Is the science which deals with the abnormal conditions in the oral cavity through the biopsy by mean of the microscope.
Biopsy: it’s the removal of tissue from a living body for the purpose of diagnosis.
Autopsy: it’s the removal of tissue from a dead body.
Biopsy:
Biopsy is the removal of a part or the whole of a lesion for the purpose of diagnostic examination.
There are several types of biopsy:
1. Surgical biopsy:
• Incisional biopsy
• Excisional biopsy
2 .Oral cytology.
3. Aspiration biopsy.
TYPES OF BIOPSY
1-Surgical:mean removal of a piece of tissue by a surgical blade, & divided into two types.
a- Excisional.
b- Incisional.
2-Fine needle aspiration: by aspirating fluid from the lesions, & is used mainly to distinguish between cystic & solid lesions
3-Needle/Core biopsy: used to take a piece of tissue from the hard lesions.
4-Exfolative cytology: by scraping the lesion, in order to examine the single cell.
Indications for biopsy:
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* Any lesion that persists for more than 2 weeks with no apparent etiologic basis.
* Any inflammatory lesion that does not respond to local treatment after 10 to 14 days.
* Persistent hyperkeratosis changes in surface tissues.
* Any persistent tumescence, either visible or palpable beneath relatively normal tissue.
* Inflammatory changes of unknown cause that persist for long periods.
* Lesion that interfere with local function.
* Bone lesions not specifically identified by clinical and radiographic findings.
* Any lesion that has the characteristics of malignancy.
Characteristics of lesions that raise the suspicion of malignancy
* Erythroplakia –lesion is totally red or has a speckled red appearance.
* Ulceration-lesion is ulcerated or presents as an ulcer.
* Duration-lesion has persisted for more than two weeks.
* Growth rate –lesion exhibits rapid growth.
* Bleeding –lesion bleeds on gentle manipulation.
* Indurations-lesion and surrounding is firm to the touch fixation.
Incisional biopsy:
* An Incisional biopsy is a biopsy that samples only a particular portion or representative part of a lesion
* If a lesion is large or has different characteristics in various locations more than one area may need to be sampled.
* Indications:
* Size limitations.
* Hazardous location of the lesion.
* Great suspicion of malignancy .
* Technique:
* Representative areas are biopsied in a wedge fashion.
* Margins should extend into normal tissue on the deep surface.
* Necrotic tissue should be avoided.
* A narrow deep specimen is better than broad shallow one.
Excisional biopsy:
* An Excisional biopsy implies the complete removal of the lesion.
* Indications:
* Should be employed with small lesions. Less than 1 cm.
* The lesion on clinical exam appears benign.
* When complete excision with a margin of normal tissue is possible without mutilation.
* Technique:
* The entire lesion with 2 to 3 mm of normal appearing tissue surrounding the lesion is excised if benign.
Oral cytology
* Developed as a diagnostic screening procedure to monitor large tissue areas for dysplastic changes.
* Most frequently used to screen for uterine cervix malignancy.
* May be helpful with monitoring post-radiation changes , herpes, pemphigus.
* The disadvantages of oral cytological procedure include:
* A- Not very reliable with many false positives.
* B-Expertise in oral cytology is not widely available.
* The lesion is repeatedly scraped with a moistened tongue depressor or spatula type instrument The cells obtained are smeared on a glass slide and immediately fixed with a fixative spray or solution.
Aspiration biopsy
* Aspiration biopsy is the use of a needle and syringe to penetrate a lesion for aspiration of i’s contents.
* Indication:
* To determine the presence of fluid within a lesion
* To ascertain the type of fluid with in lesion .
* When exploration of an intra-osseous lesion is indicated
* Aspiration:
* An 18 gauge needle on a 5 or 10 ml syringe is inserted into the area under investigation after anesthesia is obtained.
* The syringe is aspirated and the needle redirected if necessary to find the fluid cavity.
Principles of surgery:
* Anesthesia:
* Block local anesthesia techniques are employed when possible.
* The anesthetic solution should not be injected within the tissue to be removed, because it can cause artificial distortion of the specimen.
* When blocks are not possible, infiltration of local anesthesia may be used locally, but the solution should be injected at least 1 cm away from the lesion
* Tissue stabilization: specimens should be stabilized either by:
* Digital stabilization
* Specialized retractors/forceps
* Retraction sutures
* Towel clips
Homeostasis :
* Suction devices should be avoided.
* Gauze wrapped low volume suction may be used if needed.
Incision:
* Incisions should be made with a scalpel.
* They should be converging.
* Should extend beyond the suspected depth of the lesion .
* They should parallel important structures.
* Margins should include 2 to 3 mm of normal appearing tissue if the lesion is thought to be benign.
* 5mm or more may be necessary with lesions that appear malignant, vascular, pigmented, or have diffuse borders.
* Choose the most suspicious area.
* Avoid ulcers, sloughs or necrotic areas.
* In large lesions, several areas may need to be sampled.
* 10.Include every fragment for histopathological examination.
Fixation:
* The specimen should be immediately placed in 10% formalin solution, and be completely immersed.
* Fixation is necessary to prevent autolysis and destruction of the microscopic features of the specimen.
* Fixative must diffuse into the specimen completely before processing.
Margins of the biopsy
* Margins of the tissue should be identified to orient the pathologist. A silk suture is often adequate. Illustrations are also very helpful and should be included.
Surgical closure:
* Primary closure of the wound is usually possible.
* Mucosal undermining may be necessary.
. incision on the hard palate or attached gingival may be left to heal by secondary intention.
Biopsy data sheet
* A biopsy data sheet should be completed and the specimen immediately labeled. All patient’s history and descriptions of the lesion must be accurate.
Intra osseous and hard tissue biopsy
* Intra osseous lesions are most often the result of problems associated with dentition.
* Indications for intra osseous biopsy:
* Any intra osseous lesion that fails to respond to routine treatment of the dentition.
* Any intra osseous lesion that appears unrelated to the dentition .
Clinical examination
* Palpation of the area of the lesion with comparison to the opposite side.
* Any radiolucent lesion should have an aspiration biopsy performed prior to surgical exploration.
* Material obtained from the aspiration will provide valuable information about the lesion if it is:
* Solid
* Fluid filled
* Vascular
* Without contents
Principles of surgery:
* Mucperiosteal flaps should be designed to allow adequate access for Incisional& Excisional biopsy.
* Incisions should be over sound bone.
* Cortical perforation must be considered when designing flaps.
* Flaps should be full thickness
* Major neurovascular structures should be avoided
* Osseous windows should be submitted with the specimen
* Osseous perforations can be enlarged to gain access
* The tissue consistency and nature of the lesion will determine the ease of removal
* Incisional biopsies only require removal of a section of tissue
* Soft tissue overlying the lesion should be re approximated following thorough irrigation of the operative site.
* The specimen should be handled as previously described.
When to refer for biopsy
* When the health of the patient requires special management that the dentist feel unprepared to handle
* The size and surgical difficulty is beyond the level of skill that the dentist feels he / she possesses
* If the dentist is concerned about the possibility of malignancy.
Is a microbial disease of the calcified tissue of the tooth characterized by demineralization of the inorganic substances & destruction of organic substances of the tooth. it is multifactorial disease & the most common infectious diseases affecting the human race.
Pathogenesis:
require 4 main factors
1-host 2-food 3-bacteria 4-time
food +bacteria===== acid
tooth + acid ===== caries
In addition the caries affected by:
1-Intrinsic factors
a- enamel composition : there is an inverse relationship between enamel solubility & enamel fluoride concentration
b- enamel structure: in case of hypoplasia & hypo mineralization may affect the rate of progression but not initiation of caries
c- tooth morphology : deep narrow pits & fissures favor the retention of food & plaque formation .
d- tooth position, mal aligned tooth .
2-Extrinsic factors:
1- saliva: flow rate, viscosity, availability of calcium & phosphate ions, PH, & antimicrobial factors has an important value in caries.
2- diet: the quantity & quality of the diet affect the caries as e.g.. Soft sticky food .
3- systemic factors: as pregnancy may cause caries by altered dietary habit & oral hygiene.
Etiology:
Many theories were postulated in order to explain dental caries :
1-Acidogenic Theory (Miller's Theory 1890): it is the most accepted and supported theory , the acid formed from the fermentation of dietary carbohydrates by oral bacteria leads to decalcification of tooth substance with subsequent disintegration of organic matrix. Miller-isolated numerous microorganisms from the oral cavity; most important species are lacto bacillus acidophilus , streptococcus mutans, streptococcus sanguis, and streptococcus salivarius.
2) Proteolytic Theory : Main suggestion of this theory is that microorganism attack the organic part of enamel, leaving the generated acid responsible for further decalcification of inorganic part. This theory suggested that bacteria could penetrate into enamel through lamellae and inter prismatic substance.
3) Proteolysis - Chelating Theory: Organic part of the enamel is thought to be attacked first, followed by a chelating process that removes calcium from enamel and dentin without acid.
* In general, the essential requirements for development of dental caries are:
1. Plaque microorganism.
2. susceptible tooth surface.
3. bacterial substrate.
4. time for process to develop.
* Plaque: is a tenaciously adherent deposit that forms on tooth surfaces. It consists of an organic matrix containing a dense concentration of bacteria.
Etiological variables:
* Not all teeth or tooth surfaces are equally susceptible to caries. nor is the rate progression of carious lesions constant.
Clinical Classification of Dental Caries:
It is classified either according to site of attack, or according to rate of attack.
A. according to site of attack it is classified as follow:
1 . Pit and fissure caries.
2. Smooth surface caries.
3.Cemental or root caries.
4 . Recurrent caries.
P&f CA:
1. Pit and fissure caries: this is frequent in occlusal surface of premolars and molars, buccal surface of molars, lingual and palatal pits of incisors. Early caries appears as a brown or black discoloration in fissures and pits, and when inspected with dental probe, probe sticks in it. In some caries occlusal surface, where caries extends laterally into dentin, enamel above it appears chalky white in color, because of undermined caries. Caries of enamel is usually studied by ground section using a special technique, whereas in decalcified section enamel will be completely lost.
2. Smooth surface caries: this caries is frequent on proximal surface and gingival 1/3 of buccal and lingual surfaces . Initial caries or incipient caries occur just below contact point, and appear as a well-demarcated chalky white color.
3.cemental or root caries: occurs when the root face is exposed to the oral environment as a result of periodontal disease. The root face is softened and the cavities, which may be extensive, are usually shallow, saucer-shaped, with ill-defined boundaries.
4.Recurrent caries.
occurs around the margin or at the base of a previously existing restoration.
B. classification by rate of attack:
1.Rampant or acute caries: rapidly progressing caries involving many or all of the erupted teeth The rapid coronal destruction leads to early involvement of the pulp and occur mainly in children.
2.Chronic caries or slowly progressive: ordinary caries that develops slowly, and appears fully damaging in old ages, because it requires time.
3. Arrested caries:
a. arrested enamel caries:
Arrest of an a proximal smooth-surface lesion prior to cavity formation can occur when the adjacent tooth is lost so that remineralization may then occur from saliva or from the topical application of calcifying solutions.
b. arrested dentine caries:
Arrest of coronal dentinal caries may occur in lesions where there is loss of the unsupported overlying enamel following extensive lateral spread of caries along the amelodentinal junction. The loss of enamel exposes the superficially softened carious dentine to the oral environment and it is then removed by attrition and abrasion, leaving a hard, polished surface. Such dentine is deeply pigmented brown-black in color. Its surface is hyper mineralized due to re mineralization from oral fluids and has a high fluoride content.
Arrested lesions of root caries have a similar clinical appearance and develop in a similar manner following loss of the superficially softened cementum.
* Histopathology of enamel caries:
* the established early lesion (white-spot lesion) in smooth surface enamel caries is cone-shaped, with the base of the cone on the enamel surface and the apex towards the amelodentinal junction. The shape is modified in pit and fissure caries with base of the cone towards the amelodentinal junction this depend on the direction of enamel prisms. Before destruction of enamel, several zones can be distinguished in ground section.
1.translucent zone: it is more porous than normal enamel and contain 1 % by volume of spaces compare with 0.1% pore volume in normal enamel. In this demineralization has taken place (magnesium and carbonates are dissolved).
2.dark zone: this zone contain 2-4% by volume of pores ,some re mineralization happens due to re precipitation of minerals lost from translucent zone.
3.body of the lesion : pore volume of 5 and 25%.
4.surface zone: remain relatively normal despite subsurface loss of mineral, because it is an area of active re precipitation of mineral derived both the plaque and from that dissolve from deeper areas of lesion as ions diffuse outwards
* Histopathology of dentin caries:
Dentine differs from enamel in that it is a living tissue and as such can respond to caries attack. It also has high organic content. Ground and decalcified sections show a zoned lesion in which four zones are present.
1.Zone of sclerosis: the sclerotic or translucent zone is located beneath and at the site of carious lesion and is regarded as a vital reaction of odontoblasts to irritation.
2. zone of de mineralization: the inter tubular matrix is mainly affected by acid diffusing from pioneer bacteria
3. zone of bacterial invasion: the bacteria extend down and multiply within the dentinal tubules. The walls of tubules are softened and distended by Proteolytic activity and multiplying bacteria resulting in areas of liquefaction foci parallel to the direction of tubules.
4. zone of destruction: liquefaction foci enlarge and increase in number. Clefts containing bacteria and necrotic tissue also appear at right angle to dentinal tubules which is called transverse clefts.
Protective reactions of dentine and pulp under caries:
The reactions in dentine are mainly due to odontoblast activity . These reactions are not specific and may be provoked by other irritants such as attrition, erosion, abrasion and restorative procedures. Reactionary changes in dentine develop significantly under slowly progressing caries by formation tertiary or irregular dentine .
Clinical Classification of dental caries:
1-according to the sites:
a-pit & fissure.
b-smooth surface.
c-root or cementum.
2-according to rate or severity:
a-acute (rampant).
b-chronic.
c-arrested.
3-whether is new or around a restoration:
a-primary.
b-secondary.
NOTES: the shape of pit & fissure caries in enamel appears as triangle, the apex toward the surface & the base toward the DEJ , while in the dentin the triangle become inverted .
In the smooth surface the enamel caries also appears as triangle but the base toward the surface
dentin caries appear as that in pit & fissure caries.
* Clinically,
* the caries appear as chalky lesion then progress to darker color as brown or black
* toothache; sensitivity to hot or cold food or drinks
* Cementum caries:, always affect the older population ,specially whose suffering from gingival recession which enhance the accumulation of dental plaque on the exposed area.
. Arrested caries: this mean the cessation of caries in area that previously undergo caries development
* Recurrent caries: mean caries that arises around an existing restoration, & this mainly due to marginal leakage & then lead to food stagnation.
Clinical diagnosis of dental caries:
1-Visual inspection:
The tooth should be clean ,dry and well illuminated during visual examination to obtain maximum information.
2- Explorer .
Use of sharp explorer.
3-Radiographic method.
4- Fiberoptic transilluminator. (FOTI)
5-Caries detector dye.
Treatment:
*Changing the micro flora, using agents such as topical chlorhexidine and topical fluoride.
*Reducing the amount of dietary sucrose.
* Adding fluoride, particularly through daily tooth brushing .
*Increasing salivary flow, using mechanical stimulation during vigorous chewing or by using drugs .
PULPITIS:
The dental pulp is the loose C.T., containing blood vessels, lymphatic, nerves & undifferentiated C.T, cells.
Pulpitis: an inflammation of the pulpal tissue that may be reversible or irreversible.
Like any another C.T., pulpitis is characterized by redness, swelling, fever, pain.
*However, is a unique one, why
1-surrounded by hard tissue.
2-small apical foramen.
*ETIOLOGY
1-bacterial cause: caries, fracture, bacteremia, periodontal pocket
2-physical cause: sever thermal change (cavity preparation), large metallic restoration
3-trauma: from occlusion, like attrition or accident
4-chemical cause: filling (amalgam, composite), bases, disinfectant, eugenol
Classification of pulpitis
Classified into:
1-Reversible pulpitis(hyperemia).
2-Acute pulpitis.
3-Chronic pulpitis.
4-pulp polyp (chronic hyperplastic pulpitis).
1*Reversible pulpitis
Clinically
1-sharp pain & respond to sudden changes in temperature .
2-pain disappear as the stimuli removed.
3-last less than 20 min.
4-easily localized & unaffected by body position.
*Histopathology:
show dilatation of blood vessels(hyperemia)with RBC &WBC
extravasations &edema.
*Treatment
protection of the pulp from further stimulation,& placing sedative dressing for several weeks.
2*Acute pulpitis: may occur as a sequel of focal reversible pulpitis or occur due to acute exacerbation of chronic pulpitis.
clinically
1-occurs in a tooth with large carious lesion or defective margin of a restoration
2-pain is sever throbbing at time lancination keeping the patient awake.
3-pain will be spontaneous & continuous, even when stimuli removed.
4-pain lasts for a prolonged period longer than 20 min.
5-difficult to localized , & the pain initiated when the patient reclines (sleep) duo to increase blood pressure.
Histopathology
1-Show, vascular dilatation, edema & high amount of bacteria with
PML which lead to abscess formation by the macrophage action
2-odontoblast undergo degeneration at the area of inflammation.
Treatment: pulpotomy, root canal, extraction.
3*Chronic pulpitis: develop as a result of acute pulpitis, or develops as chronic once.
Clinically
1-spontaneous dull, itching pain.
2-increased pain threshold (need strong stimuli) due to degeneration of the nerve fibers.
3- the pain lasts for about 2 h.
Histopathology: show
1-infiltration of pulp by various amount of chronic inflammatory Cells mainly lymphocytes & plasma cells.
2-dilatation of capillaries & collagen fiber formation around the inflamed area.
Treatment:
Root canal or extraction
4*Chronic hyperplastic pulpitis: is a rare condition that is confined to the molars of children. It result from acute caries in young teeth that rapidly reaches the pulp before it becomes completely necrotic
Clinically:
1-polyp in the center of the tooth cavity
2-occurs in a tooth with large carious lesion
3-not sensitive to touch, due to little nerves in hyperplastic tissues
4-bleed easily
5-may confused with hypertrophic gingival polyp
Histopathology:
1-the polyp is a mass of granulation tissue
2-sometimes,the polyp covered by a layer of stratified sq.
Epith.
Treatment:
Root canal or extraction.
Essential properties of cariogenic bacteria:
1- Acidogenic.
2- Able to produce a PH low enough(usually PH below 5) to decalcify tooth substance.
3- Able to survive and continue to produce acid at low level of PH.
4- Possess attachment mechanisms for firm adhesion to smooth tooth surfaces.
5- Able to produce adhesive ,insoluble plaque polysaccharides.
Pulp necrosis
Pulpal necrosis is the term applied to pulp tissue that is no longer living.
Pulp necrosis results due to cut off of apical blood vessels as a result of blow or trauma without caries (coagulative ) .
or due to a sequel of caries ( liqueficative necrosis).
clinically:
1-symptomless or slight pain, specially in multirooted teeth.
2-discoloration of the tooth when the product of necrotic pulp pass into the dentinal tubule giving the tooth a greenish – black color.
3-bad odors smelled .
Age change in the pulp:
1-the size of pulp reduced.
2-decrease in vascularity.
3-reduction in cellularity &increase in collagen fibers.
*these changes may allow change in the response of the pulp tissue to injury & impair the healing potential.
PERIAPICAL DISEASES
mean extension of pulp inflammation Beyond the tooth root apex.
the possible changes that may occur around non vital tooth apex are:
Bacterial cause--- non vital tooth ---- non bacterial cause
acute ------ -- per apical abscess---------- chronic
This interrelation ship depends on :
1- number & virulence of the microorganism that invade the area
2- types & severity of the irritation ( mechanical or chemical )
3- host defense
4- duration of irritation.
Etiology:
1-Pulp infection due to caries (bacterial)
2-Trauma, either due to blow on the tooth or due to occlusal trauma which result from a high restoration or less frequently associated with bruxism, or from orthodontic treatment
3-Endodontic treatment, mechanical instrumentation through the root canal treatment, as well as chemical irritation from root filling materials.
Periapical abscess: acute or chronic suppurative process in the periapical area .
It can develop directly as acute or chronic depending on the host defense
some time the chronic one can transformed to acute one if invaded by more virulence microorganism
* Clinically:
* 1-sever pain in acute,&milder in chronic
* 2-pain is increase on percussion
* 3-extrusion of the tooth from its socket
* 4-the tooth dose not respond to hot &cold
stimulation .
5-fever with regional lymphadenitis.
Radiographic appearance
* In acute abscess ,may be no change but sometimes only slight widening of PdL at the root apex seen.
* In chronic one,clearly defined radiolucency around the root observed
Histopathology
* Vascular dilatation of the PdL &adjacent bone marrow.
* The abscess consists of a sea of PML with inflammatory exudate ,cellular debris ,necrotic tissue &bacterial colonies.
Periapical Granuloma (P.A.G): it’s the most common lesion in dental clinic and as a sequel of pulpitis , it represent long standing inflammation in the bone at the root apex,
is mass of granulation tissue formed due to the response of mild & chronic inflammation .
Clinically:
* 1-may be symptomless,unless invaded by virulent m.o. & cause acute inflammation
* 2-sensetive to percussion, due to edema & inflammation in PdL
* 3-tooth slightly elongated in its socket.
* 4-non vital tooth, due to pulp necrosis
Radiographically:
* Appear as oval or round radiolucency with well demarcation.
* When undergo acute exacerbation will have a less distinct line.
* Sometimes in a long standing P.A.G. finding such as hypercementosis or resorption .
It is rare, representing less than 1% of all odontogenic tumors. It originates
from epith. Rest of dental lamina & or the reduced enamel epith.
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Clinically:
Occurs in patient between 20-60 Y age.
Occurs as either central (intraosseous) or peripheral (extraosseous)
lesion.
Central one like the common ameloblastoma, mostly occur in the molar
area followed by premolar area.
Both jaw can affected
The tumor presents as a slowly growing painless mass
Peripheral one, most commonly occurs in the anterior part of the mouth,
it represents as a superficial soft tissue swelling of the gingiva.
Radiographically:
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Tend to occur as a diffuse radiolucency with faint flecks of calcified
structures.
But may appear as a mixed of radiolucency & opacity
The lesion may occur over impacted or displaced teeth,
Differential diagnosis in radiograph include:
Dentigerous cyst, adenomatoid odontogenic tumor & ameloblastic
fibro-odontoma.
Histopathology:
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It is pathognomonic
Consists of sheets of polyhedral cells with prominent intercellular
bridges.
The epith. Cells may show pleomorphism, multinucleation, prominent
nucleoli
In addition there is pools of homogenous eosinophilic material found
1within & between the epith. Sheets along with spherical calcifications
are distributed.
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The nature of the eosinophilic deposits believed to be a form of
amyloid.
The tumor is not encapsulated
Treatment:
By radical surgical removal
Adenomatoid odontogenic tumor (AOT):
It is uncommon tumor, it’s
name reflects the characteristic histologic feature of duct like structures
spread throughout the epith. Component.
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Clinically:
Is usually associated with an impacted tooth & is often cause failure of
tooth to erupt.
The lesion occurs during the 2 nd decade of life, commonly in patients
14-15 Y of age
It most often occurs in the anterior mouth, usually around an impacted
cuspid, but sometime associated with molars
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The lesion appear as an area of swelling over an unerupted tooth.
Radiographically
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Appear usually as unilocular radiolucency with well demarcated
borders & contains a tooth.
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The lesion similar to that found in a Dentigerous cyst, but by a good
examination reveals that differs from a Dentigerous cyst, in which the
radiolucency extend apically beyond the C.E.J.
Histopathology:
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AOT composed of an outer fibrous capsule surrounding a nodular mass
of epith.cells.
The epith., cells are spindle in shape scattered throughout the lesion
The characteristic feature, is the formation of duct like structure by
cuboidal or columnar cells & containing eosinophilic materials.
Treatment:
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By surgical removal & recurrency is rare
Calcifying odontogenic cyst (Gorlin cyst ):
is an uncommon odontogenic lesion.
Because the lesion often appears as a solid noncystic lesion, although it may
appear as cystic & solid part, it’s classified as an tumor.
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Clinically:
Can occur in any part of the jaw, but mostly occur anterior to the
molars.
Occur at any age but a peck incidence in the 2 nd decade of life.
Can occur extraosseously or intraosseously.
The extraosseous one appear as focal localized swelling, where as
intraosseous lesions produce a generalized expansion of the buccal &
lingual cortices.
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The lesion is usually painless.
Radiographically
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Most commonly appear as a well circumscribed unilocular
radiolucency, containing flecks of radiopacity.
Histopathology
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Varies, some lesions have a cystic center, & others are solid.
The epith., component consists of an outer layer of palisade columnar
cells & an inner layer resemble the stellate reticulum.
The characteristic feature of the lesion is the presence of eosinophilic
epith., cells without nuclei, known as Ghost cells, present within the
stellate reticulum areas.
Multiple spherical & diffuse calcifications within the epith., & the C.T.,
are also included.
Treatment:
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Required conservative treatment, usually enucleation. Recurrences are
uncommon
Squamous odontogenic tumor (SOT):
was first described in 1975. the lesion can be multifocal & have aggressive
potential if not treated in it’s early stages.
3SOT may originate from the remnants of the dental lamina, rest of Malassez,
or overlying epith.
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Clinically:
Usually occur anterior to the molars
Are affect both the max, & mand
It occur at any age, with a peak incidence in the 3 rd decade
Represent as either a painless swelling or as looseness of teeth in the
region
Radiographically
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Appear as either unilocular or multilocular radiolucency, with tooth
separation
Histopathology
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Consists of rounded & elongated islands of normal appearing stratified
squamous epith, against a cellular fibrous C.T., background.
The epith, islands have a basal cell layer of inactive-appearing cuboidal
cells.
The remainder of the islands are composed of mature intermediate cell
with prominent desmosomal bridge, with central microcyst in many
islands
Treatment:
Small lesions treated with local curettage, while large one require block
resection.
4odontogenic myxoma
It is a special tumor for the jaws locally aggressive arise from dental
mesenchymal tissue. It is infiltrative (not capsulated) benign tumor.
Clinically:-
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It occurs in young age group, most commonly involve the mandible,
appear as a painless swelling or asymptomatic. The maxillary lesion will
arise into the sinus while the mandibular lesion found in molar, premolar
area & often extend into ramus .
Radiograph
- Multilocular radiolucency with scalloped margin, soap-bubble
appearance or honey comb appearance (resemble ameloblastoma).
Histopathology
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Grossly it is a gelatinous tissue, microscopically consist of a scanty
spindle shape irregular cells with fine long anastomosing processes, and a
mucoid material & few collagen fibers & epithelial rest. The margins of
the lesion are ill defined & the bone trabeculae show resorption. They
will give difficulty in removal of the lesion . Some cases contain an
odontogenic epithelium.
Treatment & prognosis
- It is a benign tumor with infiltrative properties & not capsulated,
therefore, bone resection & curettage is the treatment, it is associated
with recurrence.
- It is important to remove all gelatinous tissue to reach an intact area in nts
of amorphous cementoid or dentinoid calcification may be seen between
the epithelium .
Treatment:- Enucleation, no recurrence .
5Odontoma
Odontomes are dental hamartomas containing the calcified dental tissue.
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Odontoma is a hamartomatous lesion found over unerupted teeth
containing enamel, dentine, pulp and cementum in either normal tooth
shape (compound) or abnormal tooth shape (complex).
- It represents nearly 70% of whole odontogenic tumors, complex
odontoma is more commonly occurred in posterior mandible than
maxilla, as asymptomatic swelling.
- Compound odontoma more commonly occurs in anterior maxilla than
in mandible and as a symptomatic swelling either over the crowns of
unerupted teeth or between the roots of erupted one .
Radiograph
- Unilocular radiolucency containing multiple radiopaque structures that
resemble small teeth , compound odontoma may contain as few as 2-3
tooth like structures or as many as 20-30 tooth like structures.
- Complex odontoma in posterior part of mandible on impacted tooth and
may reach several (cm) in size ,appear as solid radiopaque mass, lesions
are unilocular & separated from normal bone by distinct radiolucent line.
Individual tooth like structure is absent.
Histopathology
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Enamel, dentine, pulpal tissue or tooth like structure of compound
odontoma are arranged in an ordinary pattern in a fibrous capsule.
Complex odontoma differs by being composed of single disorganized
mass of enamel, dentine & pulp within abnormal tooth shape .
Treatment:- Enucleation from surrounding bone.
Are group of tumors occurs only in the jaw bones. These tumors arises from
the cells of the tooth germ & associated mesenchymal cells during the
dentinogenesis ( tooth development ).
C l a s s i f i c a t i o n
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I-Benign odontogenic tumor:
A-Epithelial:
1- Ameloblastoma 2- Pindborg tumor
3- Gorlin cyst
4- Adenomatoid odontogenic tumor
5- Squamous odontogenic tumor
B- Mesenchymal:
1- Odontogenic fibroma
2- Odontogenic myxoma
3- Cementoblastoma
4- Dentinoma
C-Mixed:
1-Ameloblastic fibroma
3- Odontoma
2- Ameloblastic fibro-odontoma
II- Malignant odontogenic tumor:
1- Ameloblastic carcinoma 2- Odontogenic carcinoma
3- Primary intra-osseous carcinoma
Benign epithelial odontogenic tumor:
* Ameloblastoma:
• Is a benign neoplasm, can arise from any of the multiple sources of
odontogenic epith. That remain within the alveolar bone& soft
tissue these include:
• a- remnants of dental lamina (rests of Serres)
• b- reduced enamel epith.
• c- rests of Malassez
• d- basal cell layer of overlying surface epith.
1•
However, three clinical types of Ameloblastomas are generally
recognized:
• 1- common ameloblastoma
• 2- unicystic ameloblastoma
• 3- peripheral ameloblastoma
Common Ameloblastoma:
is the most common form of this lesion, nearly occur in patients over 25
years of age.
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Clinically:
The lesion may cause extensive deformities of the mand. & max.
It is most commonly located in the mand., with 3⁄4 occurring in the
molar & ascending ramus area.
The tumor is slowly growing, locally aggressive, allows time for
periosteum to produce a thin shell of bone
This thinned outer shell of bone cracks easily when palpated (
diagnostic sign) known as ( eggshell cracking).
•
Radiographically:
• Mostly appear as multilocular radiolucency (soap bubble
appearance) with ill defined border.
Histopathology:
there are two main histological pattern:
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A- Follicular pattern:
It consist of epith. In the form of islands & strands against a
background stroma of fibrous C.T.
The epith. arrangement have an outer border composed of the palisades
ameloblasts-like cells with reversed polarization of nucleus.
The remainder of the islands consist of loosely arranged & widely
separated triangular shaped cells that are similar to those of the stellate
reticulum.
In some islands the stellate-like cells of the central areas degenerate,
forming central microcysts “cystic ameloblastoma”, in other islands the
central cells are transformed to squamous cells that produce keratin
within individual cell or in the form of keratin pearls “acanthomatous”.
2Sometimes the central cells of the island appear swollen & densely
packed with eosinophilic granules, this pattern termed “granular cell
variant”
B- Plexiform pattern:
this type consists of epithelium that proliferates in a fishnet or mesh
arrangement
large & small cyst like areas are present
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The tumor is not encapsulated.
Treatment:
The best chance of completely removing the lesion is with marginal
block resection.
However, recurrency may be reported.
Unicystic ameloblastoma:
•
Most of these lesions are found within the lining of a large unilocular
cyst, commonly associated with the crown of an impacted tooth in a
young patient; specially the Dentigerous cyst.
•
In many lesions, areas of normal cystic lining are adjacent to the
ameloblastomatous tissue, in other lesions, normal epith. Lining can’t
be found.
clinically
• Most commonly occur in patients who are 15-20 Y of age, & rarely
found in patients up to the age of 40 Y.
• With few exceptions, the lesion mostly occurs in a Dentigerous cyst
relationship & is usually associated with a severely displaced 3 rd
molar.
• The lesion mostly occur in the mand. Than in the max.
•
•
Radiographically:
Usually well demarcated radiolucency & the tooth is often present
within the radiolucency.
Histopathology:
• The lesion composed of island of epith. which may be follicular or
plexiform within the epith. lining of the cystic wall.
3•
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Some lesions will contain areas in which the epith. Is thickened with
papillary projections extending into the lumen, this called
“intraluminal unicystic ameloblastoma”
When the thickened lining penetrates the adjacent capsular tissue,
it’s termed “mural unicystic ameloblastoma
Treatment:
Either by enucleation or marginal resection.
Peripheral ameloblastoma (extraosseous):
•
Is a very uncommon odontogenic tumor that histologically resembles
the intraosseous common ameloblastoma but is limited to the soft
tissues of the gingiva.
•
It is believed to arise directly from the overlying epith. or from the
remnants of the dental lamina located in the extraosseous tissue.
Clinically
•
Usually appear as a firm sessile nodules of the gingiva, & they have a
smooth surface & normal coloration
Histopathologically:
•
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The tissue is composed of islands & strands of odontogenic epith.,
usually resembling the follicular pattern of intraosseous common
ameloblastoma.
The epith. Islands commonly exhibit the acanthomatous variant with
central areas of keratin formation or the cystic pattern
Treatment:
By local incision
Bone cells & their precursors react to the influences of circulating
hormones & other regulating substances. Thus the bones are
particularly sensitive to physiologic & genetic changes that can result
in alterations to their structure & mineral content.
1- Paget’s disease (Osteitis deformans)
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Is a focal alteration in the histology & morphology of bone, result
from uncoordinated increase in the osteoclastic & osteoblastic
activity of the bone cells.
Confined to one bone or multiple bones throughout the body.
Initially the process is dominated by bone resorption followed by
excessive bone formation, result in increase in volume but a
decrease in strength.
This uncoordinated function of osteoclast & osteoblastic activity
characterized by numerous reversal lines that give the bone a
characteristic mosaic pattern under the microscope.
The etiology is still unknown, but intranuclear viral inclusion
bodies have been found within some osteoclast cells.
Clinical features
Asymptomatic, seldom found in patients younger than 40 years,
& being more common in the western countries.
The disease may involved one bone (Monostotic) or multiple
bones (Polyostotic), when multiple bones are involved, there will
be some degree of incapacity, pain, & joint disease.
When involve the skull, a frequent symptom is a gradual increase
in hat size caused by increased cranial circumference. But the
serous concern is the involvement of the base of skull, in this
case diminish in the various foramens can result in compression
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of the spinal cord & cranial nerves lead to paralysis & loss of
hearing & sight.
in the jaws, the maxilla is more commonly involved than the
mandible, the first sign is spaces between the teeth, & the denture
may become tight & uncomfortable within the time.
The most important investigation is alkaline phosphates level,
which give information of osteoblastic activity. Normal level =
63 IU/ L, but in Paget’s disease may reach 1000-5000 IU/L in
polystotic & 200-500 IU/L in monostotic one.
Elevation of urinary hydroxyproline level indicate the increase
bone resorption (osteoclast activity).
Alyhough considerable Ca ++ loss from the bone occurs ,serum
Ca ++ usually remain within normal levels.
The complications, include, bone fracture, heart failure &
sarcoma
Radiographic appearance
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Varies extensively, in the early osteolytic stage the disease
exhibit a diffuse radiolucency, later on there is a diffuse
2radiopacity.
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The most common picture is a mixed radiolucent / radiopaque
resembling “cotton wool” in a diffusely radiolucent area.
The maxilla & mandible are often enlarged, with loss of the
lamina dura & hypercementosis of the roots of the teeth in the
area.
histopathology
Consist of an increase in osteoclasts, osteoblasts, & blood vessels
& a replacement of the normal bone by a less dense bone having
a mosaic appearance.
Treatment
the most common effective therapeutic agents are Calcitonin &
Diphosphonates such as Disodium etidronate.
These compound inhibit bone resorption, this provides the bone
forming cells to produce stronger, less fragile bone.
However, the treatment does not stop the lesion but does slow it.
Surgery is avoided because the diseased bone is prone to
hemorrhage & prone to a difficult to manage osteomyelitis.
Surgery is used only to relive sever pain caused by pressure on
nerves & spinal cord.
32- Hyperparathyroidism
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Loss of bone mineralization ( osteoporosis ) due to increase in the
PTH secretion ( primary ) or increased demand for serum Ca ++ (
secondary) mostly in renal disease.
The disease lead to multiple systemic complications, loss of
alveolar bone architecture, & occasionally giant cell tumor
(
brown tumor ).
Clinical features
Mostly in patients over 60 years of age & female to male ratio 2-
1.
The disease is mostly asymptomatic.
Hypercalcemia is the most common manifestation & the disease
diagnosed when serum Ca ++ is above the normal range of 8.6-
10.4 mg/100 ml, associated with decrease serum phosphates
level.
Serum alkaline phosphates & urinary hydroxyproline are normal,
but urinary phosphate may be elevated.
Radiographic appearance
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Generalized reduced bone density
mottled areas of radiolucency.
( osteoporosis ) or
In the mandible & maxilla, the normal trabecular pattern may be
lost, with lack of distinctness of lamina dura in late stage.
4•
A large radiolucency may be present, indicate giant cell tumor.
Histopathology
Non specific, However, the lesion consisting of increased osteoclastic
activity, thinning of trabecular bone, & wide zones of osteoid with
activated osteoblast. Also some replacement of marrow with loose
C.T. may occur.
Treatment
Treat the cause & dietary phosphate supplements, & Vit. D
supplements have been beneficial.
3-Osteopetrosis
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Is a generalized hereditary condition in which the bones become
more denser than normal due to excessive bone mineralization,
resulting in altered stature, frequent fracture, lack of bone
marrow hematopoietic function, & a tendency for sever
Osteomyelitis of the jaws.
Clinically
Early symptoms in infancy include difficulties in breathing &
hearing due to oversized facial & mastoid bones.
Followed by functional defects in the ocular & trigeminal nerves
as a result of compressed by sclerosis of the foramina of the base
of skull.
Delayed eruption of teeth is a common oral finding, & healing is
difficult after extraction.
5•
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Depletion of platelets, leukocytes, & erythrocytes, make a
tendency for spontaneous hematomas, multiple infections, &
anemia.
In sever cases the patient die from complications of marrow
depletion before 10 years of age.
Radiographically
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The disease characterized by a generalized increase in bone
density with obliteration of normal internal architecture.
Histopathology
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The bone is dense & sclerotic, with most of the marrow spaces
replaced with bone or fibrous tissue.
The bone is somewhat avascular & in some cases islands of
calcified cartilage are found, which normally resorbed during
development.
6•
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Treatment
Depends on the condition. Either by bone marrow
transplantation, or by oral Calcitriol combined with a calcium
deficient diet.
4- Osteogenic imperfecta
is a bone disease characterized by defective matrix formation &
lack of mineralization, resulting in multiple broken bone, blue
sclera of the eye, & associated dentinogenesis imperfecta
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Clinically
The neonatal form is lethal, the patients suffering multiple
fractures during gestation & delivery.
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Patients with moderate type, have blue sclera, & dentinogenesis
imperfecta.
X-Ray
show large areas of cyst like radiolucency, multiple fractures & healed
fractures are present. The teeth exhibit bulbous crowns with shortened
roots.
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Histopathology
The bone show markedly thinned bone cortices composed of
immature woven bone
Treatment
No therapy is capable of altering the course of the disease.
Developmental disturbances of the oral region are discussed under
three categories:
1- disturbances affecting teeth
2- disturbances limited to soft tissue
3- disturbances affecting bone.
Disturbances affecting the teeth
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A -Disturbances in the size:
1- Microdontia:
Mean tooth or teeth smaller than the normal, either localized or
generalized.
In generalized it’s either true or relative:
True: small teeth with normal size jaw bone & this occur in
dwarfism.
Relative: the jaw bone is larger than normal which lead to
spacing between teeth giving picture of false microdontia.
*in localized microdontia, usually one tooth affected & mostly in
lateral incisor (peg lateral) & max third molar.
2- Macrodontia:
Mean tooth or teeth larger than the normal, it may be generalized
or localized
In generalized it’s either true or relative
True: large teeth in normal jaw bone size, occur in Gigantism.
Relative: normal teeth in small size jaw, cause crowding of teeth
& give false picture of macrodontia.
*in localized macrodontia, usually affect one side of jaw such in
hemifacial hypertrophy.
1B- Disturbances in number:
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1- Anodontia:
Complete absence of teeth (deciduous & permanent)
It usually occurs in association with a generalized disorder such
as hereditary ectodermal dysplasia. Therefore, all tissues derived
from ectoderm are absent such as teeth, hair follicle, sweat
gland, sebaceous gland.
The patient suffer from smooth, thin & dry skin, can’t tolerate
heat due to absence of sweat glands.
However, sometimes some teeth are present such as cuspids &
molars
2- Hypodontia: (partial anodontia)
Mean congenital absence of one or more teeth.
Although any tooth can be congenitally absent, but the most
common are the 3 rd molars, followed by the max, lateral incisors
& the 2 nd premolars
Familial tendency for congenitally absent teeth is recognized.
3- Supernumerary teeth:
Teeth in excess of the normal number
They are more common in max, than in the mand
A supernumerary tooth located between max, central incisors
referred to as a mesiodens. The 4 th molar called paramolar.
A supernumerary tooth may resemble the corresponding normal
tooth, or it may be smaller or conically shaped, bearing little or no
resemblance to it’s normal counterpart.
Supernumerary teeth may be single or multiple & erupted or
impacted
Multiple supernumerary teeth, which are generally impacted, are
characteristically seen in Cleidocranial dysplasia.
2C- Disturbances in eruption:
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1- Premature eruption:
Teeth erupt earlier than it’s normal eruption time
Usually involves only one or two teeth, most commonly the
deciduous mand, central incisors, & usually are part of the
normal complement of deciduous teeth, they are not
supernumerary tooth & should therefore be retained if possible.
We have 2 types:
Natal teeth: deciduous teeth present at birth
Neonatal teeth: deciduous teeth that erupt during the 1 st 30 days
of life.
2- Delayed eruption:
Teeth fail to erupt at it’s normal time & it may be associated with:
Systemic conditions like, Cleidocranial dysplasia, cretinism &
rickets.
Local conditions like, gingival fibromatosis, insufficient space in
the dental arch, abnormal position of tooth germ, &
supernumerary teeth which prevent eruption of original one.
3- Impacted teeth:
Teeth that continue to form within bone but fail to erupt, the
causes same that of delayed eruption
We have 3 types:
*complete impaction: impacted tooth that is totally surrounded by
bone
*partial impaction: the tooth partly in bone & partly in soft tissue
*retained (embedded) tooth: teeth that fail to erupt due to
unknown reason
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D- Disturbance in shape
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1- Dilaceration: A sharp bend or angulation of the root portion of
a tooth. Cause difficulty in extraction & root canal therapy.
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2- Taurodontism: A molar with an elongated crown & apically
placed furcation of the roots, resulting in an enlarged rectangular
coronal pulpal chamber, (bull like) teeth.
There is no constriction at the area of crown & root
(cementoenamel junction).
3- Dens invaginatus: A focal area of the crown of a max, lateral
incisor is folded inward (invagination) which lead to small
opening & accumulation of food debris, then caries. Sometimes
this condition called “dens in dentin” which mean tooth inside the
tooth.
4- Dens evaginatus: Is a developmental abnormality that
primarily affects premolars. It’s characterized by the
development of an abnormal nodular or globe-shaped projection
appearing as an extra cusp centrally located on the occlusal
surface between the buccal & lingual cusps of premolars,
although any tooth may be involved
5- Talon cusp: A form of supernumerary cusp, typically seen on
the lingual aspect of max, incisors, is called a talon because it’s
resembles an eagle’s talon.
6- supernumerary roots: Additional roots, more than the expected
number, are termed supernumerary roots. This is common in
mand, premolars & cuspids.
7- Gemination: Is a developmental anomaly that affects anterior
teeth, they result from partial division “twinning” of a single tooth
germ, resulting in a tooth with two separated or partly separated
crowns & a single root & root canal.
8- Fusion: Result from the union of two normally separated tooth
germs, it can be complete or incomplete.
* we can differentiate between gemination & fusion clinically by
counting the teeth in each arch, if one tooth is missing mean
fusion, but if with normal number mean gemination.
9- Concrescence: Is a type of fusion of two teeth through
cementum. The condition is thought to occur as a result of
4traumatic injury to the area or crowding where interseptal bone is
lost, allowing close proximation of the tooth roots.
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10- Hypercementosis: Excess cementum at the root area
(usually at the apex) & known as bulbous root.
11- Cervical enamel projection: A focal apical extensions of the
coronal enamel beyond the cervical margin (cementoenamel
junction) & onto the root of the tooth.
Their clinical significant is that they could contribute to
periodontal pocket formation.
12- Enamel pearls: Globular droplets of enamel that present
usually at the bifurcation or trifurcation area of the molars; it’s
also called Enameloma.
Are group of tumors occurs only in the jaw bones. These tumors arises from
the cells of the tooth germ & associated mesenchymal cells during the
dentinogenesis ( tooth development ).
C l a s s i f i c a t i o n
•
I-Benign odontogenic tumor:
A-Epithelial:
1- Ameloblastoma 2- Pindborg tumor
3- Gorlin cyst
4- Adenomatoid odontogenic tumor
5- Squamous odontogenic tumor
B- Mesenchymal:
1- Odontogenic fibroma
2- Odontogenic myxoma
3- Cementoblastoma
4- Dentinoma
C-Mixed:
1-Ameloblastic fibroma
3- Odontoma
2- Ameloblastic fibro-odontoma
II- Malignant odontogenic tumor:
1- Ameloblastic carcinoma 2- Odontogenic carcinoma
3- Primary intra-osseous carcinoma
Benign epithelial odontogenic tumor:
* Ameloblastoma:
• Is a benign neoplasm, can arise from any of the multiple sources of
odontogenic epith. That remain within the alveolar bone& soft
tissue these include:
• a- remnants of dental lamina (rests of Serres)
• b- reduced enamel epith.
• c- rests of Malassez
• d- basal cell layer of overlying surface epith.
1•
However, three clinical types of Ameloblastomas are generally
recognized:
• 1- common ameloblastoma
• 2- unicystic ameloblastoma
• 3- peripheral ameloblastoma
Common Ameloblastoma:
is the most common form of this lesion, nearly occur in patients over 25
years of age.
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Clinically:
The lesion may cause extensive deformities of the mand. & max.
It is most commonly located in the mand., with 3⁄4 occurring in the
molar & ascending ramus area.
The tumor is slowly growing, locally aggressive, allows time for
periosteum to produce a thin shell of bone
This thinned outer shell of bone cracks easily when palpated (
diagnostic sign) known as ( eggshell cracking).
•
Radiographically:
• Mostly appear as multilocular radiolucency (soap bubble
appearance) with ill defined border.
Histopathology:
there are two main histological pattern:
•
•
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•
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A- Follicular pattern:
It consist of epith. In the form of islands & strands against a
background stroma of fibrous C.T.
The epith. arrangement have an outer border composed of the palisades
ameloblasts-like cells with reversed polarization of nucleus.
The remainder of the islands consist of loosely arranged & widely
separated triangular shaped cells that are similar to those of the stellate
reticulum.
In some islands the stellate-like cells of the central areas degenerate,
forming central microcysts “cystic ameloblastoma”, in other islands the
central cells are transformed to squamous cells that produce keratin
within individual cell or in the form of keratin pearls “acanthomatous”.
2Sometimes the central cells of the island appear swollen & densely
packed with eosinophilic granules, this pattern termed “granular cell
variant”
B- Plexiform pattern:
this type consists of epithelium that proliferates in a fishnet or mesh
arrangement
large & small cyst like areas are present
•
•
•
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The tumor is not encapsulated.
Treatment:
The best chance of completely removing the lesion is with marginal
block resection.
However, recurrency may be reported.
Unicystic ameloblastoma:
•
Most of these lesions are found within the lining of a large unilocular
cyst, commonly associated with the crown of an impacted tooth in a
young patient; specially the Dentigerous cyst.
•
In many lesions, areas of normal cystic lining are adjacent to the
ameloblastomatous tissue, in other lesions, normal epith. Lining can’t
be found.
clinically
• Most commonly occur in patients who are 15-20 Y of age, & rarely
found in patients up to the age of 40 Y.
• With few exceptions, the lesion mostly occurs in a Dentigerous cyst
relationship & is usually associated with a severely displaced 3 rd
molar.
• The lesion mostly occur in the mand. Than in the max.
•
•
Radiographically:
Usually well demarcated radiolucency & the tooth is often present
within the radiolucency.
Histopathology:
• The lesion composed of island of epith. which may be follicular or
plexiform within the epith. lining of the cystic wall.
3•
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Some lesions will contain areas in which the epith. Is thickened with
papillary projections extending into the lumen, this called
“intraluminal unicystic ameloblastoma”
When the thickened lining penetrates the adjacent capsular tissue,
it’s termed “mural unicystic ameloblastoma
Treatment:
Either by enucleation or marginal resection.
Peripheral ameloblastoma (extraosseous):
•
Is a very uncommon odontogenic tumor that histologically resembles
the intraosseous common ameloblastoma but is limited to the soft
tissues of the gingiva.
•
It is believed to arise directly from the overlying epith. or from the
remnants of the dental lamina located in the extraosseous tissue.
Clinically
•
Usually appear as a firm sessile nodules of the gingiva, & they have a
smooth surface & normal coloration
Histopathologically:
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The tissue is composed of islands & strands of odontogenic epith.,
usually resembling the follicular pattern of intraosseous common
ameloblastoma.
The epith. Islands commonly exhibit the acanthomatous variant with
central areas of keratin formation or the cystic pattern
Treatment:
By local incision
It is rare, representing less than 1% of all odontogenic tumors. It originates
from epith. Rest of dental lamina & or the reduced enamel epith.
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Clinically:
Occurs in patient between 20-60 Y age.
Occurs as either central (intraosseous) or peripheral (extraosseous)
lesion.
Central one like the common ameloblastoma, mostly occur in the molar
area followed by premolar area.
Both jaw can affected
The tumor presents as a slowly growing painless mass
Peripheral one, most commonly occurs in the anterior part of the mouth,
it represents as a superficial soft tissue swelling of the gingiva.
Radiographically:
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Tend to occur as a diffuse radiolucency with faint flecks of calcified
structures.
But may appear as a mixed of radiolucency & opacity
The lesion may occur over impacted or displaced teeth,
Differential diagnosis in radiograph include:
Dentigerous cyst, adenomatoid odontogenic tumor & ameloblastic
fibro-odontoma.
Histopathology:
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It is pathognomonic
Consists of sheets of polyhedral cells with prominent intercellular
bridges.
The epith. Cells may show pleomorphism, multinucleation, prominent
nucleoli
In addition there is pools of homogenous eosinophilic material found
1within & between the epith. Sheets along with spherical calcifications
are distributed.
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The nature of the eosinophilic deposits believed to be a form of
amyloid.
The tumor is not encapsulated
Treatment:
By radical surgical removal
Adenomatoid odontogenic tumor (AOT):
It is uncommon tumor, it’s
name reflects the characteristic histologic feature of duct like structures
spread throughout the epith. Component.
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Clinically:
Is usually associated with an impacted tooth & is often cause failure of
tooth to erupt.
The lesion occurs during the 2 nd decade of life, commonly in patients
14-15 Y of age
It most often occurs in the anterior mouth, usually around an impacted
cuspid, but sometime associated with molars
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The lesion appear as an area of swelling over an unerupted tooth.
Radiographically
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Appear usually as unilocular radiolucency with well demarcated
borders & contains a tooth.
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The lesion similar to that found in a Dentigerous cyst, but by a good
examination reveals that differs from a Dentigerous cyst, in which the
radiolucency extend apically beyond the C.E.J.
Histopathology:
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AOT composed of an outer fibrous capsule surrounding a nodular mass
of epith.cells.
The epith., cells are spindle in shape scattered throughout the lesion
The characteristic feature, is the formation of duct like structure by
cuboidal or columnar cells & containing eosinophilic materials.
Treatment:
2•
By surgical removal & recurrency is rare
Calcifying odontogenic cyst (Gorlin cyst ):
is an uncommon odontogenic lesion.
Because the lesion often appears as a solid noncystic lesion, although it may
appear as cystic & solid part, it’s classified as an tumor.
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Clinically:
Can occur in any part of the jaw, but mostly occur anterior to the
molars.
Occur at any age but a peck incidence in the 2 nd decade of life.
Can occur extraosseously or intraosseously.
The extraosseous one appear as focal localized swelling, where as
intraosseous lesions produce a generalized expansion of the buccal &
lingual cortices.
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The lesion is usually painless.
Radiographically
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Most commonly appear as a well circumscribed unilocular
radiolucency, containing flecks of radiopacity.
Histopathology
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Varies, some lesions have a cystic center, & others are solid.
The epith., component consists of an outer layer of palisade columnar
cells & an inner layer resemble the stellate reticulum.
The characteristic feature of the lesion is the presence of eosinophilic
epith., cells without nuclei, known as Ghost cells, present within the
stellate reticulum areas.
Multiple spherical & diffuse calcifications within the epith., & the C.T.,
are also included.
Treatment:
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Required conservative treatment, usually enucleation. Recurrences are
uncommon
Squamous odontogenic tumor (SOT):
was first described in 1975. the lesion can be multifocal & have aggressive
potential if not treated in it’s early stages.
3SOT may originate from the remnants of the dental lamina, rest of Malassez,
or overlying epith.
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Clinically:
Usually occur anterior to the molars
Are affect both the max, & mand
It occur at any age, with a peak incidence in the 3 rd decade
Represent as either a painless swelling or as looseness of teeth in the
region
Radiographically
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Appear as either unilocular or multilocular radiolucency, with tooth
separation
Histopathology
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Consists of rounded & elongated islands of normal appearing stratified
squamous epith, against a cellular fibrous C.T., background.
The epith, islands have a basal cell layer of inactive-appearing cuboidal
cells.
The remainder of the islands are composed of mature intermediate cell
with prominent desmosomal bridge, with central microcyst in many
islands
Treatment:
Small lesions treated with local curettage, while large one require block
resection.
4odontogenic myxoma
It is a special tumor for the jaws locally aggressive arise from dental
mesenchymal tissue. It is infiltrative (not capsulated) benign tumor.
Clinically:-
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It occurs in young age group, most commonly involve the mandible,
appear as a painless swelling or asymptomatic. The maxillary lesion will
arise into the sinus while the mandibular lesion found in molar, premolar
area & often extend into ramus .
Radiograph
- Multilocular radiolucency with scalloped margin, soap-bubble
appearance or honey comb appearance (resemble ameloblastoma).
Histopathology
-
Grossly it is a gelatinous tissue, microscopically consist of a scanty
spindle shape irregular cells with fine long anastomosing processes, and a
mucoid material & few collagen fibers & epithelial rest. The margins of
the lesion are ill defined & the bone trabeculae show resorption. They
will give difficulty in removal of the lesion . Some cases contain an
odontogenic epithelium.
Treatment & prognosis
- It is a benign tumor with infiltrative properties & not capsulated,
therefore, bone resection & curettage is the treatment, it is associated
with recurrence.
- It is important to remove all gelatinous tissue to reach an intact area in nts
of amorphous cementoid or dentinoid calcification may be seen between
the epithelium .
Treatment:- Enucleation, no recurrence .
5Odontoma
Odontomes are dental hamartomas containing the calcified dental tissue.
-
Odontoma is a hamartomatous lesion found over unerupted teeth
containing enamel, dentine, pulp and cementum in either normal tooth
shape (compound) or abnormal tooth shape (complex).
- It represents nearly 70% of whole odontogenic tumors, complex
odontoma is more commonly occurred in posterior mandible than
maxilla, as asymptomatic swelling.
- Compound odontoma more commonly occurs in anterior maxilla than
in mandible and as a symptomatic swelling either over the crowns of
unerupted teeth or between the roots of erupted one .
Radiograph
- Unilocular radiolucency containing multiple radiopaque structures that
resemble small teeth , compound odontoma may contain as few as 2-3
tooth like structures or as many as 20-30 tooth like structures.
- Complex odontoma in posterior part of mandible on impacted tooth and
may reach several (cm) in size ,appear as solid radiopaque mass, lesions
are unilocular & separated from normal bone by distinct radiolucent line.
Individual tooth like structure is absent.
Histopathology
-
Enamel, dentine, pulpal tissue or tooth like structure of compound
odontoma are arranged in an ordinary pattern in a fibrous capsule.
Complex odontoma differs by being composed of single disorganized
mass of enamel, dentine & pulp within abnormal tooth shape .
Treatment:- Enucleation from surrounding bone.
Bone cells & their precursors react to the influences of circulating
hormones & other regulating substances. Thus the bones are
particularly sensitive to physiologic & genetic changes that can result
in alterations to their structure & mineral content.
1- Paget’s disease (Osteitis deformans)
•
•
•
•
•
•
•
•
Is a focal alteration in the histology & morphology of bone, result
from uncoordinated increase in the osteoclastic & osteoblastic
activity of the bone cells.
Confined to one bone or multiple bones throughout the body.
Initially the process is dominated by bone resorption followed by
excessive bone formation, result in increase in volume but a
decrease in strength.
This uncoordinated function of osteoclast & osteoblastic activity
characterized by numerous reversal lines that give the bone a
characteristic mosaic pattern under the microscope.
The etiology is still unknown, but intranuclear viral inclusion
bodies have been found within some osteoclast cells.
Clinical features
Asymptomatic, seldom found in patients younger than 40 years,
& being more common in the western countries.
The disease may involved one bone (Monostotic) or multiple
bones (Polyostotic), when multiple bones are involved, there will
be some degree of incapacity, pain, & joint disease.
When involve the skull, a frequent symptom is a gradual increase
in hat size caused by increased cranial circumference. But the
serous concern is the involvement of the base of skull, in this
case diminish in the various foramens can result in compression
1•
•
•
•
•
•
of the spinal cord & cranial nerves lead to paralysis & loss of
hearing & sight.
in the jaws, the maxilla is more commonly involved than the
mandible, the first sign is spaces between the teeth, & the denture
may become tight & uncomfortable within the time.
The most important investigation is alkaline phosphates level,
which give information of osteoblastic activity. Normal level =
63 IU/ L, but in Paget’s disease may reach 1000-5000 IU/L in
polystotic & 200-500 IU/L in monostotic one.
Elevation of urinary hydroxyproline level indicate the increase
bone resorption (osteoclast activity).
Alyhough considerable Ca ++ loss from the bone occurs ,serum
Ca ++ usually remain within normal levels.
The complications, include, bone fracture, heart failure &
sarcoma
Radiographic appearance
•
Varies extensively, in the early osteolytic stage the disease
exhibit a diffuse radiolucency, later on there is a diffuse
2radiopacity.
•
•
•
•
•
•
•
•
The most common picture is a mixed radiolucent / radiopaque
resembling “cotton wool” in a diffusely radiolucent area.
The maxilla & mandible are often enlarged, with loss of the
lamina dura & hypercementosis of the roots of the teeth in the
area.
histopathology
Consist of an increase in osteoclasts, osteoblasts, & blood vessels
& a replacement of the normal bone by a less dense bone having
a mosaic appearance.
Treatment
the most common effective therapeutic agents are Calcitonin &
Diphosphonates such as Disodium etidronate.
These compound inhibit bone resorption, this provides the bone
forming cells to produce stronger, less fragile bone.
However, the treatment does not stop the lesion but does slow it.
Surgery is avoided because the diseased bone is prone to
hemorrhage & prone to a difficult to manage osteomyelitis.
Surgery is used only to relive sever pain caused by pressure on
nerves & spinal cord.
32- Hyperparathyroidism
•
•
•
•
•
•
Loss of bone mineralization ( osteoporosis ) due to increase in the
PTH secretion ( primary ) or increased demand for serum Ca ++ (
secondary) mostly in renal disease.
The disease lead to multiple systemic complications, loss of
alveolar bone architecture, & occasionally giant cell tumor
(
brown tumor ).
Clinical features
Mostly in patients over 60 years of age & female to male ratio 2-
1.
The disease is mostly asymptomatic.
Hypercalcemia is the most common manifestation & the disease
diagnosed when serum Ca ++ is above the normal range of 8.6-
10.4 mg/100 ml, associated with decrease serum phosphates
level.
Serum alkaline phosphates & urinary hydroxyproline are normal,
but urinary phosphate may be elevated.
Radiographic appearance
•
•
Generalized reduced bone density
mottled areas of radiolucency.
( osteoporosis ) or
In the mandible & maxilla, the normal trabecular pattern may be
lost, with lack of distinctness of lamina dura in late stage.
4•
A large radiolucency may be present, indicate giant cell tumor.
Histopathology
Non specific, However, the lesion consisting of increased osteoclastic
activity, thinning of trabecular bone, & wide zones of osteoid with
activated osteoblast. Also some replacement of marrow with loose
C.T. may occur.
Treatment
Treat the cause & dietary phosphate supplements, & Vit. D
supplements have been beneficial.
3-Osteopetrosis
•
•
•
•
Is a generalized hereditary condition in which the bones become
more denser than normal due to excessive bone mineralization,
resulting in altered stature, frequent fracture, lack of bone
marrow hematopoietic function, & a tendency for sever
Osteomyelitis of the jaws.
Clinically
Early symptoms in infancy include difficulties in breathing &
hearing due to oversized facial & mastoid bones.
Followed by functional defects in the ocular & trigeminal nerves
as a result of compressed by sclerosis of the foramina of the base
of skull.
Delayed eruption of teeth is a common oral finding, & healing is
difficult after extraction.
5•
•
Depletion of platelets, leukocytes, & erythrocytes, make a
tendency for spontaneous hematomas, multiple infections, &
anemia.
In sever cases the patient die from complications of marrow
depletion before 10 years of age.
Radiographically
•
The disease characterized by a generalized increase in bone
density with obliteration of normal internal architecture.
Histopathology
•
•
The bone is dense & sclerotic, with most of the marrow spaces
replaced with bone or fibrous tissue.
The bone is somewhat avascular & in some cases islands of
calcified cartilage are found, which normally resorbed during
development.
6•
•
Treatment
Depends on the condition. Either by bone marrow
transplantation, or by oral Calcitriol combined with a calcium
deficient diet.
4- Osteogenic imperfecta
is a bone disease characterized by defective matrix formation &
lack of mineralization, resulting in multiple broken bone, blue
sclera of the eye, & associated dentinogenesis imperfecta
•
•
Clinically
The neonatal form is lethal, the patients suffering multiple
fractures during gestation & delivery.
•
Patients with moderate type, have blue sclera, & dentinogenesis
imperfecta.
X-Ray
show large areas of cyst like radiolucency, multiple fractures & healed
fractures are present. The teeth exhibit bulbous crowns with shortened
roots.
•
•
•
•
Histopathology
The bone show markedly thinned bone cortices composed of
immature woven bone
Treatment
No therapy is capable of altering the course of the disease.
C- Gingival Cyst: is located in the gingival soft tissues outside of the bone, & is derived from the rests of the dental lamina (rests of Serres).
We have 2 types of gingival cyst:
* 1-Gingival cyst of the adult:
* Occurs as a firm but compressible, swelling on the mand. or max. facial gingiva in the premolar, canine, incisor region.
* The cyst not appear on radiograph because it confined to the gingival soft tissue.
* Histopathologically, include a thin lining of non-keratinized epith. about 1-3 cells in thickness with a number of clear cells.
* Treatment: by conservative surgical enucleation.
* 2- Gingival cyst of the newborn:
* Generally seen on the alveolar ridges of newborn infants as small, often multiple swelling, & appear whitish in color.
* Microscopically, consist of a thin walled cystic lesion lined by a thin, stratified squamous epith., & containing compact desquamated keratin.
* The lesion resolved spontaneously in response to normal function, therefore no treatment required.
Non-odontogenic cyst
* Also called fissural cyst or occlusion cyst, because they arise from embryonic epith. that become entrapped during embryogenesis.
* There are 2 types of these cysts:
1- Nasopalatine duct cyst (incisive canal cyst):
It’s the most common & most important non-odontogenic cyst arises from embryonic remnants of the nasopalatine duct after it’s closure, it occur at any age, but mostly discovered in the 4th or 5th decay of life, it is asymptomatic discovered by routine X-ray or it may infected & cause pain & swelling in the incisive papilla.
* Radiographically:
* Appear as well circumscribed round or oval or inverted heart shape radiolucency between the root of the upper 2 central incisors or above the apices of the roots.
* Histopathology:
* The cyst lined by a layer of ciliated columnar (respiratory), cuboidal (ductal), or stratified squamous epith. or by a mixture of these epith. types.
* The C.T. capsule typically exhibits the prominent component of blood vessels & nerves that comprise normal incisive canal contents.
* N.B.: to distinguish between the nasopalatine cyst & P.A. cyst:
* 1- N.P.cyst, the tooth is vital, but in case of P.A. cyst the associated tooth is nonvital.
* 2- because the N.P.cyst is not related (attached) to the apex of the root, so when change the direction of the X-ray beam to see if the lesion remain attach to the apex of the root, if so it mean it’s radicular cyst, if not it mean N.P. cyst.
2- Nasolabial cyst
* A rare cyst occurs entirely in the soft tissues of the anterior maxillary vestibule, below the ala of the nose & may cause swelling of the mucobuccal fold or in floor of the nose & may cause deviation of the nose to the other side.
* Because this cyst is located entirely within the soft tissue, it’s not apparent radiologically.
* The cyst lined by a layer of pseudo-stratified columnar epith. Showing variable numbers of mucus (goblet) cell, or by cuboidal or stratified squamous epith.
* A narrow zone of dense, homogeneous, fibrous tissue is usually seen adjacent to the epith. lining.
*Non epith. Cyst (bone cyst) (false cyst):
1- Simple bone cyst: it’s unusual lesion occurs in the jaw & other bones. The etiology is unknown but trauma to the bone (spongy bone) may lead to bleeding in the marrow, with failure of organization of the blood clot with subsequent degeneration of the clot that eventually produce an empty cavity within the bone.
* Clinically:
* Most frequently occur in young patients, & mainly in the mand. In the posterior region.
* The lesion is asymptomatic & discovered during routine X-ray examination, but sometime produce expansion of the bone
* The associated tooth is vital.
* Radiographically:
* Smoothly outlined radiolucency, vary from small or may involve the body of mand., extending between the roots of the teeth showing a scalloped appearance with an intact lamina dura.
* Histologically:
* Show thin C.T. membrane lining the cavity.
* Treatment:
* May heal spontaneously, or you open into the cavity to reestablish bleeding into the lesion that will heal later.
2- Aneurysmal bone cyst: A very rare lesion of the jaw bone, it’s etiology is not clear but it considered as vascular malformation.
* Clinically:
* Occurs in young patients (10-20 Y), painful, in the posterior part of the mand., & max.
* When the surgeon open the lesion excessive bleeding is in counter, & the lesion is described as blood soaked spongy.
* Radiographically:
* Appear as air bubbles radiolucency.
* Histologically:
* Stroma contain many cavernous or sinusoidal spaces filled with blood & there is multinucleated giant cell & varying amount of haemosidrine.
* Treatment:
* By curettage, but some cases show recurrence (20%)
3- Stafine cyst
* It is uncommon condition that presents as a localized deep concavity located on the lingual aspect of the mand., mostly in the molar region, but can occasionally involve the lingual aspect of the anterior mand. The condition generally reveals normal salivary gland tissue.
* Radiographically:
* Appear as ovoid radiolucency between the mandibular canal & the inferior border of the mand.
* Treatment:
* No treatment is required.
Soft tissue cyst;
1- Thyroglossal tract cyst: it’s an uncommon developmental cyst that formed any were along the embryonic thyroglossal tract between the foramen caecum of the tongue & the thyroid gland.
* Clinically:
* Occur in young person, but may occur at any age.
* Forming a mobile cystic mass which may lie on one side of the midline, but mostly in midline
* It is asymptomatic, but when occur high near the tongue it may cause dysphagia, sometime infected causing abscess with fistula.
* Histopathology:
* The cyst lined by stratified squamous epith., ciliated columnar epith., transitional epith, or a mixture of epith. Types.
* The capsule include lymphoid aggregation, thyroid tissue, mucus gland.
* Treatment: complete surgical excision.
2-Lymphoepithelial cyst
* It develop either from epithelial invaginations that detached from the surface mucosa & entrapped within the lymphoid tissue, or from epithelium of minor salivary gland ducts that traverse oral lymphoid tissue.
* Clinically:
* Most commonly found on the anterior floor of the mouth & posterior lateral borders of the tongue.
* It’s an asymptomatic, yellowish, superficial submucosal mass, usually less than 1cm in diameter.
* Histopathology:
* The cyst lined by a thin layer of parakeratinized squamous epith. Surrounded by a well defined mass of normal lymphoid tissue showing variable numbers of germinal centers.
3-dermoid & epidermoid cyst
* These represents a simple form of cystic teratoma derived from skin epith. entrapped during embryonic development.
* Most of these cysts occur in the head & neck region, primarily in the skin around the eyes & the anterior upper neck, extending superiorly into the floor of the mouth.
* Clinically:
* Mostly occur in young adults, present as painless swelling exhibiting a doughy consistency on palpation,& may cause elevation of the tongue & can interfere with eating & speaking.
* Histopathology:
* The cyst lined by a layer of orthokeratinized squamous epith., surrounding by C.T. capsule.
* In dermoid cyst in addition to these the lesion exhibiting variable numbers of dermal appendages including hair follicles, sebaceous glands.
* Treatment: this is best treated by surgical excision.
Cyst: it’s a pathological cavity lined by epithelium & filled with fluid or semi fluid material
In the jaw bones & oral tissue there are remnant of epith. come mostly from odontogenic apparatus & most of these remnants are embryonic in origin .for this reason the jaw bone are affected by a large numbers of cysts in comparism to other bones in the body.
The epith. remnants that give rise to these cysts are:
1- Reduced enamel epithelium.
2- remnants of dental lamina.
3- epithelial rests of Malassez.
Classification of the jaw cysts
I-Epithelial cysts
A- odontogenic:
1- developmental cyst (odontogenic keratocyst, dentigerous cyst, eruption cyst, lateral periodontal cyst, gingival cyst, glandular cyst)
2- inflammatory cyst (radicular cyst, paradental cyst).
B- non-odontogenic:
Nasopalatine duct cyst, nasolabial cyst
II-Non epith. (primary bone cysts)
Solitary bone cyst (traumatic, simple), aneurysmal bone cyst, Stafine cyst.
III-Soft tissue cysts:
1-Salivary mucoceles (mucus extravasation, mucus retention)
2-Dermoid & epidermoid cyst
3-Lymphoepithelial cyst
4-Thyroglossal tract cyst.
Odontogenic cysts
A cyst in which the lining of the lumen is derived from epithelium produced during tooth development, these include:
1- cysts derived from epith rests of Malassez: Periapical cyst (radicular)
2- cysts derived from reduced enamel epithelium: reduced enamel epithelium refers to the layer of epith. That remains around the tooth’s crown after enamel formation is complete. This layer of epith. Is derived from the specialized epith. Components of the enamel organ (inner enamel epith., stratum intermedium, stellate reticulum, & outer enamel epith.)That were active during amelogenesis, & collapse into a thinned dormant membrane of two or three cells in thickness.
A- Dentigerous cyst : an odontogenic cyst that surrounds the crown of an impacted tooth, caused by fluid accumulation between the reduced enamel epith. & the enamel surface, resulting in a cyst in which the crown is located within the lumen & root outside.
Clinically:
These cysts are commonly associated with unerupted mand. or max. third molars or max. canine.
The cyst usually remains asymptomatic but may produce some swelling or pain, particularly if it is large or inflamed.
Radiographically:
Mostly diagnosed by their radiographic appearance. They present as well circumscribed radiolucency surrounding the crown of a tooth.
Histopathology:
* The epith. Lining is relatively uniform layer of non-keratinized, stratified, squamous epith., measuring 2-10 cells in thickness.
* This lining may alters by inflammation & may become hyperplastic, atrophic, or ulcerated.
* Variable numbers of mucus cells are occasionally seen in the epith. Lining .
* Like the periapical cyst, crystalline cholesterol deposits, hemosiderin deposits, hyaline (Rushton ) bodies, & lipid laden macrophage are also seen in dentigerous cyst.
* Long standing cyst will occasionally exhibit areas of keratinization or premalignant (dysplastic) changes of their epith. Lining.
* Treatment: either by enucleation or marsupilization, recurrency is uncommon.
B- Eruption cyst: Is a variant of the dentigerous cyst that develops in the alveolar soft tissue around the crown of an erupting tooth.
* Clinically, appear as fluctuant swelling of the alveolar ridge, the lesion may bleed during mastication giving rise to the term eruption hematoma
* Histologically, same as those of a dentigerous cyst.
* Most of these cysts require no treatment because rupture spontaneously during mastication. But sometime surgical exposure of the crown of affected tooth may be needed.
3- cysts derived from dental lamina:
A- Odontogenic Keratocyst ( okc): A cyst derived from remnants of the dental lamina. It’s less common than the dentigerous cyst but more serous because epith. Lining show high rate of growth.
* Clinically:
* Occurs in young patient, however, it can occur at any age.
* The mand. Is affected more commonly than max. in the mand., the cyst occur mostly in the 3rd molar area, while in the max., the 3rd molar & canine areas are usually affected.
* The cyst is slowly growing & asymptomatic, but later it may cause bone expansion.
* Although okc is usually present as a single lesion, it can occasionally occur as multiple cysts that sometimes occupy all four quadrants of the jaws as in nevoid basal cell carcinoma.
Radiographically:
* appear as a well defined, solitary lesion or as a multilocular radiolucency with a thin cortical margin & displacement of the adjacent tooth.
Histopathology: the microscopic appearance of okc is pathognomonic, characterized by:
* A thin, uniform lining of parakeratinized squamous epith. usually 6-10 cells in thickness.
* A palisaded layer of columnar or cuboidal basal cell.
* A corrugated (snaky appearance) layer of parakeratin on it’s luminal surface.
* Commonly, there is focal separation of the epith. Lining from the adjacent C.T., which is often loose & usually free of inflammation.
* In the C.T. capsule there is satellite (daughter) cysts.
* Lumen containing variable amount of desquamated parakeratin.
Treatment
* By surgical enucleation, However, the cyst show recurrence rate of 25%-60%, similar to that of a neoplasm.
* The causes of recurrency are:
* Loose attachment between the epith. & C.T.
* Presence of daughter cysts
B- glandular odontogenic cyst:
an unusual large unilocular or multilocular odontogenic cyst, first described in 1987.
it originated from epith. of the dental lamina & it has greater growth potential
* Radiographically:
* Appear as well defined, unilocular, or multilocular radiolucencies, mostly in the mandible.
* Histopathology:
* It’s composed of a thin squamous epith. lining that may show areas of focal epith. thickening.
* The epith. contain glandular structures or microcysts lined by columnar or cuboidal cells.
* Treatment:
* By surgical enucleation.
B- glandular odontogenic cyst
1- Torus
* 1- Torus: rounded, smooth surfaced, non-neoplastic growth of nodular dense bone found in the midline of the palate & lingual surfaces of the mandible. In the palate called Torus palatinus, & on the lingual surface of the mand. In the cuspid / premolar region, termed Torus mandibularis.
* 2- Exostosis: An exophytic nodular growth of dense cortical bone commonly located on maxilla. Or mand. Alveolar bone, usually in bicuspid-molar area.
* 3- Osteoma: An exophytic nodular growth of dense cortical bone on or within the mand. Or max. In location other than those occupied by tori or exostosis. When it occur as multiple, they are often associated with Gardner Syndrome.
* Note: the tori & exostosis are thought to be reactions to bone stresses, while the osteomas are considered benign neoplasm.
Treatment: lesions are only treated if the patient encounters problems or a prosthetic appliance is necessary. The treatment is done by surgery
* Histopathology:
* Each of the lesions is composed of dense cortical bone with a lamellar pattern. The cortical bone is sclerotic & relatively avascular, & the medullary bone is denser than normal with reduced marrow spaces.
1-Torus,exostosis,osteoma
2- Osteoid osteoma / osteoblastoma: Benign intraosseous lesions with similar clinical, radiographic, & histopathologic features.
* Clinically:
* 1- the lesion produce swelling & pain on palpation.
* 2- occur in young patients.
* 3- osteoid osteoma is small (0.5-2 cm ), while osteoblastoma are larger (< 2 cm).
Radiographically: Are distinctive & pathognomonic, they are round, with a well defined central radiolucency (nidus) surrounded by a zone of radiopacit
Histopathology:
The lesion consist of osteoid bone, then become well calcified with small focus of active osteoblasts. The center usually remain vascular with increased number of osteoblasts & osteoclast
* Treatment:
* Surgical removal. Osteoid osteoma by curettage or block resection, while osteoblastoma requires large surgical block resection.
3- Cemento-Ossifying fibroma:
A well-demarcated, encapsulated, expansile intraosseous lesion of the jaws composed of cellular fibrous tissue containing spherical calcifications & irregular, randomly oriented bony structures
* Clinically:
* 1- Most often located in the mandible posterior to the canines & occasionally occurs in max.
* 2- it occurs twice as often in females & mainly in the 20-30 years age group.
* 3- the lesion is usually painless & grow slowly, show marked buccal & lingual bone expansion.
* Radiographically:
* It may be either unilocular or multilocular. In early stage the lesion is small & completely radiolucent. As they enlarge, amounts of irregular shaped radiopacities appear within the radiolucent area.
* In the later stage, the lesion often forming a nearly radiopaque with a thin radiolucency separating it from the surrounding normal bone.
Treatment:
by surgical removal, the extent depending on the size & location of the lesion.
* Histopathology:
* Composed of cellular fibrous tissue, with spherical amorphous calcifications (cementicle) as well as irregular small bone trabeculae. A thin outer fibrous C.T. separating the lesion from surrounding normal bone.
4-Central giant cell granuloma (CGCG):
An intraosseous destructive lesion of the anterior mand. & max., cause movement of the teeth, & produce root resorption; composed of multinucleated giant cell in a background of mononuclear fibrohistocytic cells & RBC.
* Clinically:
* Mostly occurs between 10-30 years of age.
* It occurs in the anterior mand. & max, but 75% in the mand. & crossing the midline.
* Expansion of the buccal & lingual cortical plates is common, & sometime the lesion perforate the cortex & resorption of the root apices.
Radiographically:
* is not specific, but show diffuse radiolucency (relatively large), with resorption of tooth roots
Treatment:
are successfully treated by curettage, but sometime will recur & require one or more retreatments. Block resection is done in large lesions.
* Histopathology:
* The lesion is composed of giant cells, usually containing 5-10 nuclei, in a background of mononuclear cells & fibrous tissue.
5-Peripheral giant cell granuloma(PGCG):
Most common of the giant cell lesions of the jaws, arising from the periosteum or periodontal membrane as a purplish-red nodular consisting of multinucleated giant cells in a background of mononuclear cells & RBCs.
* Clinically:
* Is the most common giant cell lesion occurring in the jaws.
* Occurs at any age, with peaks in the incidence during the mixed dentition years & 30-40 year old age group. & mostly affect the females.
* Mostly appear as a sessile focal purplish nodule on the gingiva, may reach 2 cm in size. Spreading through penetration of the PdL.
Radiographically:
small lesions show little radiographic changes, while larger one show superficial erosion of the cortical bone, & some widening of the PdL.
* Histopathology:
* Composed of multinucleated giant cells in a background of mononuclear cells & extravasated RBCs ., the lesion are surrounded by bands of fibrous C.T. stroma. Osteoid deposits or speckles of new bone are often present in the base of the lesion.
* Treatment:
* By surgical removal, & when PdL is involved, the associated teeth may need to be extracted.
BENIGN FIBRO-OSSEOUS LESIONS
• Fibro-osseous lesions are a diverse group of processes that are characterized by
replacement of normal bone by fi brous tissue containing a newly formed
mineralized product.
• The designation fi bro-osseous lesion is not a specifi c diagnosis and describes
only a process.FIBROOSSEOUS LESIONS OF
THE JAWS INCLUDE:
• Developmental (hamartomatous) lesions,
• Reactive or dysplastic processes, and
• NeoplasmsFIBRO-OSSEOUS LESIONS OF
THE JAWS COMMONLY INCLUDE
THE FOLLOWING:
● Fibrous dysplasia
● Cemento-osseous dysplasia
● Focal cemento-osseous dysplasia
● Periapical cemento-osseous dysplasia
● Florid cemento-osseous dysplasia
● Ossifying fibromaFIBROUS DYSPLASIA
• An asymptomatic self-limiting regional alteration of bone in
which the normal structure is replaced by fibrous tissue &
non-functional trabeculae-like osseous structures
(metaplastic woven bone).FIBROUS DYSPLASIA
• Fibrous dysplasia is a sporadic condition that results from a
postzygotic mutation in the GNAS1
• It may be Monostotic or Polystotic.MONOSTOTIC JUVENILE F.D
• It’s the most common type
• It grows slowly & ceases in the late teens or early twenties
• Clinically appears as facial asymmetry, mostly affect the max., & cause
displacement of the teeth
• This type affect a single boneRADIOGRAPHIC APPEARANCE
• It has different appearance, in the early stage appear as radiolucency, then in
the late stage with bone formation they becoming more radiopaque giving “
ground glass” or “ cotton wool” appearance, in addition to expansion of the
cortical plates & displacement of the root .
• The lamina dura is usually obscured, & the lesion in general diffused & there is
no demarcated line .HISTOPATHOLOGY
the lesion mainly consist of cellular fibrous connective
tissue that replaced the bone trabeculae & marrow
spaces, with irregular islands of metaplastic bone.TREATMENT:
Surgical correction for cosmetic reason, but this done when the patient
reaches adulthood age.
Radiotherapy is excluded because of risk of malignant transformation.MONOSTOTIC ADULT
FIBROUS DYSPLASIA
• Appears as asymptomatic diffuse expansion of the cortices with
teeth movement.X-RAY:
• It show a mixed radiolucency-radiopacity (cotton wool)
pattern, it blends with the surrounding bone, & expansion
with thinning of the cortical platesHISTOPATHOLOGY:
Show cellular fibrous connective tissue with immature
metaplastic woven bone that diffused with the surrounding
normal bone, this distinguished it from ossifying fibroma.TREATMENT:
• it differ from juvenile type. It is not self-limiting. & complete
surgical removal of smaller lesions. While in larger one bone
shaving is done.C- POLYOSTOTIC F.D.
Is affect more than one bone, mostly confined to the cranio-
facial area or distributed throughout the skeleton. &
accompanied by skin pigmentation & endocrine
dysfunction.CLINICALLY
• 1-The lesion give the patient an unpleasant
appearance
• 2-The lesion most commonly involve the ribs,
cranium, max. ,femur, tibiaCLINICALLY
• 3-Many patients have large light pigmentation known as café au lait
spots (coffee with milk) on the skin the process is termed Jaffe-
Lichtenstein syndrome.
• 4-When endocrine dysfunction present (McCune-
Albrightsyndrome) clinical features begin in early childhood, like
premature vaginal bleeding, breast development in femaleX-RAY & HISTOPATHOLOGY
• Is similar to that of Monostotic typeTREATMENT
• By surgical management to correct the functional disturbances &
cosmetic surgery to improve appearanceCHERUBISMCHERUBISM
• It’s autosomal dominant fibro-osseous lesion of the jaws involving more than
one quadrant that stabilizes after the growth period usually leaving deformity
and malocclusion.
• Involving more than one quadrant, usually the mand. In a bilateral symmetrical
manner at early childhood. The maxilla is less commonly involved.
• The disease is slowly growing, associated with sever malocclusion.
• The condition stopped when the patient reaches pubertyCHERUBISM
• When expansile lesions are present in the mandible and maxilla, they
give the face a “chubby” appearance and often produce some
elevation of the floor of the orbits, causing the pupils to be elevated
upward
• Lesions begin in early childhood as slow-growing expansions of the
posterior portions of the mandible or maxillaX-RAY APPEARANCE
In early stage show large area of radiolucency, exhibit massive
expansion with malaligned & disturbed eruption of teeth.
Later when the disease mature it appears with more radiopaque & give
“ground glass” appearance.HISTOPATHOLOGY
It consist of giant cell tissue (multinucleated giant cells) with mononuclear cells.
Then during maturation it replaced by cellular fibrous tissue with metaplastic
woven bone.
Then the lesion show a bony dominant.• Treatment: cosmetic surgery after puberty.CEMENTO-OSSEOUS
LESIONSCEMENTO-OSSEOUS LESIONS
• They are benign fibro-osseous lesions closely associated with the
apices of the teeth and containing amorphous spherical
calcifications through out resembling an aberrant form of
cementum; lesions are usually without signs and symptomsA. FOCAL CEMENTO-
OSSEOUS DYSPLASIA
• Focal cemento-osseous dysplasia exhibits single site of involvement.
• About 90% of cases of focal cemento-osseous dysplasia occur in
females, with an approximate mean age of 38 years and a
predilection for the third to sixth decades.A. FOCAL CEMENTO-
OSSEOUS DYSPLASIA
• Focal cemento-osseous dysplasia may occur in any area of the jaws,
but the posterior mandible is the predominant site.
• The disease is typically asymptomatic and is detected only on a
radiographic examination. Most lesions are smaller than 1.5 cm in
diameter.FOCAL CEMENTO-OSSEOUS
DYSPLASIA.B-PERIAPICAL CEMENTAL
DYSPLASIA:
• 1- The disease characterized by the replacement of normal bone by
cemento-osseous tissue
• 2-mainly affect the anterior portion of the mand.
• 3-The lesion is asymptomatic & the teeth overlying the lesion remain
vitalX-RAY:
it has 3 pictures, depending on the stage of maturation.
1- osteolytic stage: appear as well defined radiolucency at the apex of
one or more teeth, which are free from caries or restoration.
2- cementoblastic stage: appear as demarcated radiolucency
containing nodular radiopaque deposits.
3- mature stage: appear as well defined, dense nodular radiopaque.
The Pd membrane can be seen separating the lesion from the teeth.HISTOPATHOLOGY:
the osteolytic stage consists primarily of cellular C.T. replacing the normal trabecular bone with
small calcified structures
then in cementoblastic stage, further displays a mixture of spherical calcification & irregular
shaped deposits of osteoid & mineralized bone, surrounding by osteoblasts & containing
osteocytes
at mature stage, the lesion composed of coalesced spherical calcification & sclerotic mineralized
bone with little C.T.FLORID CEMENTO-OSSEOUS
DYSPLASIA
• It’s a diffuse asymptomatic intra-osseous lesion, that involve one or both arches
• Mostly affect the females young age
• Some time the patient may experience pain or discomfort due to secondary
infection from periapical lesion or after extraction.CONSIST OF MULTIPLE RADIOLUCENT-
RADIOPAQUE DIFFUSED LESION
• consist of multiple radiolucent-radiopaque diffused lesionHISTOPATHOLOGY
the lesion show cellular C.T. containing many small & large spherical
calcifications & bones.TREATMENT:
• no treatment unless secondary infection & complicated
osteomyelitis, in this case debridment, drainage & antibiotics is
Oral Mucosal Lesions
The oral cavity is lined by a mucous
membrane that is composed of stratified
squamous epithelium and underlying
connective tissue. The epithelium serves as
a cover for the oral soft tissues as a barrier
to the entry of external pathogenic factors.
Ecchymosis: Non-elevated area of hemorrhage,
larger than a petechia.
Cyst: Pathologic epithelium-lined cavity often
filled with liquid or semi-solid contents.
Unilocular: Describing a radiolucent lesion
having a single compartment.
Multilocular: Describing a radiolucent lesion
having several or many compartments.
To better describe the appearances of
lesions and communicate these features to
others, the clinician should be familiar with
the following terms:
Oral Infections
Fungal infections
Macule: Focal area of color change which is not
elevated or depressed.
I. Candidiasis
Candidiasis is the most common oral
fungal infection in humans that is caused by
Candida albicans, which may be a
component of the normal oral microflora.
Papule: Solid, raised lesion which is less than 5
mm in diameter.
Nodule: Solid, raised lesion which is greater
than 5 mm in diameter.
Sessile: Describing a tumor or growth whose
base is the widest part of the lesion.
Generally, predisposing factors are local
(poor oral hygiene, xerostomia, mucosal
damage, antibiotic mouthwashes and
dentures) and systemic (broad-spectrum
antibiotics, steroids, immunosuppressive
drugs, radiation, HIV infection, iron-
deficiency anemia, and immunodeficiency).
Pedunculated: Describing a tumor or growth
whose base is narrower than the widest part of
the lesion.
Papillary: Describing a tumor or growth
exhibiting numerous surface projections.
Verrucous: Describing a tumor or growth
exhibiting a rough, warty surface.
Clinical features
Vesicle: Superficial blister, 5 mm or less in
diameter, usually filled with clear fluid.
Candidiasis of the oral mucosa may
exhibit a variety of clinical patterns,
including the following clinical types:
Bulla: Large blister, greater than 5 mm in
diameter.
Pustule: Blister filled with purulent exudate.
1. Pseudomembranous Candidiasis
(Oral Thrush)
Ulcer: Lesion characterized by loss of the
surface epithelium and frequently some of the
underlying connective tissue.
The best-recognized form of candidal
infection, characterized by the presence of
white plaques on the oral mucosa that can
be scrapped off. The underlying mucosa
may appear normal or erythematous.
Symptoms, if present at all, are usually
mild, consisting of a burning sensation or an
Erosion: Superficial lesion, characterized by
partial or total loss of the surface epithelium.
Fissure: Narrow, slit-like ulceration or groove.
Plaque: Lesion that is slightly elevated and is
flat on its surface.
Petechia: Round, pinpoint area of hemorrhage.
2Lec.1: Oral Mucosal Lesions
Dr. Mustafa Al-Talqani
unpleasant taste. The white plaques are
characteristically distributed on the buccal
mucosa, palate, and dorsal tongue.
e. Cheilocandidiasis: Infrequently,
candidiasis involves the peri-oral skin,
usually secondary to actions that keep the
skin moist (e.g., thumb sucking, chronic use
of petrolatum-based ointments).
2. Erythematous Candidiasis
Erythematous candidiasis is more
common than oral thrush. In contrast to the
pseudomembranous form, patients with
erythematous candidiasis either do not show
white flecks, or a white component is not a
prominent feature. Several clinical forms of
erythematous candidiasis may be seen:
a. Acute atrophic candidiasis: Typically
follows a course of broad-spectrum anti-
biotic therapy. Patients often complain of
burning sensation that is usually
accompanied by a diffuse loss of the
filiform papillae of the dorsal tongue,
resulting in a reddened, “bald” appearance.
f. Denture stomatitis: This condition is
characterized by varying degrees of
erythema, localized to the denture-bearing
areas of a maxillary removable denture. The
process is rarely symptomatic. Whether this
represents actual infection by C. albicans or
caused by other local factors remains
controversial. The clinician should rule out
other local factors such as: improper denture
design, allergy to the denture base, and
inadequate curing of the denture acrylic.
3. Chronic Hyperplastic Candidiasis
(Candidal Leukoplakia)
b. Median rhomboid glossitis (Central
papillary atrophy): Clinically, median
rhomboid glossitis appears as a well-
demarcated erythematous zone that affects
the midline, posterior dorsal tongue. It is
often asymptomatic. It was thought to be a
developmental defect of the tongue, but
candidal infection has been proven.
White patches that cannot be removed by
scraping. This form of candidiasis is the
least common. Such lesions are usually
located on the anterior buccal mucosa and
tongue. Clinically, it cannot be distinguished
from a leukoplakia. The diagnosis is
confirmed by the presence of candidal
hyphae and by complete resolution of the
lesion after antifungal therapy, otherwise,
biopsy is mandatory.
c. Chronic multifocal candidiasis:
Multifocal oral candidiasis characterized by
central papillary atrophy of the tongue and
other areas of involvement.
d. Angular cheilitis (perlèche):
Candidiasis at the angles of the mouth is
characterized by erythema, fissuring, and
scaling. It is seen typically in old patients
with reduced vertical dimension. Saliva
tends to pool in these areas, keeping them
moist and thus favoring a fungal infection.
Histopathology
There is parakeratosis, neutrophilic
microabscesses,, and chronic inflammation
of the underlying connective tissue. The
candidal hyphae are embedded in the
parakeratin layer.
Treatment
Dealing with predisposing factors.
Topical and/or systemic anti-fungal.
3Lec.1: Oral Mucosal Lesions
Dr. Mustafa Al-Talqani
Viral infections
During the primary infection, only a
small percentage of individuals show
clinical signs and symptoms of infectious
systemic disease, whereas a vast majority
experience only subclinical disease. After
resolution of primary herpetic infection, the
virus is believed to migrate, through an
unknown mechanism, to the trigeminal
ganglion (most commonly). The virus uses
the axons of the sensory neurons to travel
back and forth to the skin or mucosa.
Human herpesviruses
The human herpesvirus (HHV) family
constitutes a large family of double-stranded
DNA viruses. This family includes:
✦ Herpes simplex virus (HSV): two types:
✴ Type 1 (HSV-1 or HHV-1): The
pharynx, intraoral mucosa, lips, eyes,
and skin above the waist are involved
most frequently.
✴ Type 2 (HSV-2 or HHV-2): Typically
involves the genitalia and skin below the
waist.
✦ Epstein-Barr virus (EBV or HHV-4) Viral reactivation may follow aging,
ultraviolet light, stress, fatigue, heat, cold,
pregnancy, allergy, trauma, dental treatment,
respiratory illnesses, fever, menstruation,
systemic diseases, and malignancy.
✦ Cytomegalovirus (CMV or HHV-5) Clinical features
✦ More recently discovered members,
HHV-6, HHV-7, and HHV-8. a. Acute herpetic gingivostomatitis
(primary herpes): Primary disease is
usually seen in children between the ages of
6 months and 5 years. The affected mucosa
develops numerous pinhead vesicles, which
rapidly collapse to form numerous small,
red lesions. These lesions enlarge slightly
and develop central ulceration covered by
yellow fibrin. In all cases, the gingiva is
enlarged, painful, and erythematous.
✦ Varicella-zoster virus (VZV or HHV-3)
Humans are the only natural reservoir for
these viruses, which are endemic
worldwide. All eight types cause a primary
infection and remain latent within specific
cell types for the life of the individual.
I. Herpes Simplex Virus (HSV)
Infections
Herpes simplex virus (HSV) is the best-
known member of the human herpesvirus
(HHV) family. HSV infections occur in two
forms: primary (systemic) and secondary
(localized). Both forms are self-limited, but
recurrences of the secondary form are
common because the virus can remain
within ganglionic tissue in a latent state.
Physical contact with an infected individual
or with body fluids is the typical route of
HSV inoculation and transmission.
The primary lesions are accompanied by
fever, malaise, anorexia, headache, and
cervical lymphadenopathy. After the
systemic primary infection runs its course of
about 7 to 10 days, lesions heal without scar
formation. By this time, the virus may have
migrated to the trigeminal ganglion to reside
in a latent form.
b. Herpetic pharyngotonsillitis: The age
of initial infection affects the clinical
presentation of primary HSV infection, with
4Lec.1: Oral Mucosal Lesions
Dr. Mustafa Al-Talqani
Treatment
individuals infected at an early age tending
to exhibit gingivostomatitis and those
exposed later in life often demonstrating
pharyngotonsillitis. Sore throat, fever,
malaise, and headache are the initial
symptoms. Numerous small vesicles
develop on the tonsils and posterior
pharynx. The vesicles rapidly rupture to
form shallow ulcers. The clinical
presentation closely resembles pharyngitis
secondary to streptococcal infection.
Early administration of anti-virals
(acyclovir or valacyclovir) accelerates
clinical resolution and ceases the
development of new lesions. Besides,
associated eating and drinking difficulties,
pain, healing time, duration of fever, and
viral shedding are shortened dramatically.
NSAIDs may be used; in conjunction with
acyclovir; for more immediate pain relief.
Patients also should be instructed to
avoid contact with active lesions to prevent
auto-inoculation or spread to others.
c. Recurrent herpes simplex infections
(secondary herpes): Secondary herpes
represents the reactivation of the latent
virus. Patients usually have prodromal
symptoms of tingling, burning, or pain in
the site at which lesions will appear. Within
a matter of hours, multiple fragile and short-
lived vesicles appear. The vesicles rupture
and crust within 2 days. The lesions heal
without scarring in 1 to 2 weeks and rarely
become secondarily infected.
II. Varicella-Zoster Virus (VZV)
Infections
The primary varicella-zoster virus (VZV)
infection is called varicella (chickenpox).
S u b s e q u e n t l y, l a t e n c y e n s u e s , a n d
recurrence is possible as herpes zoster
(shingles), often after many decades.
Varicella is believed to be transmitted
predominantly through the inhalation of
contaminated droplets or direct contact with
active lesions. The condition is very
contagious and is known to spread readily
from person to person.
Most secondary lesions appear on the
vermilion and surrounding skin, known as
herpes labialis. While intraoral recurrences
are restricted to the hard palate or gingiva.
d. Herpetic whitlow: Herpetic whitlow
is a HSV infection involving the finger(s).
Before the universal use of gloves, this type
of infection typically occurred in dental
practitioners who had been in physical
contact with infected individuals. Contact
could result in a vesiculoulcerative eruption
on the digit (rather than in the oral region).
The duration may be about 4 to 6 weeks.
Clinical features of varicella
(chickenpox)
Varicella is characterized by a skin rash
of the trunk and head and neck that is
accompanied by fever. The rash quickly
develops into a vesicular eruption that
becomes pustular and eventually ulcerates.
The infection is self-limiting and lasts
several weeks. Oral mucosa may be
involved, demonstrating multiple shallow
ulcers that are preceded by vesicles.
5Lec.1: Oral Mucosal Lesions
Dr. Mustafa Al-Talqani
Clinical features of herpes zoster
(shingles)
Signs and symptoms are usually mild to
moderate and generally last less than a
week.
Herpes zoster is essentially a condition
of adults. The sensory nerves of the trunk
and head and neck are commonly affected.
The involvement of various branches of the
trigeminal nerve may result in unilateral
oral, facial, or ocular lesions. Involvement
of facial and auditory nerves produces the
Ramsay Hunt syndrome, in which facial
paralysis is accompanied by vesicles of the
external ear, tinnitus, deafness, and vertigo.
Treatment
No treatment usually is required because
herpangina is self-limiting, mild, of short
duration, and causes few complications.
IV. Hand-Foot-and-Mouth Disease
Hand-foot-and-mouth disease is a highly
contagious viral infection that usually is
caused by Coxsackie virus or enterovirus.
The virus is transferred from one individual
to another through airborne spread or fecal-
oral contamination.
After days of prodromal symptoms of
pain and/or paresthesia in the area of the
involved dermatome, a well-delineated
unilateral maculopapular rash appears. The
rash quickly becomes vesicular, pustular,
and then ulcerative. Remission usually
occurs in several weeks.
Clinical features
Predominantly affects children younger
than 5 years of age. Signs and symptoms are
usually mild to moderate in intensity and
include fever, malaise, lymphadenopathy,
and sore mouth. Pain from oral lesions is
often the patient’s chief complaint. Oral
lesions begin as vesicles that quickly
rupture to become ulcers. The palate,
tongue, and buccal mucosa are favored oral
sites.
Treatment
Treatment is generally supportive.
Corticosteroids are contraindicated.
III. Herpangina
Herpangina is an acute viral infection
caused by the Coxsackie virus. It is
transmitted by contaminated saliva and
occasionally through contaminated feces.
Multiple maculopapular lesions, typically
on the feet, toes, hands, and fingers, appear
concomitantly with or shortly after the onset
of oral lesions. These cutaneous lesions
progress to a vesicular state; they eventually
become ulcerated.
Clinical features
Herpangina is usually endemic, with
outbreaks occurring typically in summer or
early autumn. It is more common in
children. Those infected generally complain
of malaise, fever, dysphagia, and sore throat
after a short incubation period. Intraorally, a
vesicular eruption appears on the soft
palate, faucial pillars, and tonsils. No
associated skin lesions are typically seen.
Treatment
Because of the relatively short duration,
generally self-limiting nature, and general
lack of virus-specific therapy, treatment is
usually symptomatic.
6Lec.1: Oral Mucosal Lesions
Dr. Mustafa Al-Talqani
Bacterial infections
II. Necrotizing Ulcerative Gingivitis
(NUG)
I. Streptococcal Tonsillitis and
Pharyngitis
Necrotizing ulcerative gingivitis (NUG)
is a relatively rare specific infectious
gingival disease of young persons.
Tonsillitis and pharyngitis are extremely
common. The most common causes are
beta-hemolytic streptococci, adenoviruses,
enteroviruses, influenza, and Epstein-Barr
virus. Although the majority of cases caused
by viral infections, bacterial infection is also
evident to a lesser extent. Spread is typically
by person-to-person contact, through
respiratory droplets or oral secretions.
Clinical features
The characteristic clinical feature is
painful necrosis of the gingiva. Spontaneous
gingival bleeding, halitosis, and intense
salivation are common. Fever, malaise, and
lymphadenopathy are less common. The
process sometimes can lead to a loss of
attachment and the development of
periodontitis (necrotizing ulcerative
periodontitis) or spread to adjacent soft
tissue (necrotizing stomatitis).
Clinical features
Most cases arise in temperate climates in
winter or early spring. Common findings
include sudden onset of sore throat, fever,
dysphagia, tonsillar hyperplasia, redness of
the oropharynx and tonsils, palatal
petechiae, cervical lymphadenopathy, and a
yellowish tonsillar exudate. Systemic
symptoms, such as headache, malaise,
anorexia, abdominal pain, and vomiting,
especially in younger children.
Histopathology
Non-specific; surface ulceration, mixed
inflammatory infiltrate, necrotic material
and extensive bacterial colonization
Treatment
Debridement by scaling, curettage, or
ultrasonic instrumentation. Rinses with
chlorhexidine or warm saltwater. Antibiotic
medications (metronidazole and penicillin
have been suggested as the drugs of choice).
Treatment
Usually self-limited and spontaneously
resolves within 3 to 4 days after onset of
symptoms. The main goal of therapy is to
prevent peritonsillar abscess formation and
prevent systemic complications, such as
acute rheumatic fever.
E-mail: mustafab.altalqani@uokufa.edu.iq
The antibiotic of choice is either
penicillin or amoxicillin. Other choices
(such as azithromycin and cephalosporins)
can be given for penicillin-allergic patients.
Antibiotics should not be prescribed without
confirmation of bacterial infection (majority
of cases are caused by a viral infection).
Oral ulcerative lesions
Primary oral ulceration
I. Traumatic Ulcerations
Variety of pathological conditions that
affect the oral mucosal lining are
characterized by loss of mucosal tissue and
present as erosions (superficial loss of tissue
that involves only the epithelium) or
ulcerations (deeper lesions that extend into
the connective tissue); ulcerations in human
beings are most commonly encountered in
the mucosa of the oral cavity as well as
stomach, intestines, and genitourinary tract.
Traumatic ulcers are usually caused by
biting, denture trauma or chemical trauma
and arise at trauma-prone sites such as
tongue, lip, buccal mucosa or adjacent to a
denture flange.
Clinical features
Traumatic ulcers are tender, have a
yellowish-grey floor of fibrin slough and
red margins. Inflammation, swelling and
erythema are variable, depending on the
cause and time since trauma. There is no
induration unless the site is scarred from
repeated episodes of trauma. Occasionally, a
large ulcer is caused by biting after a dental
local anaesthetic. Biting trauma may
produce two small adjacent ulcers matching
cusps of upper and lower opposing teeth.
In general, the morphology of the
ulcerative lesion including its shape, size,
borders and base characteristics, as well as
the presence of a pseudomembrane and/or
peripheral component, provide important
and sometimes definitive clues to the
diagnosis. Equally important to the accurate
description of the morphologic features of
ulcerative lesions is the assessment of their
number (single or multiple), onset and
duration (acute or chronic), and potential for
recurrence (recurrent or non-recurrent).
Chemical trauma may be self-inflicted or
iatrogenic. Etchant, hypochlorite and silver
nitrate are just a few of the caustic agents
used in dentistry that can cause mucosal
ulcers. Some patients continue to believe
that aspirin is effective for toothache if held
against the alveolus to dissolve. The result
is local whitening caused by epithelial
necrosis, followed by ulceration.
Causes of oral ulcerations
1. Infective: (Bacterial, Viral, Fungal)
2. Traumatic: (Mechanical, Chemical,
Thermal, Factitious injury, Radiation)
3. Idiopathic: (Aphthous stomatitis,
Necrotizing sialometaplasia)
Histopathology
4. Associated with systemic disease:
(Hematological disease, GIT disease,
Behçet’s disease, HIV-associated)
Non-specific. Surface ulceration with
mixed inflammatory infiltrate.
Treatment
5. Associated with dermatologic diseases:
(Lichen planus, Erythema multiforme,
Lupus erythematous, Vesiculobullous
disease)
Treatment is symptomatic. Traumatic
ulcers heal in days after elimination of the
cause. If they persist for more than 10 days,
biopsy should be carried out to exclude
other diseases.
6. Neoplasms: (Oral squamous cell
carcinoma)
2Lec. 2: Oral Ulcerative Lesions
Dr. Mustafa Al-Talqani
Riga-Fede disease typically appears on
the tongue of neonates between 1 week and
1 year of age. The condition often develops
in association with natal or neonatal teeth.
The anterior ventral surface of the tongue is
the most common site of involvement.
II. Traumatic Ulcerative Granuloma
with Stromal Eosinophilia (TUGSE) and
Riga-Fede Disease
Traumatic ulcerative granuloma with
stromal eosinophilia (TUGSE) is a chronic
oral ulcerative lesion with uncertain
etiopathogenesis. Mucosal trauma appeared
to be the major instigating factor of this
lesion. However, it was assumed that if the
trauma was the sole cause, TUGSE would
be more common; therefore, other causes
were suggested such as: viral or toxic
agents, cell-mediated pathogenesis or lack
of expression of certain growth factors.
Histopathology
Histopathologically, TUGSE is presented
as an ulcerated lesion composed of a poorly
formed granulation tissue showing a mixed
inflammatory infiltrate with large atypical
mononuclear cells; the eosinophilic
infiltrate in TUGSE lesions is characteristic
and fundamental for the diagnosis. Large
atypical mononuclear cells are scattered and
may be mitotically active.
Generally speaking, TUGSE is not an
uncommon oral lesion, but in Iraq, it seems
to be considered as a rare and recently
delineated oral lesion that might be reflected
by the general lack of awareness of it.
Treatment
The irritating cause should be removed.
Interestingly, many of these lesions undergo
resolution after incisional biopsy.
Similar sublingual ulcerations may occur
in infants as a result of chronic mucosal
trauma from adjacent anterior primary teeth,
often associated with nursing. These
distinctive ulcerations of infancy have been
termed Riga-Fede disease and should be
considered a variation of TUGSE.
Extraction of the anterior primary teeth
has resolved the ulcerations in Riga-Fede
disease.
Idiopathic oral ulceration
III. Necrotizing Sialometaplasia
Uncommon, locally destructive condition
of the salivary glands. This lesion is
important because it mimics a malignant
process; clinically and microscopically. The
cause is uncertain, however, ischemia with
subsequent local infarction is suggested.
Clinical features
TUGSE is characterized as a solitary
benign chronic oral ulcer, with the tongue
being the most common site to be affected.
It could be painful or painless. Most of
cases develop in patients older than age 40
years. It has an important clinical
significance, since it may be provisionally
diagnosed as oral squamous cell carcinoma
due to its worrisome clinical presentation as
a chronic ulcer with elevated and rolled
margins that fails to heal by local treatment.
Clinical features
Mostly develops in the minor salivary
glands of the posterior palate. The major
salivary glands can be affected. Necrotizing
sialometaplasia is most common in adult
males. The condition appears initially as a
3Lec. 2: Oral Ulcerative Lesions
Dr. Mustafa Al-Talqani
non-ulcerated swelling, often associated
with pain or paresthesia. Within 2 to 3
weeks, necrotic tissue sloughs out, leaving a
crater-like ulcer (1 to 5 cm in diameter).
children and young adults. There are three
recognized clinical variations of aphthous
stomatitis: (Minor, Major, and Herpetiform).
All forms present as painful recurrent
ulcers. Patients may have prodromal
symptoms of burning, itching, or stinging.
The ulcers are not preceded by vesicles
formation.
Histopathology
Acinar necrosis and squamous metaplasia
of the salivary ducts. The overall lobular
architecture of the glands is still preserved
—a helpful histopathologic clue. The
squamous metaplasia of the salivary ducts
can be striking and produce a pattern that is
easily misdiagnosed as squamous cell
carcinoma or mucoepidermoid carcinoma.
Here, immunohistochemistry is helpful.
Minor aphthous ulcerations: the most
common clinical variant, but has the fewest
recurrences and the shortest duration.
Classically, minor aphthous ulcerations
measure less than 10 mm in diameter,
demonstrate a variable recurrence rate, and
heal without scarring in 7 to 14 days.
During a single episode, one to five lesions
typically are present. The buccal and labial
mucosae are affected most frequently.
Treatment
Because of the worrisome clinical
presentation, biopsy usually is indicated to
rule out the possibility of malignant disease.
Once the diagnosis has been established, no
specific treatment is indicated or necessary.
The lesion resolves spontaneously.
Major aphthous ulcerations: are less
common, larger (1 to 3 cm), deeper, longer
duration (2 to 6 weeks to heal) and may
cause scarring, in comparison with the
minor variant. In addition, the number of
lesions varies from 1 to 10. Any oral surface
area may be affected, but the labial mucosa,
soft palate, and tonsillar fauces are involved
most commonly. The onset of major aphthae
is after puberty, and recurrent episodes may
continue to develop for up to 20 years.
IV. Recurrent Aphthous Stomatitis
Recurrent aphthous stomatitis is one of
the most common oral mucosal pathoses.
The exact etiopathogenesis is not known,
but it is evident that mucosal destruction is
resulted from a T cell–mediated immune
reaction. However, several triggering factors
for aphthous stomatitis have been reported,
including: (Allergens, Genetic
predisposition, Hormonal influences,
Infectious agents, Nutritional deficiencies,
Smoking cessation, Stress, and Trauma)
Herpetiform aphthous ulcerations: have
the greatest number of lesions and the most
frequent recurrences. The individual lesions
are small, averaging 1 to 3 mm in diameter,
with as many as 100 ulcers present in a
single recurrence. Because of their small
size and large number, they bear a
resemblance to HSV infection, leading to
the confusing designation, herpetiform.
Clinical features
Aphthous is, almost exclusively, present
on non-keratinized oral mucosa. Aphthous
ulcerations are noted more frequently in
4Lec. 2: Oral Ulcerative Lesions
Dr. Mustafa Al-Talqani
Unlike herpes infection, herpetiform
aphthous ulcers are not preceded by vesicles
and exhibit no virus-infected cells. It is
common for individual lesions to coalesce
into larger irregular ulcerations. The
ulcerations heal within 7 to 10 days, but the
recurrences tend to be closely spaced.
slightly increased prevalence and tend to
have a worse clinical course. Typically,
Behçet syndrome has a relapsing and
remitting pattern. Virtually, all affected
patients demonstrate oral ulcerations that
often herald the onset of the disease. The
oral lesions are similar to aphthous
ulcerations, mostly the minor type.
Histopathology
The genital lesions occur in 75% of the
patients. Ocular involvement occurs in up to
70% of the cases. Arthritis is one of the
more common minor manifestations.
Cutaneous lesions include erythematous
papules, vesicles, acneiform eruptions, and
erythema nodosum–like lesions.
Because the histopathologic features are
non-specific and the diagnosis is usually
evident clinically, a biopsy is usually
unnecessary and rarely performed.
Treatment
The mainstay of therapy is the use of
corticosteroids in various forms. Most
patients with mild aphthosis receive either
no treatment, therapy with a number of
over-the-counter anesthetics, or periodic
topical medicaments to minimize the
frequency and severity of the attacks.
From a diagnostic standpoint, one of the
most important skin manifestations is the
presence of positive “pathergy”. One or 2
days after the oblique insertion of a 20-
gauge or smaller needle under sterile
conditions, a sterile pustule develops. This
reaction is termed cutaneous pathergy.
Oral ulcerations associated with systemic
disease
Diagnosis
V. Behçet Syndrome (Behçet Disease)
Definitive criteria have been developed:
Although Behçet disease traditionally has
been thought to be a classic triad of oral,
genital, and ocular lesions, it now is
recognized to be a rare multisystem
inflammatory disease in which recurrent
oral aphthae are a consistent feature.
Etiology is not clear, however, Behçet
syndrome appears to represent an abnormal
immune process triggered by an infectious
or environmental antigens in a genetically
predisposed individual.
Criteria for the Diagnosis of Behçet Disease*
✓ Recurrent oral ulceration (must)
Plus two of the following minor manifestations:
✓
✓
✓
✓
Recurrent genital ulcerations
Eye lesions
Skin lesions
Positive pathergy test
*Proposed by the Behçet International Study Group.
Histopathology
The histopathologic features are not
specific. There is surface ulceration. The
small blood vessels classically demonstrate
invasion by neutrophils (vasculitis),
extravasation of red blood cells, and
necrosis of the vessel wall.
Clinical features
Behçet syndrome usually arises in the
third and fourth decades. Males exhibit a
5Lec. 2: Oral Ulcerative Lesions
Dr. Mustafa Al-Talqani
Treatment
These lesions are typically not static but
wax and wane over weeks or months.The
reticular form usually causes no symptoms
and involves the posterior buccal mucosa
bilaterally. Other oral mucosal surfaces may
also be involved concurrently, such as the
lateral and dorsal tongue, the gingivae, the
palate, and vermilion border.
Therapy is tailored to the disease
severity. Many patients are treated
symptomatically, with the disease often
going into remission as the patient ages.
Oral ulcerations associated with
dermatologic disease
Erosive Lichen Planus
VI. Lichen Planus
Erosive lichen planus, although not as
common as the reticular form, is more
significant for the patient because the
lesions are usually symptomatic. Clinically,
there are atrophic, erythematous areas with
central ulceration of varying degrees. The
periphery of the atrophic regions is usually
bordered by fine, white radiating striae.
Sometimes the atrophy and ulceration are
confined to the gingival mucosa, producing
the reaction pattern called desquamative
gingivitis.
Lichen planus is a common, chronic,
immunologically mediated mucocutaneous
disorder that often affects the oral mucosa.
The exact etiology is unknown. Implication
of stress, anxiety, certain medications,
foreign material and hepatitis C infection, as
predisposing factors, is still controversial.
Clinical features
Most patients with lichen planus are
middle-aged adults. Women are affected
more than men. The skin lesions of lichen
planus present as Purple, Pruritic, Polygonal
Papules. These usually affect the flexor
surfaces of the extremities. Careful
examination of the surface of the skin
papules reveals a fine, lace-like network of
white lines (Wickham striae). Other
extraoral sites include the glans penis, the
vulvar mucosa, and the nails.
Histopathology
Classically present as six clinical types
(Reticular, Atrophic, Papular, Bullous,
Plaque, and Erosive or Ulcerative). The
discussion will be focused on the former
and the latter clinical types. Varying degrees of hyperkeratosis (ortho-
or para-) may be present. The rete ridges
classically have a pointed or a “saw-
toothed” shape. Destruction of the basal
cell layer of the epithelium is evident. This
is accompanied by an intense, band-like
infiltrate of predominantly T lymphocytes
immediately subjacent to the epithelium.
Degenerating keratinocytes may be seen in
the area of the epithelium and connective
tissue interface and have been termed
Civatte bodies.
Reticular lichen planus Treatment
Reticular lichen planus is thus named
because of its characteristic pattern of
interlacing white lines (Wickham striae). Reticular lichen planus produces no
symptoms, and no treatment is needed.
Erosive type is treated by corticosteroids.
6Lec. 2: Oral Ulcerative Lesions
Dr. Mustafa Al-Talqani
dehydrated because they are unable to
ingest liquids as a result of mouth pain.
VII. Erythema Multiforme (EM)
EM is an ulcerative mucocutaneous
condition of uncertain etiopathogenesis. In
about half of the cases, precipitating causes
are apparent including infection such as
herpes simplex, and less commonly, drugs.
A clinical recognition of EM major can
be made if two or more mucosal sites are
affected in conjunction with widespread
skin lesions. In most cases the oral mucosa
is involved in addition to either the ocular or
genital mucosae.
For many years it was thought that
erythema multiforme (EM) exhibited a
spectrum of severity, ranging from EM
minor through major thought Stevens-
Johnson syndrome and toxic epidermal
necrolysis. EM minor and major represent a
distinctly different process from the latter
two conditions, so that they were separated.
Histopathology
The histopathological picture is non-
specific; the diagnosis is often based on the
clinical presentation. However, subepithelial
or intraepithelial vesicles may be seen with
necrotic basal keratinocytes. Connective
tissue shows mixed inflammatory infiltrate
arranged in a perivascular orientation.
Clinical features
EM typically has an acute onset and
usually affects young adults, with a slight
female predilection. EM minor is the mild
type. Target lesions (characteristic skin
lesions of EM) appear as concentric circular
erythematous rings resembling a target or
bull’s-eye. The oral cavity is the most
frequently involved mucosal site, although
the conjunctival, genitourinary and
respiratory mucosa also may be affected.
Involvement of extraoral mucosal areas is
usually associated with the more severe
form; EM major.
Treatment
Even though the disease is self-limiting,
usually lasting 2 to 6 weeks, about 20% of
patients experience recurrent episodes. The
use of systemic or topical corticosteroids is
beneficial.
VIII. Stevens- Johnson Syndrome and
Toxic Epidermal Necrolysis
Rare severe blistering and ulcerative
mucocutaneous diseases. One of differences
between Stevens-Johnson syndrome and
toxic epidermal necrolysis is the degree of
skin involvement (10%, 30% respectively).
Both of them are almost always triggered by
drug exposure, with more than 200 different
medications having been implicated.
The oral lesions begin as erythematous
patches that undergo epithelial necrosis and
evolve into large, shallow ulcerations with
irregular borders. Hemorrhagic crusting of
the vermilion zone of the lips is common
distribution. The lips, labial mucosa, buccal
mucosa, tongue, floor of the mouth, and soft
palate are the most common sites of
involvement. Sometimes patients are
Clinical features
Stevens-Johnson syndrome is usually
seen in younger patients, while toxic
epidermal necrolysis tends to occur in
7Lec. 2: Oral Ulcerative Lesions
Dr. Mustafa Al-Talqani
people over 60 years of age. A female
predilection is observed. Unlike EM, the
cutaneous lesions initially appear on the
trunk, presenting as erythematous macules
with subsequent sloughing of the skin and
flaccid bullae development. Target lesions
are present.
often makes the lesions worse. Oral lesions
of SLE appear as nonspecific lichenoid
areas, with presence of ulcerations, usually
affect palate, buccal mucosa, and gingivae.
The prevalence of clinical and laboratory
manifestations, on which the diagnosis can
be made, are given below:
Virtually all patients have mucosal sites
involvement, particularly the oral mucosa.
Diffuse sloughing of the skin and mucosal
surfaces makes it appear as if the patient
had been badly scalded.
PREVALENCE of CLINICAL and LABORATORY
MANIFESTATIONS of SLE*
Histopathology
Necrosis of the whole skin thickness by
apoptosis with little inflammation.
Treatment
One of the most important aspects is
identifying and immediately discontinuing
any drug that might be initiating the
condition. Treatment is controversial. There
is a high risk of death when the area of skin
involved in toxic epidermal necrolysis is
great.
Systemic Signs and Symptoms:
(Fatigue, Malaise, Fever, Anorexia,
Weight Loss) 95%
Musculoskeletal symptoms:
(Arthralgia/myalgia, polyarthritis) 95%
Cutaneous signs:
(Photosensitivity, Malar rash, Oral ulcers) 80%
Hematologic signs:
(Anemia, Leukopenia, Lymphopenia) 85%
Neurologic signs and symptoms:
(Cognitive disorder, Headache ache) 60%
Cardiopulmonary signs:
(Pleurisy, Pericarditis, Effusions) 60%
Renal signs:
(Proteinuria, Nephrotic syndrome, Renal 30-50%
failure)
*established by the American Rheumatism Association.
Chronic cutaneous lupus erythematosus
(CCLE): may represent a different, but
related, process. It primarily affects the skin
and oral mucosa. The skin lesions of CCLE
most commonly present as discoid lupus
erythematosus (most common subtype).
They begin as scaly, erythematous patches
that are frequently distributed on sun
exposed skin. With time, the lesions may
heal spontaneously in one area, only to
appear in another area.
IX. Lupus Erythematosus
Lupus erythematosus is a classic
example of an immunologically mediated
condition. It may exhibit any one of several
clinicopathologic forms.
Clinical features
Systemic lupus erythematosus (SLE):
is a serious multisystem disease having
various cutaneous and oral manifestations.
Women are affected 8 to 10 times more than
men; patients usually are adults.
The oral lesions are characterized by an
ulcerated or atrophic, erythematous central
zone, surrounded by white, fine, radiating
striae (clinically resembling the lesions of
erosive lichen planus).
A characteristic rash of SLE, having the
pattern of a butterfly, develops over the
malar area and nose (Malar rash). Sunlight
8Lec. 2: Oral Ulcerative Lesions
Dr. Mustafa Al-Talqani
borders of the tongue. This erythema is due
to atrophy of the filiform papillae, and these
atrophic areas are typically surrounded at
least partially by a slightly elevated, yellow-
white, serpentine or scalloped border.
Subacute cutaneous lupus erythematosus
(SCLE): is a third form of the disease,
which has clinical features intermediate
between those of SLE and CCLE.
Histopathology
The patient who is aware of the process
is often able to describe the lesions as
appearing quickly in one area, healing
within a few days or weeks, and then
developing in a very different area. The
lesions are usually asymptomatic, although
a burning sensation or sensitivity to hot or
spicy foods may be noted when the lesions
are active.
The oral lesions show hyperkeratosis,
alternating atrophy and thickening of the
spinous cell layer, degeneration of the basal
cell layer, and subepithelial lymphocytic
infiltration in a perivascular orientation.
Treatment
Patients with SLE should avoid exposure
to sunlight because UV light may
precipitate disease activity. The therapy, in
general, include NSAIDs, corticosteroids
(systemic or topical), immunosuppressive
agents, given according to disease severity.
Histopathology
Diagnosis is usually achieved on clinical
basis. If a biopsy specimen of the peripheral
region of erythema migrans is examined, a
characteristic histopathologic pattern is
observed. Hyperparakeratosis, spongiosis,
acanthosis, and elongation of the epithelial
rete ridges are seen.
Because most of the manifestations of
CCLE are cutaneous, topical corticosteroids
are often reasonably effective, which is also
helpful in treating the oral lesions.
X. Erythema Migrans (Geographic
Tongue; Benign Migratory Glossitis)
Treatment
Generally no treatment is indicated for
patients with erythema migrans. Reassuring
the patient that the condition is completely
benign is often all that is necessary. When
lesions are associated with tenderness or a
burning sensation, topical corticosteroids
may provide relief.
Erythema migrans is a common benign
condition that primarily affects the tongue.
It is often detected on routine examination
of the oral mucosa. The lesion occurs in 1%
to 3% of the population with slight female
predilection. The etiopathogenesis is still
unknown; however, an association of
allergy has been suggested.
E-mail: mustafab.altalqani@uokufa.edu.iq
Clinical features
The characteristic lesions of erythema
migrans are seen on the anterior two-thirds
of the dorsal tongue mucosa. They appear as
multiple, well-demarcated zones of
erythema, concentrated at the tip and lateral
VESICULOBULLOUS LESIONS
condition because, if untreated, it often
results in the patient’s death.
Several conditions in this lecture are
caused by inappropriate production of
antibodies by the patient (autoantibodies).
These autoantibodies are directed against
various constituents of the molecular
apparatus that hold epithelial cells together
or that bind the surface epithelium to the
underlying connective tissue. The damage
produced by the interaction of these
autoantibodies with the host tissue is seen
clinically as a disease process often termed
an immunobullous disease. Because each
disease is characterized by production of
specific autoantibodies, identification of the
antibodies and the tissues against which
they are targeted is important diagnostically.
Etiopathogenesis
The oral mucosal blisters of pemphigus
vulgaris are resulted from an intraepithelial
clefting (separation). This clefting is due to
an abnormal production, for unknown
reasons, of autoantibodies that are directed
against desmosomes (structures that bond
epithelial cells to each other) and effectively
inhibit the molecular interaction that is
responsible for epithelial adherence.
Clinical features
The oral lesions are often the first sign of
the disease, and they are the most difficult
to resolve with therapy. This has prompted
the description of the oral lesions as “the
first to show, and the last to go”. The
average age at diagnosis is 50 years.
Patients usually complain of superficial,
ragged erosions and ulcerations distributed
haphazardly on the oral mucosa. Patients
rarely report vesicle or bulla formation
intraorally, and such lesions can seldom be
identified by the examining clinician,
probably because of early rupture of the
thin, friable roof of the blisters.
I. Pemphigus Vulgaris
Pemphigus vulgaris is an autoimmune,
intraepithelial, blistering disease affecting
the skin and mucous membranes. It is the
most common disorder of a condition
known as PEMPHIGUS, which represents
four related autoimmune diseases:
1. Pemphigus vulgaris
2. Pemphigus vegetans
3. Pemphigus erythematosus
The skin lesions appear as flaccid
vesicles and bullae that rupture quickly,
usually within hours to a few days, leaving
an erythematous, denuded surface. Ocular
involvement may be seen, usually appearing
as bilateral conjunctivitis.
4. Pemphigus foliaceus
Only the first two of these affect the oral
mucosa. Pemphigus vegetans is suggested
to be a rare variant of pemphigus vulgaris.
Despite pemphigus vulgaris is the most
common of pemphigus group, it is not seen
very often with an annual incidence of one
to five cases per million people diagnosed
in the general population. Nevertheless,
pemphigus vulgaris is an important
A characteristic feature of pemphigus
vulgaris is that a bulla can be induced on
normal-appearing skin if firm lateral
pressure is exerted. This is called a positive
Nikolsky sign.
2Lec. 3: Vesiculobullous Lesions
Dr. Mustafa Al-Talqani
Histopathology
paraneoplastic pemphigus developed before
a neoplasm was identified. Signs and
symptoms usually begin suddenly. The oral
mucosa shows multiple areas of erythema
and diffuse irregular ulceration affecting
virtually any oral mucosal surface.
Biopsy specimens of perilesional tissue
show intraepithelial separation. Sometimes
the entire superficial layers of the
epithelium are stripped away, leaving only
the basal cells, which have been described
as resembling a “row of tombstones”. The
cells of the spinous layer of the surface
epithelium typically appear to fall apart, a
feature that has been termed acantholysis,
and the loose cells (Tzanck cells) tend to
assume a rounded shape. A chronic
inflammatory cell infiltrate is usually seen
in the underlying connective tissue.
Palmar or plantar bullae may be evident,
a feature that is uncommon in pemphigus
vulgaris. For other patients, skin lesions can
appear more papular and pruritic, similar to
cutaneous lichen planus. The lips often
show hemorrhagic crusting similar to that of
erythema multiforme.
Other mucosal surfaces are also
commonly affected, including conjunctival,
anogenital, nasopharyngeal, esophageal, and
respiratory tract mucosae.
Treatment
The treatment primarily consists of
systemic and/or topical corticosteroids,
often in combination with other
immunosuppressive drugs.
Histopathology
The histopathological features of
paraneoplastic pemphigus may be as diverse
as the clinical features. A subepithelial
clefting (like pemphigoid) or intraepithelial
clefting (like pemphigus) can be seen.
II. Paraneoplastic Pemphigus
Paraneoplastic pemphigus (neoplasia
induced pemphigus) is a rare vesiculo-
bullous disorder that affects patients who
have a neoplasm, usually lymphoma or
chronic lymphocytic leukemia (CLL).
Paraneoplastic pemphigus is often a very
serious condition with a high morbidity and
mortality rate.
Treatment
Systemic corticosteroids combined with
immunosuppressive agents.
III. Mucous Membrane Pemphigoid
Mucous membrane pemphigoid is a
chronic, blistering, mucocutaneous
autoimmune disease. The term pemphigoid
is used because clinically it often appears
similar to pemphigus; the prognosis and
microscopic features of pemphigoid,
however, are very different. Its prevalence is
twice as common as pemphigus vulgaris.
Etiopathogenesis
The precise pathogenetic mechanisms are
unknown, however it is suggested that it is
an immune-mediated condition in response
to the patient’s tumor.
Clinical features
Patients typically have a history of a
malignant neoplasm. In some cases,
3Lec. 3: Vesiculobullous Lesions
Dr. Mustafa Al-Talqani
Etiopathogenesis Histopathology
Autoantibodies are directed against one
or more components of the basement
membrane, mostly hemidesmosomes
(structures that bind the basal cell layer of
the epithelium to the basement membrane
and the underlying connective tissue)
resulting in formation of subepithelial
vesicles. Biopsy of perilesional mucosa shows a
split between the surface epithelium and the
underlying connective tissue in the region of
the basement membrane (subepithelial
clefting) with no acantholysis. A mild
chronic inflammatory cell infiltrate is
present in the submucosa.
Clinical features Topical or systemic corticosteroids, for
mild to moderate cases. Severely affected
patients are treated by corticosteroids plus
other immunosuppressive agents.
Treatment
Mucous membrane pemphigoid usually
affects older adults (50 to 60 years) with
higher female predominance. The oral
lesions begin as either vesicles or bullae that
may be identified clinically, in contrast to
pemphigus. The most likely explanation for
this difference is that the pemphigoid blister
forms in a subepithelial location, producing
a thicker, stronger roof. Eventually, the oral
blisters rupture, leaving large, superficial,
ulcerated, and denuded areas of mucosa.
The ulcerated lesions are usually painful
and persist for weeks to months if untreated.
Often this process is seen diffusely
throughout oral mucosa, however, it may be
limited to gingiva, producing a clinical
reaction pattern termed desquamative
gingivitis.
IV. Bullous Pemphigoid
Bullous pemphigoid is the most common
of the vesiculobullous lesions, occurring at
an estimated rate of ten cases per million
population per year. In many respects,
bullous pemphigoid resembles mucous
membrane pemphigoid. One significant
difference is that the clinical course in
patients with bullous pemphigoid is usually
characterized by periods of remission
followed by relapse, whereas the course in
patients with mucous membrane
pemphigoid is usually progressive.
Etiopathogenesis
The disease is characterized by the
production of autoantibodies directed
against components of the basement
membrane.
The most significant complication is
ocular involvement. Patients with ocular
involvement may show adhesions
(symblepharons) between the bulbar and
palpebral conjunctivae. Without treatment
the patient may develop entropion (upper
eyelid turn inward), trichiasis (eyelashes
rubbing against the eye itself), obliteration
of the lower fornix of the eye, adhesions of
eyelids, with subsequent blindness.
Clinical features
Bullous pemphigoid typically develops
in older people (75 and 80 years) with no
apparent sex predilection. Oral mucosal
involvement is uncommon, with
4Lec. 3: Vesiculobullous Lesions
Dr. Mustafa Al-Talqani
approximately 10% to 20% of patients
being affected. The oral lesions, like the
skin lesions, begin as bullae, but they tend
to rupture sooner, probably as a result of the
constant low-grade trauma to which the oral
mucosa is subjected. Large, shallow
ulcerations with smooth, distinct margins
are present after the bullae rupture. Clinical features
Histopathology Oral lesions are commonly observed in
the dystrophic type. Vesiculobullous lesions
with scarring may lead to contracture of the
mouth opening (microstomia) and severe
stricture of the esophagus.
The initial lesions are vesicles or bullae,
which are seen early in life and develop on
areas exposed to low-grade, chronic trauma,
such as the knees. The bullae rupture,
resulting in erosions or ulcerations that
ultimately heal with scarring. In the process,
appendages such as fingernails may be lost.
Microscopic examination of tissue
obtained from the perilesional margin of a
bulla shows separation of the epithelium
from the connective tissue at the basement
membrane zone, resulting in a subepithelial
separation.
Histopathology
The histopathologic features of
epidermolysis bullosa include intraepithelial
or subepithelial clefting according to the
type being examined. Immunohistochemical
evaluation and molecular analysis may be
helpful for confirming the diagnosis.
Treatment
Topical or systemic corticosteroids, with/
without systemic immunosuppressive
therapy according to the severity.
V. Epidermolysis Bullosa
Treatment
The term epidermolysis bullosa describes
a heterogeneous group of inherited
blistering mucocutaneous disorders. There
are four broad categories: (Simplex,
Junctional, Dystrophic, and Kindler
syndrome). A variety of inheritance patterns
may be seen (autosomal dominant and
autosomal recessive). The degree of severity
can range from relatively mild, annoying
forms, such as the simplex types, through a
spectrum that includes severe, fatal disease.
For example, many cases of junctional
epidermolysis bullosa result in death at birth
because of the significant sloughing of the
skin during passage through the birth canal.
Unfortunately, because of the genetic
nature of these diseases, no cure exists.
Genetic counseling of affected families is
indicated. Supportive therapy, symptomatic
treatment and preventive measures usually
carried out to improve the general status of
the patient.
Benign epithelial lesions associated th human papillomavirus
Human papillomavirus (HPV) comprises a group of double-stranded DNA viruses, belonging to the family Papillomaviridae HPV exhibits tropism for squamous epithelium and may infect skin or mucosa of anogenital region, upper aerodigestive tract, and other sites. More than 130 HPV types have been identified, including more than 30 types known to infect the oral mucosa HPV is associated with a variety of benign, premalignant, and malignant epithelial lesions
Proposed modes of transmission for oral HPV infection include sexual and nonsexual contact, salivary transfer, contaminated objects, auto-inoculation, breastfeeding, perinatal and prenatal transmission. The incubation period for benign HPV disease is ranging from 3 weeks to 2 years.
In nomal-appearing skin or mucosa, the virus may remain in a latent state within the nuclei of basal epithelial cells in such cases, the viral DNA is present in low numbers. In contrast, in benign and low grade premalignant HPV-associated lesions, the viral DNA typically is present within the various epithelial cell layers in increased numbers, with shedding of mature virions
from the superficial cells. Benign epithelial lesions associated with
HPVs include
Squamous papilloma 11. Verruca vulgaris (common wart) III. Condyloma acuminatum (venereal wart)
IV. Multifocal epithelial hyperplasia (Heck
disease)
Lec.4: Epithelial Pathology 1
Clinical features
Verruca vulgaris most often arises in children. It is common on the skin but frequently develops on oral mucosa. The skin of the hands is the most commonly involved site. Oral mucosal lesions usually are found on the vermilion border, labial mucosa, or anterior tongue. Typically, the verruca appears as a white painless papule or nodule with papillary projections or a rough, pebbly surface (usually 5 mm in size). It may be pedunculated or sessile. Histopathology
2
Dr. Mustafa Al-Talqani
1. Squamous Papilloma
The squamous papilloma is a benign, common, HPV-induced proliferation of stratified squamous epithelium. HPV types 6 and 11 are identified most commonly with a low virulence and infectivity rate Clinical features
It can arise at any age, but children are mostly affected. Sites of predilection include the palate, tongue, and lips.
Clinically, the squamous papilloma is a soft, painless, pedunculated, exophytic nodule with numerous finger like surface projections that impart a "cauliflower" wart-like appearance. The lesion may be white, slightly red, or normal in color, depending on the amount of surface
keratinization. Its maximum size is 0.5 cm It is sometimes difficult to distinguish this lesion clinically from verruca vulgaris, condyloma acuminatum, or multifocal epithelial hyperplasia. Histopathology
There is a proliferation of keratinized stratified squamous epithelium arranged in finger-like projections with fibrovascular connective tissue cores,
Treatment
Conservative surgical excision
II. Verruca Vulgaris (Common Wart)
Verruca vulgaris is a focal, benign, HPV induced hyperplasia of stratified squamous epithelium. HPV type 2 is present most often. Verruca vulgaris is contagious and can spread to other parts of a person's skin or mucosa by auto-inoculation Verruca vulgaris most often arises in children It is common on the skin but infrequently develops on oral mucosa. The skin of the hands is the most commonly involved site. Oral mucosal lesions usually are found on the vermilion border, labial mucosa, or anterior tongue. Typically, the benign proliferation of acanthotic stratified verruca appears as a white painless papule squamous epithelium with mildly keratotic or nodule with papillary projections or a papillary surface projections rough, pebbly surface (usually <S mm in size). It may be pedunculated or sessile.
Condyloma acuminatum appears as a
Treatment
Conservative surgical excision IV. Multifocal Epithelial Hyperplasia
(Heck Disease)
Multifocal epithelial hyperplasia is a squamous epithelial proliferation primarily attributed to HPV 13 and 32 It often affects multiple members of a given family either due to genetic susceptibility or HPV transmission between family members Crowded living conditions, poor hygiene, and malnutrition appear to be risk factors
Clinical features
Histopathology
Verruca vulgaris is characterized by a proliferation of hyperkeratotic stratified squamous epithelium arranged in fingerlike, pointed projections with connective tissue cores. Chronic inflammatory cells often
infiltrate the supporting connective tissue. Oral lesions are excised surgically, or they may be destroyed by laser.
Treatment
III. Condyloma Acuminatum (Venereal Wart)
Condyloma acuminatum is a HPV induced proliferation of stratified squamous epithelium of the anogenital region, mouth, and larynx. Mostly attributed to HPV 6 and 11. It represents a common sexually transmitted disease. Auto-inoculation of additional mucosal sites is possible.
Multifocal epithelial hyperplasia arises in children and adolescents. The most common sites of involvement include the labial, buccal, and lingual mucosa. It either presents as pink, smooth-surfaced papules and nodules (papulonodular) or as white to pale pink nodules (papillomatous).
Histopathology The hallmark is acanthosis of the surface epithelium. The rete ridges are widened.
Treatment
Conservative surgical excision, however spontaneous regression has been reported.
Dr. Mustafa Al-Talqani
Clinical features
Usually affects teenagers and young adults. Oral lesions most frequently occur on the labial mucosa and lingual frenum, The typical condyloma appears as a sessile, pink, well-demarcated, non-tender. V. Linea alba
Linea alba ("white line") is a common alteration of the buccal mucosa that most likely is associated with pressure, frictional irritation, or sucking trauma from the facial surfaces of the teeth. As the name implies. the alteration consists of a white line that usually is bilateral. It may be scalloped and is located on the buccal mucosa at the level of the occlusal plane of the adjacent teeth The line varies in prominence and usually is restricted to edentulous areas. No treatment is required for patients with linea alba, and spontaneous regression may occur.
VI. Morsicatio Mucosae Oris (Chronic Mucosal Chewing)
Chronic mucosal nibbling produces lesions that are located most frequently on the buccal mucosa (morsicatio buccarum), however, the labial mucosa (morsicatio labiorum) and the lateral border of the tongue morsicatio linguarum also may be involved. A higher prevalence of classic morsicatio mucosae oris has been found in people who are under stress or who exhibit psychological conditions.
Most frequently, the lesions are found bilaterally on the anterior buccal mucosa, also may be unilateral. Thickened white areas may be combined with intervening zones of erythema, erosion or focal traumatic ulceration. The patient may describe being able to remove shreds of white material from the involved area
No treatment is required, only patient reassurance with preventive measures
Lec.4: Epithelial Pathology
Treatment
No treatment is required. Discomfort or aesthetic concerns may necessitate therapy IX. Hairy Tongue (Black Hairy Tongue)
Because of the similarity in names, care should be taken to avoid confusing hairy tongue with hairy leukoplakia. Hairy tongue is characterized by accumulation of keratin on the filiform papillae of the dorsal tongue resulting in a hair-like appearance. Hairy tongue is a benign condition with no serious sequelae. The cause is uncertain, many affected people are heavy smokers.
Hairy tongue most commonly affects the
spontaneous regression has been reported.
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VII, Frictional keratosis
Frictional keratosis is a white lesion that is related to chronic rubbing or friction against mucosa. This results in a protective keratotic white lesion that is analogous to a callus on the skin. Keratoses of this type are reversible after elimination of the trauma Traumatic lesions such as linea alba, morsicatio types, and toothbrush gingival abrasion have not been documented to transform into malignancy. Alveolar ridge keratosis, involving the retromolar pad or crest of an edentulous ridge. represent a form of frictional keratosis caused by masticatory function or denture trauma
VIIL Oral Hairy Leukoplakia
Oral Hairy leukoplakia is caused by Epstein-Barr virus and is highly associated with immunosuppressive conditions (mostly HIV infection). However, the name may cause some confusion because it neither hairy nor leukoplakia (have a known cause) Clinical features
Hairy leukoplakia presents as a white lesion that varies in architecture from a flat to a papillary or corrugated lesion that does not rub off. The vast majority of cases have been located along the lateral margins of the tongue, with occasional extension onto the dorsal surface
Histopathology
The epithelium is hyper parakeratinized The epithelium is acanthotic and exhibits a band-like zone of lightly stained cells with abundant cytoplasm (balloon cells) in the upper spinous layer Dysplasia is not noted Treatment
No treatment is required. Discomfort or aesthetic concerns may necessitate therapy.
IX. Hairy Tongue (Black Hairy Tongue)
Because of the similarity in names, care should be taken to avoid confusing hairy tongue with hairy leukoplakia. Hairy tongue is characterized by accumulation of keratin on the filiform papillae of the dorsal tongue. resulting in hair-like appearance. Hairy tongue is a benign condition with no serious sequelae. The cause is uncertain, many affected people are heavy smokers
Hairy tongue most commonly affects the
midline just anterior to the circumvallate
papillae. The elongated papillae are usually
brown, yellow, or black as a result of
growth of pigment-producing bacteria or staining from tobacco and food. The major concern is often the aesthetic appearance and associated bad breath. Any predisposing factors should be eliminated, and excellent oral hygiene should be encouraged Periodic tongue scraping or
brushing can promote desquamation of the
papillae and surface debris.
Premalignant lesions
Many squamous cell carcinomas have been documented to be associated with or preceded by a precancerous lesion, including the following arranged from the highest to lowest potential for malignant transformation):
Proliferative verrucous leukoplakia (PVL) 2 Nicotine stomatitis in reverse smokers 3 Erythroplakia
Lec. 4: Epithelial Pathology 1
cessation. Usually, habit cessation leads to a normal mucosal appearance within 2 weeks
XI. Nicotine Stomatitis
Although nicotine stomatitis is associated with tobacco smoking (cigar, pipe), it is not considered a premalignant, perhaps because it develops in response to heat rather than the chemicals in tobacco smoke. Similar changes also can be produced by the long- term use of extremely hot beverages.
But, reverse smoking is more serious. In some cultures, hand-rolled cigarettes and cigars are smoked with the lit end held within the mouth. This reverse smoking habit produces a pronounced palatal keratosis which has a significant potential to develop dysplasia or carcinoma
Clinical features Nicotine stomatitis most commonly affects men older than 45 years. With long-
upper spinous layer Dysplasia is not noted.
Dr. Mustafa Al-Talqani
4. Oral submucous fibrosis
5. Who Akulaku
Leukoplakia (Granular type) 7. Actinic cheilitis
& Leukoplakia (Smooth and thick types). 9. Smokeless tobacco keratosis
10. Lichen planus (erosive forms) 11. Smooth, thin leukoplakia
X. Smokeless Tobacco Keratosis (Tobacco Ponch Keratosis)
Chronic use of smokeless tobacco is considered to be carcinogenic, although the risk is less than that associated with cigarette smoking and alcohol abuse. Clinical features
Smokeless tobacco keratosis represents a characteristic white or gray plaque involving the mucosa in direct contact with tobacco, The altered mucosa typically is thin with an indistinct border. Sometimes mild peripheral erythema is present
Upon palpation, the lesion may feel soft and velvety. Stretching of the mucosa often reveals a distinct "pouch caused by flaccidity in the area of chronic tobacco placement. The mucosa appears fissured, in a fashion resembling the sand on a beach after an ebbing tide. Induration, ulceration and pain are not associated with this lesion. Histopathology
There is hyperkeratosis and acanthosis. Epithelial dysplasia is uncommon.
Treatment
Treatment depends on histopathologic diagnosis: Keratosis without dysplasia malignancy may require only continued monitoring and encouraged tobacco
Dr. Mustafa Al-Talgani
palate is minimal (except in individuals who reverse smoke), nicotine stomatitis is a marker or indicator of intense tobacco use and hence may indicate increased risk of epithelial dysplasia and neoplasia elsewhere in the oral cavity and respiratory tract
XII. Oral Submucous Fibrosis Oral submucous fibrosis is a high-risk, precancerous condition characterized by chronic, progressive scarring of the oral mucosa. It is seen primarily in the Indian subcontinent. The etiology is linked to the use of betel quid (paan) products. Clinical features
Typical chief complaints include trismus
and burning sensation with intolerance spicy foods. The buccal mucosa, retromolar area, and soft palate are the most commonly affected sites. Subsequently, the mucosa develops a blotchy, marble-like pallor and
5luye Sven LUMII WILL LIU SCIOUS
sequelae. The cause is uncertain, many
affected people are heavy smokers
Hairy tongue most commonly affects the midline just anterior to the circumvallate papillon. The elongated papillae are usually brown, yellow, or black as a result of growth of pigment-producing bacteria or staining from tobacco and food
The major concern is often the aesthetic appearance and associated bad breath Any predisposing factors should be eliminated, and excellent oral hygiene should be encouraged. Periodic tongue seraping or brushing can promote desquamation of the papillae and surface debris.
Premalignant lesions
Many squamous cell carcinomas have been documented to be associated with or preceded by a precancerous lesion. including the following arranged from the highest to lowest potential for malignant transformation:
Proliferative verrucous leukoplakia (P2) 2 Nicotine stomatitis in reverse smokers 3 Erythroplakia
Lec.4: Epithelial Pathology 1
cessation. Usually, habit cessation leads to a normal mucosal appearance within 2 weeks. XI. Nicotine Stomatitis
Although nicotine stomatitis is associated with tobacco smoking (cigar, pipe), it is not considered a premalignant, perhaps because it develops in response to heat rather than the chemicals in tobacco smoke. Similar changes also can be produced by the long term use of extremely hot beverages
But, reverse smoking is more serious. In some cultures, hand-rolled cigarettes and cigars are smoked with the lit end held within the mouth. This reverse smoking habit produces a pronounced palatal keratosis which has a significant potential to develop dysplasia or carcinoma. Clinical features
Nicotine stomatitis most commonly affects men older than 45 years. With long term exposure to heat the palatal mucosa he comes diffusely gray or white numerous slightly elevated papules are noted, usually with punctate red centers. Such papules represent inflamed minor salivary glands and their ductal orifices
Histopathology Nicotine stomatitis is characterized by hyperkeratosis and acanthosis of the palatal epithelium and subepithelial mild, patchy. chronic inflammation. Squamous metaplasia of the excretory ducts is usually seen Epithelial dysplasia rarely is seen
Treatment Nicotine stomatitis is reversible within to 2 weeks of smoking cessation. Although the risk of carcinoma development in the
considered to be carcinogenic, although the risk is less than that associated with cigarette smoking and alcohol abuse. Clinical features
Smokeless tobacco keratosis represents a characteristic white or gray plaque involving the mucosa in direct contact with tobacco. The altered mucosa typically is thin with an indistinct border. Sometimes mild peripheral erythema is present
Upon palpation, the lesion may feel soft and velvety. Stretching of the mucosa often reveals a distinct "pouch" caused by flaccidity in the area of chronic tobacco placement The mucosa appears fissured, a fashion resembling the sand on a beach after an ebbing tide. Induration, ulceration, and pain are not associated with this lesion
Histopathology There is hyperkeratosis and acanthosis Epithelial dysplasia is uncommon
Treatment Treatment depends on histopathologic diagnosis. Keratoses without dysplasia or malignancy may require only continued
monitoring and encouraged tobacco
Dr. Mustafa Al-Talqani
palate is minimal (except in individuals who reverse smoke), nicotine stomatitis is a marker or indicator of intense tobacco use and hence may indicate increased risk of epithelial dysplasia and neoplasia elsewhere in the oral cavity and respiratory tract.
XIL Oral Submucous Fibrosis Oral submucous fibrosis is a high-risk, precancerous condition characterized by chronic, progressive scarring of the oral mucosa. It is seen primarily in the Indian subcontinent. The etiology is linked to the use of betel quid (paan) products.
Clinical features
Typical chief complaints include trismus and burning sensation with intolerance to spicy foods. The buccal mucosa, retromolar area, and soft palate are the most commonly affected sites. Subsequently, the mucosa develops a blotchy, marble-like pallor and progressive stiffness. The tongue may become immobile, diminished in size, and devoid of papillae
Histopathology
Oral submucous fibrosis is characterized by deposition of densely collagenized, hypovascular connective tissue: Epithelial dysplasia is found in about 15% of cases submitted for biopsy, and carcinoma is found in at least 6% of sampled cases,
Treatment
Oral submucous fibrosis does not regress with habit cessation Treatment includes intralesional corticosteroids or excision of the fibrous bands: relapse is common
Originally defined by the World Health Organization (WHO): oral leukoplakia (leuko - white; plakia patch) represents "a white patch or plaque that cannot be characterized clinically or pathologically as any other disease
The definition of leukoplakia is unusual in that it makes the diagnosis dependent not so much on definable appearances as on the exclusion of other entities that appear as oral white plaques such lesions as lichen planus, frictional keratosis, tobacco pouch keratosis, nicotine stomatitis, leukoedema and white sponge nevus must be ruled out before a clinical diagnosis of leukoplakia can be made.
As with most oral white lesions, the clinical color results from a thickened surface keratin layer, which appears white when wet, or a thickened spinous layer which masks the normal vascularity of the underlying connective tissue,
Etiopathogenesis
The cause of leukoplakia remains unknown, although hypotheses abound. Among the various proposed contributory factors, tobacco smoking appears to be the most closely associated with leukoplakia. More than 80% of patients with leukoplakia are smokers, and smokers are much more likely to have leukoplakia than nonsmokers
Alcohol exerts a strong synergistic effect with tobacco in oral cancer development. Nevertheless, there is conflicting evidence as to whether alcohol is associated independently with leukoplakia. Ultraviolet (UV) radiation is a causative factor for leukoplakia of the lower lip vermilion,
C Albicans and human papilloma virus (HPV) have been implicated in the etiology of leukoplakia, but still controversial. Clinical Features
Leukoplakia usually affects persons older
than 40 years Prevalence increases rapidly with age, especially for males. Mostly found on the lip vermilion, buccal mucosa, gingiva, the tongue, and floor of the mouth.
Although leukoplakia does not constitute a specific histopathologic diagnosis, it is considered a precancerous (premalignant) That is, the frequency of transformation into frequency of malignancy is greater than that for normal or unaltered mucosa. Leukoplakia is by far appears as a flat or slightly elevated, gray or the most common oral pre-cancer, representing 85% of such lesions. In addition, more than one-third of oral carcinomas exhibit leukoplakia in close proximity
2.
Lec. 5: Epithelial Pathology 2
Granular (nodular) leukoplakia such presentation is often seen when some homogenous leukoplakia develop increased surface irregularities.
Verrucous (verruciform) leukoplakia in which lesions develop sharp or blunt, wart like projections.
Proliferative verrucous leukoplakia (PPL) is s special high-risk form of leukoplakia that is characterized by the development of multiple, slowly spreading keratotic plaques with rough surface projections
Many leukoplakic lesions are a mixture of the previously mentioned subtypes Leukoplakia may become dysplastic or even malignant, with no change in its clinical appearance. However, some lesions eventually demonstrate scattered patches of redness, called erythroplakia. Such areas usually represent sites in which epithelial cells are so immature or atrophic that they can no longer produce keratin. This intermixed red-and-white lesion, called erythroleukoplakia or speckled leukoplakia, frequently exhibits advanced dysplasia.
Histopathology/Epithelial Dysplasia Leukoplakia is characterized by hyperkeratosis, with or without acanthosis.
Leukoplakia may have a varied clinical appearance and tend to change over time. Clinical presentations include: Thin leukoplakia mild leukoplakia that
white plaque, with demarcated borders homogeneous (thick) leukoplakia a progressive stage of thin leukoplakia in tobacco smokers who do not reduce their habit Clinically characterized by a thickened, leathery, distinctly white plaque with deepened fissures
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Dysplastic changes typically begin in the basilar and p basilar portions of the epithelium. The more dysplastic the epithelium becomes, the more the atypical epithelial changes extend to involve the entire thickness of the epithelium. The histopathological alterations of dysplastic epithelial cells are similar to those of SCC, For the sake of clarity, one has to distinguish between cellular changes and architectural changes of epithelial dysplasia. Cellular alterations:
1. Enlarged nuclei and cells
2. Large and prominent nucleoli. 3. Increased nuclear-to-cytoplasmic (NC)
mtio
4. Hyperchromatic (dark-staining) nuclei 5. Cellular and nuclear pleomorphism . Dyskeratosis (premature keratinization
of individual cells). 7. Increased mitotic activity (excessive
bers of mitosis). & Booru Mitotic figures (tripolar or star-shaped mitosis mitotic figures
above the basal layer)
Architectural alterations
1. Bulbous or teardrop-shaped rete ridges 2. Loss of polarity lack of progressive maturation toward the surface)
3. Keratin or epithelial pearls focal, round collections of concentrically layered
keratinized cells)
4. Loss of epithelial cell cohesiveness The grade of epithelial dysplasia refers to
ite
r intensity In this context usually represent sites in which epithelial cells are so immature or atrophic that they can no longer produce keratin This intermixed red-and-white lesion called erythroleukoplakia or speckled leukoplakia, frequently exhibits advanced dysplasia.
Histopathology/Epithelial Dysplasia Leukoplakia is characterized by hyperkeratosis, with or without acanthosis. Frequently variable numbers of chronic inflammatory cells are noted within the connective tissue. The keratin layer may
consist of parakeratin (hyperparakeratosis), orthokeratin (hyperorthokeratosis), or a combination of both Histopathologic changes range from hyperkeratosis, dysplasia, and carcinoma in situ to invasive SCC
Lec. 5: Epithelial Pathology 2
III. Severe epithelial dysplasia demonstrates alterations from the basal layer to a level above the midpoint of the epithelium. IV. Carcinoma in situ:
is defined as dysplasia involving the entire thickness of the epithelium. Some authorities consider carcinoma in situ to be a precancerous lesion, whereas others believe that it represents a genuine malignancy discovered before invasion
11. Erythroplakia Similar to leukoplakia, erythroplakia is defined as a red patch or plaque that cannot be clinically or pathologically diagnosed as any other condition. Predominantly a any Predominantly a disease of middle-aged to older adults with no significant sex predilection. The causes of erythroplakia are presumed to be the same as those associated with SCC
The floor of mouth, tongue, and soft palate are the most common sites of involvement, and multiple lesions may be present. The lesion appears as a well demarcated, erythematous patch or plaque with a soft, velvety texture It is usually asymptomatic and may be associated with an adjacent leukoplakia (erythroleukoplakia)
Almost all erythroplakia demonstrate significant epithelial dysplasia, carcinoma in situ, or invasive SCC. The epithelium lacks keratin production and often is atrophic, thereby allowing the underlying vasculature to produce a red appearance. The underlying connective tissue frequently demonstrates chronic inflammation
Lec 5: Epithelial Pathology 2
carcinoma is about four times greater than that among the general population. The relative risk (smoker's risk for oral cancer compared with that of a nonsmoker) is dose-dependent and time-dependent
star-shaped mitoses or mitotic flies above the basal layer)
Architectural alterations:
1 Bulbous or tear drop-shaped rete ridges 2. Loss of polarity lack of progressive
maturation toward the surface). 3. Keratin or epithelial pearls local, round
collections of concentrically layered keratinized cells). 4 Loss of epithelial cell cohesiveness
The grade of epithelial dysplasia refers to its "severity or intensity. In this context,
dysplasia has been classified as follows: Mild epithelial dysplasia:
refers to alterations limited principally to the basal and parabasal layers. IL. Moderate epithelial dysplasia: demonstrates involvement from the basal layer to the mid-portion of spinous layer.
Dr. Mustafa Al-Talqani
III. Squamous Cell Carcinoma (SCC)
Oral squamous cell carcinoma (SCC) is the most common oral cancer, which accounts for more than 90% of oral malignancies SCC is a malignant neoplasm of the stratified squamous epithelium that is capable of locally destructive growth and distant metastasis
The incidence of oral cancer varies enormously around the world. In both United Kingdom and USA, oral cancer accounts for less than 4% of all cancers, but in India and South East Asia, it accounts for up to 40% of all malignant tumors.
Interestingly, over the past several decades, a significant increase in the incidence of oral tongue cancer has been noted among young individuals, especially white women aged 18 to 44 years; some of patient were otherwise healthy. The underlying cause for this trend is uncertain Etiology
The cause of oral SCC is multifactorial No single causative agent or factor (carcinogen) has been clearly defined or accepted, but both extrinsic and intrinsic factors may be involved. Many SCCs have been documented to be associated with preceded by a precancerous lesion. especially leukoplakia. Etiological and risk factors for SCC include the following:
1 Tobacco Smoking Tobacco smoke contains more than 70 carcinogens. In addition, smoking produces free radicals and oxidants that promote the destruction and counteract the protective effects of endogenous antioxidants. The proportion of smokers (80%) among patients with oral
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6. Radiation: UV radiation represents a major risk factor for lip carcinoma. X-ray decreases immune reactivity and produces chromosomal abnormalities. Radiotherapy to the head and neck area increases the risk carcinoma is about four times greater than that among the general population. The relative risk (smoker's risk for oral cancer compared with that of a nonsmoker) is dose-dependent and time-dependent.
2 Smokeless Tobacco Approximately 50% of oral cancers in smokeless tobacco users occur at the site where the tobacco is habitually placed
3. Betel Quid (Paan): Carcinogenicity of betel quid traditionally has been attributed to tobacco although areca nut alone also appears to be carcinogenic. This habit is associated with development of precancers. such as leukoplakia and oral submucous fibrosis
4. Alcohol: It is well established that alcohol in combination with tobacco is a significant risk factor for oral cancer development Studies have reported a twofold to fourteenfold increased risk for oral cancer among heavy drinkers. The risk generally appears to be dose-dependent and time-dependent.
Ethanol in alcoholic beverages is metabolized into acetaldehyde, which is a known carcinogen. In addition, carcinogen impurities may be present in some alcoholic beverages. Moreover, alcohol may help solubilize other carcinogenic compounds and may increase the permeability of oral epithelium to these compounds
5. Occupational Exposures and Environmental Pollutants: Workers in the wood products industry and regions with heavy metal pollutants showed an increased risk for oral cancer
Lec. 5: Epithelial Pathology 2
immortalize the host cell, thereby facilitating malignant transformation. Human papillomavirus (HPV) and human immunodeficiency virus (HIV) are implicated in the oral carcinogenesis.
A strong link between high-risk HPV (16 and 18 types) and oropharyngeal carcinoma has been established. The mechanisms by which HPV is believed to contribute to carcinogenesis are linked to the production of viral oncogenes.
HIV-infected individuals have increased risk to develop oral and pharyngeal SCC. In addition, HIV-related immunosuppression contributes to elevated cancer risk and accelerated cancer development 11. Immunosuppression Persons with
HIV infection and those who are undergoing immunosuppressive therapy are at increased risk for oral SCC and other malignancies. 12. Oncogenes and Tumor Suppressor Genes. The molecular basis of carcinogenesis involves an accumulation of
mutations in two broad classes w
6, Radiation UV radiation represents a major risk factor for lip carcinoma. X-ray decreases immune reactivity and produces chromosomal abnormalities. Radiotherapy to the head and neck area increases the risk for later development of a new primary oral malignancy. It is controversial whether dental radiography may pose an increased risk to develop various tumors, however, dental imaging has not been proven to be associated with oral SCC development
7. Vitamin/Mineral Deficiencies and Dietary Factors Iron deficiency is associated with an elevated risk for SCC. Iron deficiency may cause impaired cell mediated immunity and impaired epithelial turnover with associated degenerative changes (mucosal atrophy) that increase susceptibility to malignant transformation.
Vitamin-A is thought to be inversely proportional to the risk of SCC and leukoplakia. It is suggested that high intake of fruits and vegetables decreases the risk for numerous cancers.
8. Bacteria certain oral bacteria (such as
some Streptococcus species and Neisseria
species) may interact with tobacco and
alcohol and contribute to carcinogenesis via acetaldehyde production (a carcinogen). 9. Candida: Candida may contribute to acetaldehyde production, but its role in oral carcinogenesis is largely circumstantial 10, Oncogenic Viruses: Oncogenic
(tumor producing) viruses may play a major role in a wide variety of cancers. Vital integration into the host's genetic material may result in abnormal cell growth and proliferation The oncogenic viruses may
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Clinical and Radiographic Features
Persons with oral SCC are most often older men who have been aware of an alteration for several months before seeking professional help. There is minimal pain during the early growth phase, which may explain the delay in seeking professional care. If the health care professional does not have a high index of suspicion, then additional weeks or months may elapse before a biopsy is performed. Early diagnosis is of prime importance and has great impact on prognosis the earlier the diagnosis the better the prognosis)
SCC has a varied clinical presentation, including the following:
Exophytic (mass-forming)
Endophytic invasive, and ulcerated) Leukoplakia (white patch)
Erythroplakia (red patch)
Erythroleukoplakia (combined red and
white patch)
Leukoplakia and erythroplakia forms of viral oncogenes.
HIV-infected individuals have increased risk to develop oral and pharyngeal SCC. In addition, HIV-related immunosuppression contributes to elevated cancer risk and accelerated cancer development,
perio diagnosis is of prime importance and has great impact on prognosis the earlier the diagnosis, the better the prognosis). SCC has a varied clinical presentation,
including the following
11. Immunosuppression: Persons with HIV infection and those who are undergoing immunosuppressive therapy are at increased risk for oral SCC and other malignancies
12. Oncogenes and Tumor Suppressor Genes. The molecular basis of carcinogenesis involves an accumulation of mutations in two broad classes of genes proto-oncogenes and tumor suppressor genes. Proto-oncogenes may be transformed into activated oncogenes by environmental agents (eg viruses, irradiation, and chemical carcinogens) or inherited changes, Activated oncogenes promote uncontrolled cell division and are involved in the initiation and progression of a wide variety of malignancies. Tumor suppressor genes, on the other hand, inhibit cell division and indirectly allow tumor production when they become inactivated or mutated.
Lec. 5: Epithelial Pathology 2
red, or white mucosa. The rolled border results from invasion of the tumor under adjacent epithelium
Destruction of underlying bone, when
present, may be painful or completely painless it appears on radiographs as a "moth-eaten" radiolucency with ill-defined or ragged margins (an appearance similar to osteomyelitis). Perineural invasion may cause paresthesia.
From an epidemiological and clinico pathological perspective. SCC can be divided into three categories: Lip Vermilion Carcinoma
Intraoral Carcinoma
Oropharyngeal Carcinoma Lip Vermilion Carcinoma
Carcinoma of the lip vermilion is somewhat different from intraoral carcinoma. It has a pathophysiology more akin to SCC of sun-exposed skin White males are affected most commonly. The low incidence among women may be related to little outdoor occupational activity and prevalent use of lip protective agents. In nonwhites, racial pigmentation may provide protection against sun exposure (UV light).
Carcinoma of the lip vermilion typically is found in light skinned persons with chronic exposure to sunlight (UV radiation). It may arise at the site where the patient holds a cigarette, cigar, or pipe Almost 90% of lesions are located on the lower lip. The typical vermilion carcinoma is a small crusted, oozing, non-tender, and indurated ulceration. The tumor usually grows slowly
Exophytic (mass-forming) Endophytic invasive, and ulcerated) Leukoplakia (white patch)
Erythroplakia (red patch) Erythroleukoplakia (combined red and
white patch)
Leukoplakia and erythroplakia forms are probably early cases that have not yet produced a mass or ulceration, and the clinical features are identical to those described for leukoplakia and erythroplakia.
An exophytic lesion typically has a surface that is irregular, fungating, papillary, or verruciform, and its color may vary from normal to white or red, depending on the amount of keratin and vascularity. The surface is often ulcerated, and the tumor feels hard (induration) on palpation.
The endophytic growth pattern has a central, depressed, irregularly shaped ulcer with a surrounding "rolled" border of pink,
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Intraoral Carcinoma
The majority of intraoral carcinomas are concentrated in the lower part of the mouth, particularly posterior lateral and ventral surfaces of the tongue, the floor of the mouth and the lingual aspect of the alveolar margins, forming a U-shaped area extending back towards the oropharynx. Two major factors help to explain why this region is at such a high risk: First any carcinogen may mix with saliva, pool in the floor of the mouth, and constantly bathe these anatomic sites. Second these regions are covered by a thin non-keratinized mucosa which provides less protection from carcinogens However, other sites of SCC involvement (in descending order of frequency) are the gingiva, buccal mucosa, labial mucosa, and hard palate. The tongue represents an increasingly common site of involvement in young patients(for unknown reasons).
Of all intraoral carcinoma, floor of mouth lesions are the most likely to arise from a preexisting leukoplakia or erythroplakia Gingival and alveolar carcinomas are usually painless and most frequently arise from keratinized, posterior mandibular mucosa Gingival and alveolar carcinomas have a special propensity to mimic common, benign inflammatory and reactive lesions, such as the pyogenic granuloma, gingivitis, and periodontal disease. Gingival tumors often destroy the underlying bone and cause tooth mobility. The lesion may go unrecognized until after tooth extraction, when it proliferates out of the socket to mimic the granulation tissue of an epulis granulomatosa >
Oropharyngeal Carcinoma
Lip Vermilion Carcinoma
Carcinoma of the lip vermilion is somewhat different from intraoral carcinoma. It has a pathophysiology more akin to SCC of sun-exposed skin White males are affected most commonly. The low incidence among women may be related to little outdoor occupational activity and prevalent use of lip protective agents. In nonwhites, racial pigmentation may provide protection against sun exposure (UV light),
Carcinoma of the lip vermilion typically is found in light skinned persons with chronic exposure to sunlight (UV radiation). It may arise at the site where the patient holds a cigarette, cigar or pipe Almost 90% of lesions are located on the lower lip. The typical vermilion carcinoma is a small. crusted, oozing, non-tender, and indurated ulceration The tumor usually grows slowly
Lec. 5: Epithelial Pathology 2
Cancers that develop in an edentulous
area may "wrap around" a denture flange and superficially resemble inflammatory fibrous hyperplasia (epulis fissuratum). Tumors of the maxillary alveolar ridge may extend onto the hard palate. The buccal mucosa is an especially common site for oral carcinoma in regions of the world where betel quid use is prevalent Oropharyngeal Carcinoma
Oropharyngeal carcinomas exhibit the same basic clinical appearance as more anterior carcinomas: however, in this posterior location, lesions often go unrecognized for long periods. By the time of diagnosis, tumor size is typically greater than that of oral carcinomas, and the proportion of cases with cervical and distant metastasis is higher Common presenting symptoms for oropharyngeal carcinoma include persistent sore throat, difficulty in swallowing (dysphagia), and pain on swallowing (odynophagia). The pain may be dull or sharp and is referred to the ear.
Metastasis
Metastasis of oral SCC occurs largely via the lymphatics to the ipsilateral cervical lymph nodes. A cervical lymph node that contains metastatic carcinoma is usually firm to stony hard, non-tender, and enlarged. If the malignant cells have perforated the capsule of the node and invaded into surrounding tissues, then the node will feel fixed. The most common sites of distant metastasis are the lungs, liver, and bones, but any part may be affected
Lec. 5: Epithelial Pathology 2
(in descending order of frequency) are the gingiva, buccal mucosa, labial mucosa, and hard palate. The tongue represents an increasingly common site of involvement in young patients(for unknown reasons)
Of all intraoral carcinoma, floor of mouth lesions are the most likely to arise from a preexisting leukoplakia or erythroplakia Gingival and alveolar carcinomas are usually painless and most frequently arise from keratinized, posterior mandibular mucosa, Gingival and alveolar carcinomas have a special propensity to mimic common, benign inflammatory and reactive lesions, such as the pyogenic granuloma, gingivitis, and periodontal disease. Gingival tumors often destroy the underlying bone and cause tooth mobility. The lesion may go unrecognized until after tooth extraction, when it proliferates out of the socket to mimic the granulation tissue of an epulis granulomatosa.
Dr. Mustafa Al-Talqani
Lymph node involvement may occur early in oral carcinomas, but enlarged regional nodes do not necessarily indicate metastatic spread as they may show only non-specific reactive hyperplasia.
Staging/ TNM system
Assigning the proper clinical and pathological stage is one of the key activities for clinicians caring for those afflicted with cancer Tumor size and the extent of metastatic spread are the best prognostic indicators for oral SCC Quantifying these clinical parameters is called staging. Table (1) summarizes the tumor-node-metastasis (TNM) system for staging oral carcinoma. This staging protocol depends on three basic clinical features:
T: Size of the primary tumor, in centimeters N: Regional lymph node involvement M: Distant metastasis Updates of the TNM staging system
1. Elimination of the TO (unknown primary) category because greater than 90% of these TO designations (lymph nodes in patients with no detectable primary) reflect high-risk human papillomavirus-associated oropharyngeal and nasopharyngeal cancers 2 Depth of invasion (DOI) has been included in the Category that will better discriminate the higher risk small cancers as
demonstrated by deeply invasive tumors
from those with less invasive cancers.
3. Extranodal extension (ENE) has been added as a prognostic variable for regional lymph node metastases (N category). ENE-positive cases have higher N score than ENE-negative
Histopathology
SCC is characterized histopathologically by invasive islands and cords of malignant squamous epithelial cells. Invasion is represented by irregular extension of lesional epithelium through the basement membrane and into subepithelial connective tissue. The invading tumor destroys normal tissue and may extend deeply into underlying adipose tissue, muscle, or bone. Lesional cells may breach the perineurium that encases nerve bundles (perineural invasion) or may invade the lumina of veins or lymphatics (vascular invasion. There is a strong inflammatory response to invading
epithelium, and necrosis may be present. The malignant epithelial cells generally show abundant eosinophilic cytoplasm with large darkly staining (hyperchromatic) large, darkly staining (hyperchromatic) nuclei and an increased N/C ratio.
Lec. 5: Epithelial Pathology 2
Treatment and Prognosis
Many patients lives have been shortened by having malignant tumors treated with Repeated courses of antibiotics. Health care professional should have a high index of suspicion, especially for worrisome lesions at early stages. EARLY DETECTION is the most effective approach to reduce morbidity and mortality from oral cancer.
Clinical staging guides the treatment of SCC. Generally, treatment strategies include: surgical excision (with safe margin), radiation therapy, or combined chemoradiation therapy. The treatment plan is tailored by the surgeon according the stage of the tumor and the general medical health of the patient.
Patients with one carcinoma are at increased risk for additional concurrent (synchronous) or more commonly, later (metachronous) primary surface epithelial malignancies. The development of multiple mucosal cancers is hypothesized to be
Dr. Mustafa Al-Talqani
Varying degrees of cellular and nuclear pleomorphism are seen. The normal product of squamous epithelium is keratin, and keratin pearls (a round focus of concentrically layered, keratinized cells) may be produced within lesional epithelium
Histopathologic grading of SCC is based upon the degree of resemblance to normal squamous epithelium and the amount of keratin production. Lesions are graded on a three-point (grades I to III). The less differentiated tumors receive the higher numerals. The histopathologic grade of a tumor is related somewhat to its biologic behavior. The clinical staging correlates much better with the prognosis than microscopic grading. The histopathological grades of SCC include:
Grade In well-differentiated, low-grade Tumor is closely resemble its tissue of origin, grow slightly slow, and metastasizes later in its course, Keratin pearls are often found within the masses of infiltrating cells. Nuclear and cellular pleomorphism is not prominent and there are few mitoses,
Grade 11 (moderately-differentiated Tumors show less keratinization and more nuclear and cellular pleomorphism and mitotic activity, but are still readily identified as squamous in type.
Grade II noor differentiated, high grade): Tumor with marked pleomorphism and little or no keratin production that may be so immature that it becomes difficult to identify the tissue of origin Such tumors often enlarge rapidly and metastasize early
Dr. Mustafa Al-Talqani
elongated rete ridges that appear to "push" into the underlying connective tissue. The lesional epithelial cells generally show no
significant cytologic atypia. The treatment of choice is surgical excision. The surgery generally need not be as extensive as that required for routine SCC of a similar size.
V. Basal cell carcinoma (rodent ulcer)
Basal cell carcinoma represents the most common skin cancer, and the most common of all cancers. It is a locally invasive, slowly spreading, epithelial malignancy that arises from the basal cell layer of the skin and its appendages. It is mainly results from UV radiation exposure. The risk generally increases with age. proximity to the equator, and lighter skin pigmentation.
Basal cell carcinoma most often affects white adults. It typically presents as a slow growing nodule that eventually ulcerates centrally Untreated lesions continue to Histopathology
SCC is characterized histopathologically by invasive islands and cords of malignant squamous epithelial cells. Invasion is represented by irregular extension of transitional epithelium through the basement membrane and into subepithelial connective tissue. The invading tumor destroys normal tissue and may extend deeply into underlying adipose tissue, muscle, or bone. Lesional cells may breach the perineurium that encases nerve bundles (perineural invasion or may invade the lumina of veins or lymphatics (vascular invasion). There is a strong inflammatory response to invading epithelium, and necrosis may be present
Grade I (well-differentiated, low-grade) Tumor is closely resemble its tissue of origin, grow slightly slow, and metastasizes later in its course. Keratin pearls are often found within the masses of infiltrating cells Nuclear and cellular pleomorphism is not prominent and there are few mitoses.
Grade Il moderately-differentiated) Tumors show less keratinization and more nuclear and cellular pleomorphism and mitotic activity, but are still readily identified as squamous in type.
Grade III (nuort-differentiated, high gradel Tumor with marked pleomorphism and little or no keratin production that may be so immature that it becomes difficult to identify the tissue of origin. Such tumors often enlarge rapidly and metastasize early
Dr. Mustafa Al-Talqani
The malignant epithelial cells generally show abundant eosinophilic cytoplasm with show abundant eosinophilic cytoplasm with large, darkly staining (hyperchromatic) nuclei and an increased N/C ratio.
Lec. 5: Epithelial Pathology 2
Treatment and Prognosis
Many patients' lives have been shortened by having malignant tumors treated with repeated courses of antibiotics. Health care professional should have a high index of suspicion, especially for worrisome lesions at early stages. EARLY DETECTION is the most effective approach to reduce
elongated rete ridges that appear to "push" into the underlying connective tissue. The lesional epithelial cells generally show no significant cytologic atypia.
The treatment of choice is surgical excision. The surgery generally need not be
morbidity and mortality from oral cancer Clinical staging guides the treatment of SCC Generally, treatment strategies include: surgical excision (with safe margin) radiation therapy, or combined chemoradiation therapy. The treatment plan is tailored by the surgeon according the stage of the tumor and the general medical health of the patient.
as extensive as that required for routine SCC of a scimitar size.
V. Basal cell carcinoma (rodent ulcer)
Basal cell carcinoma represents the most common skin cancer, and the most common of all cancers. It is a locally invasive, slowly spreading, epithelial malignancy that arises from the basal cell layer of the skin and appendages. It is mainly results from UV radiation exposure. The risk generally increases with age, proximity to the equator, and lighter skin pigmentation.
Patients with one carcinoma are at increased risk for additional concurrent (synchronous) or more commonly, later (metachronous) primary surface epithelial malignancies. The development of multiple mucosal cancers is hypothesized to be resulted from field cancerization. IV. Verrucous carcinoma
(Ackerman's tumor) Verrucous carcinoma is an uncommon distinctive low-grade variant of SCC, which presents as a diffuse, well-demarcated, painless thick plaque with papillary or verruciform surface projections. The most common sites of oral mucosal involvement include the mandibular vestibule, buccal
mucosa, gingiva, tongue, and hard palate. It has a good prognosis and extremely rare to metastasize Verrucous carcinoma has a deceptive benign microscopic appearance; it is characterized by wide and
Basal cell carcinoma most often affects white adults. It typically presents as a slow growing nodule that eventually ulcerates centrally. Untreated lesions continue to enlarge slowly, with ulceration and destruction of underlying structures-hence the term rodent ulcer. Histopathologically, it consists of cytologically malignant basaloid cells, arranged in a variety of patterns, invading adjacent tissue. Lesions are treated by routine surgical excision
Field cancerization a process whereby exposure to carcinogens, such as tobacco, UV light and alcohol, creates a diffuse field of altered epithelial cells with increased potential for malignant transformation.Lec. 6: Connective Tissue Pathology
It is a common lesion that occurs in the
vestibular mucosa where the denture flange contacts tissue. Chronic irritation may result in the appearance of painless folds of fibrous tissue reparative response) surrounding the overextended flanges or ill fitting denture
Treatment
Surgical removal The ill-fitting denture should be remade or relitted to prevent a recurrence of the lesion. V. Inflammatory Papillary hyperplasia
Inflammatory papillary hyperplasia (known as Denture Papillomatosis) is a reactive tissue growth that usually develops beneath a denture. The exact pathogenesis is unknown, however, the condition most often appears to be related to an ill-fitting denture, poor denture hygiene and/or wearing the denture 24 hours a day Clinical features
Inflammatory papillary hyperplasia usually occurs on the hard palate benesta denture base. It is usually asymptomatic. The mucosa is erythematous and has a pebbly or papillary surface Histopathology
Fibrous and epithelial hyperplasia resulting in papillary surface projections. Denture removal, antifungals or surgical
Treatment
removal according to the lesions extent.
VI. Peripheral Ossifying Fibroma The peripheral ossifying fibroma is a relatively common gingival growth bar is
Lec. 6: Connective Tissue Pathology
Fibrosarcoma is often diagnosis of exclusion. Well-differentiated examples consist of fascicles of spindle-shaped cells that classically form a herringbone pattern. Pleomorphism and mitotic activity may be seen.
Treatment
Wide surgical excision,
recurrence rate.
with high
VIII, Pyogenic Granuloma (Lobular Capillary Hemangioma)
The pyogenic granuloma is a common tumor-like growth of the oral cavity: Pyogenic granulomas (lobular capillary hemangioma) currently are categorized ns vascular tumors. The term (pyogenic granuloma) is a misnomer. Although it was originally thought to be caused by pyogenic organisms, it is now believed to he unrelated to infection Furthermore, it represents an exuberant tissue response to local irritation or trauma (it is not a true granuloma)
Clinical features
The pyogenic granuloma is a smooth or lobulated mass that is usually pedunculated. The surface is usually ulcerated and ranges from pink to red to purple Typically, the mass is painless although it often bleeds casily because of its extreme vascularity. Oral pyogenic granulomas show a striking predilection for the gingiva. The lips, tongue, and buccal mucosa are the next most common sites. Pyogenic granuloma can develop at any age it is most common in children and young adults. Most studies
also demonstrate a definite female
Lec. 6: Connective Tissue Pathology
Vascular malformations are structural anomalies of blood vessels with normal
endothelial cell turnover By definition, vascular malformations are present at birth and persist throughout life. Vascular malformations can be categorized according to the type of vessel involved (capillary,
Dr. Mustafa Al-Talani
considered to be reactive rather than
neoplastic in nature. The pathogenesis of this lesion is uncertain Researchers believe that she peripheral ossifying fibromas develop initially as pyogenic granuloma that undergo fibrous maturation and subsequent clarification
Clinical features The peripheral ossifying
fibroma occurs exclusively on the gingiva It appears as a nodular mass, cither pedunculated or sessile, that usually originates from the interdental papilla It is predominantly a lesion of teenagers and young adults. Almost two-thirds of all cases occur in females with a slight predilection for the maxillary arch
Histopathology
There is fibrous proliferation associated with the formation of a mineralized product (bone, cementum-like material, and/or dystrophic calcifications) Treatment
Surgical excision. Recurrence is possible
VIL Fibrosarcoma
The fibrosarcoma is a rare malignant tumor of fibroblasts. The tumor is most common in the extremities.
Clinical features
Fibrosarcomas most often present as slow-growing masses that may reach considerable size before they produce pain They can develop at any age and occur anywhere in the head and neck region
Dr. Mustafa Al-Talqani
predilection, possibly because of the
vascular effects of female hormones Pyogenic granuloma frequently develops in pregnant women (may be related to high levels of estrogen and progesterone), so that the term pregnancy tumor often is used.
Epulis granulomatosa is a term used to describe hyperplastic growth of granulation tissue that sometimes arise in healing extraction sockets. These lesions resemble pyogenic granulomas and usually represent granulation tissue reaction to bony sequestra in the socket Histopathology
Microscopic examination of pyogenic granulomas shows highly vascular proliferation that resembles granulation tissue. Numerous vascular channels are formed and organized in lobular aggregates -hence, its name The surface is usually ulcerated. A mixed inflammatory cell infiltrate is evident
Treatment
Conservative surgical excision; rarely recur Treatment of pregnancy tumor should be deferred unless significant functional or anesthetic problems develop. The recurrence rate is bigger and some lesions may resolve
spontaneously after delivery
IX. Hemangiomas and Vascular Malformations
Hemangiomas are the most common
benign tumors of infancy, predominantly of white females. Most hemangiomas cannot be recognized at birth, but arise during the first 8 weeks of life Lec. 6: Connective Tissue Pathology
Fibrosarcoma is often a diagnosis of exclusion Well differentiated examples consist of fascicles of spindle-shaped cells that classically form a herringbone pattern. Pleomorphism and mitotic activity may be
Seen Treatment
Wide surgical excision, with high recurrence rate
VI. Pyogenic Granuloma (Lobular Capillary Hemangioma
The pyogenic granuloma is a common tumor-like growth of the oral cavity Pyogenic granulomas (lobular capillary hemangiomas) cumently are categoxized as vascular tumors. The term (pyogenic granuloma) is a misnomer. Although it was originally thought to be caused by pyogenic organisms, it is now believed to be unrelated to infection. Furthermore, it represents an exuberant tissue response to local irritation or trauma is not a true
granuloma). Clinical features
The pyogenic granuloma is a smooth or
lobulated mass that is usually pedunculated The surface is usually ulcerated and ranges from pink to red to purple Typically, the mass is painless, although it often bleeds easily because of its extreme vascularity Oral pyogenic granulomas show a striking predilection for the gingiva The lips, tongue, and buccal mucosa are the next most common sites. Pyogenic granuloma can develop at any age it is most common in children and young adults. Most studies also demonstrate a definite female
Lec 6: Connective Tissue Pathology
Vascular malformations are structural
anomalies of blood vessels with real endothelial cell turnover. By definition, vascular malformations are present at birth and persist throughout life. Vascular malformations can be categorized according to the type of vessel involved (capillary,
venous, or arteriovenous). Clinical features
During the first few weeks of life, hemangiomas will demonstrate rapid development that is followed, several years Bater, by an involution phase. Superficial tumors of the skin appear raised and bosselated with a bright red color
No.
2
3
4
6
7
8
Criteria
Description
Elements
Growth Radars
Thrill & bruit
Involution Resection
Recurrence
Histopathology
Dr. Mustafa Al-Taqani
predilection, possibly because of the
vascular effects of female hormones Pyogenic granuloma frequently develops in pregnant women (may be related to high levels of estrogen and progesterone). so that the term pregnancy tumor often used.
is
Epulis granulomatosa is a term used to describe hyperplastic growth of granulation tissue that sometimes arise in healing extraction sockets. These lesions resemble pyogenic granulomas and usually represent a granulation tissue reaction to bony sequestra in the socket Histopathology Microscopic examination of pyogenic
granulomas shows a highly vascular
proliferation that resembles granulation
tissue: Numerous vascular channels are
formed and organized in lobular aggregates
-hence, its name The surface is usually
ulcerated. A mixed inflammatory cell
intikate is evident
Treatment
Conservative surgical Excision, rarely recur. Treatment of pregnancy tumor should be deferred unless significant functional or aesthetic problems develop. The recurrence rate is higher and some lesions may resolve spontaneously after delivery
IX.Hemangiomas and Vascular
Malformations Hemangiomas are the most common benign tumors of infancy, predominantly of white females Most hemangiomas cannot be recognized ut birth, but arise during the first 8 weeks of life
Dr. Mustafa Al-Talqani
strawberry hemangioma) Majority of hemangiomas will show complete
resolution by 9 years of age. In contrast to hemangiomas, vascular malformations are present at birth and persist throughout life. They are most common on the face, particularly along the distribution of the trigeminal nerve. Lesions that affect bone (commonly the mandible) usually represent vascular malformations rather than congenital hemangioma
The following table shows a comparison between hemangiomas and vascular malformations
Congenital hemangioma
Benign congenital neoplasms of proliferating endothelial cells
Results in increase in No of capillaries
Rapid congenital growth Ole circumscribed, rarely affects bone
No associated thrill or bruit
Spontaneously involves Persistent lesion resection
Uncomo
Congenital hemangiomas are composed of abundant capillary spaces lined by endothelium without muscular support Vascular malformation may consist not only of capillaries, hut also af venous, arteriolar and lymphatic channels
Lec. 6: Connective Tissue Pathology
X. Lymphangioma
Lymphangioma is benign growth of lymphatic vessels. Oral lymphangioma
OCCURS frequently on the tongue, often
Vascular malformation Lesions resulting from animal vessels morphologies
A mix of arteries, veins, capillaries
Grow with the patient Poorly circumscribed, may affects
bone
Maybe produced
Docs not Difficult to be reset
Common
Treatment
Congenital hemangioma may involute spontaneously during childhood if not surgery, arterial embolization, sclerosing therapy and laser therapy. Vascular malformation, the same approach but difficult to eradicate Lec. 6: Connective Tissue Pathology
X. Lymphangioma
Lymphangioma is benign growth of lymphatic vessels. Oral lymphangioma
occurs frequently on the tongue, often resulting in macroglossia. Usually, it is superficial in location with a pebbly surface that resembles cluster of translucent vesicles (looks like frog eggs). Secondary hemorrhage may cause some of these "vesicles" to become purple Deeper tumors present as soft ill-defined masses
Lymphangioma of the lip cause a macrocheilia, Lymphangioma of the neck (cystic hygroma) is a diffuse soft tissue swelling that may be life threatening beçause it may involve vital structures. Histopathology
Endothelial-lined lymphatic channels are diffusely distributed in the submucosa Treatment .
Surgical removal or sclerotherapy. XI. Traumatic Neuroma
Caused by injury to a peripheral nerve, such as a tooth extraction, from local anesthetic injection, or from an accident Transection of a sensory nerve can result in inflammation and scarring in the area of injury. As the proximal nerve segment proliferates in an attempt to regenerate into to the distal segment, it becomes entangled and trapped in the developing scar, resulting in a mass of fibrous tissue, Schwann cells and axons.
Clinical features Pain ranges from occasional tenderness to constant, severe pain. Injection of local
Lec. 6: Connective Tissue Pathology
It may appear as a solitary lesion or as multiple lesions as part of the syndrome "neurofibromatosis" (von-Recklinghausen's Clinical features
disease of skin).
Solitary neurofibroma presents at any
age as an asymptomatic, submucosal mass The tongue, buccal mucosa, and vestibule are most commonly affected
Histopathology
Spindle shaped cells, with fusiform or wavy nuclei found in a delicate connective
tissue matrix
Treatment Surgical excision
XIV. Neurofibromatosis Type (Von Recklinghausen Disease of the Skin)
Neurofibromatosis is a common hereditary condition, at least, eight types have been recognized but the most common is neurofibromatosis type I (NFI) or von Recklinghausen disease of the skin
Diagnostic Criteria
I-Six or more cafe-au-lait macules with variable size depend on puberty
2-Two or more neurofibromas of any type 3-Freckling in the axillary or inguinal regions
4-Optic glioma
5-Two or more Lisch nodules
Treatment
No specific therapy for NFL. Treatment is directed for management of complications Development of cancer has been reported in 5% of cases.
Dr. Mustafa Al-Talqani
anesthesia relieves the pain. The mental foramen is the most common location, followed by extraction site, in the anterior maxilla and posterior mandible. he lower lip, tongue, buccal mucosa and palate are also relative common soft tissue locations
Histopathology
Bundles of nerves in a haphazard or tortuous arrangement are found admixed with dense collagenous fibrous tissue Treatment
Surgical removal
XI. Schwannoma (Neurilemmoma)
Schwannoma is a benign neoplasm that is derived from a proliferation and Schwann cells, or nerve sheath.
Clinical features
The lesion is an encapsulated submucosal mass The tongue is the most common site
Histopathology Spindle cells that exhibit two different patterns the first, so-called Antoni-A areas consist of spindle cells organized in palisaded manner. The second, so-called Antoni-B, consists of spindle cells haphazardly distributed in a delicate fibrillar
microcystic matrix
Treatment
Surgical excision
XIII. Neurofibroma
The neurofibroma is the most common type of peripheral nerve neoplasm It arises from a mixture of cell types, including Schwann cells and perineural fibroblasts.
Dr. Mustafa Al-Taljani
XV. Rhabdomyomas Rhabdomyomas are extremely rare
benign neoplasms of skeletal muscle, they have a predilection for the soft tissue of the head and neck. Rhabdomyomas of the head and neck can be sub classified into two major categories: 1) adult rhabdomyomas and 2) fetal rhabdomyomas.
XVI. Rhabdomyosarcoma Rhabdomyosarcoma is a malignant neoplasm that is characterized by skeletal muscle differentiation. These tumors are common in young children, accounting for 50% of soft tissue sarcomas in childhood The most frequent site is the head and neck. Microscopically, rhabdomyosarcoma has several patterns including: pediatric rhabdomyosarcoma (embryonal & alveolar) and adult rhabdomyosarcoma (pleomorphic).
Treatment typically consists of local surgical excision followed by multi-agent chemotherapy and radiotherapy if needed
XVIL Lipoma
Uncommon neoplasm of oral cavity,
tongue, buccal mucosa and floor of the mouth among common locations, Appear as asymptomatic, yellowish submucosal mass. overlying epithelium intact and superficial blood vessels are evident over the tumor. Histologically it composed of a well-circumscribed lobulated mass of adipocytes in various degree of maturation
XVIII. Liposarcoma
Rare slow growing malignant neoplasm of adipose tissue of the head and neck.
E
al mustafa altalganlu okufa.edula Lec. 7: Salivary Glands Pathology
Salivary Glands Pathology
Salivary glands are tubulo-acinar exocrine organs responsible for the production and secretion of saliva They comprise the three-paired major glands parotid, submandibular, and sublingual There are also several hundreds minor salivary glands 5001000 which are widely distributed throughout the oral and oropharyngeal submucosa. The functional unit of salivary glands is the secretory acinus and related ducts and myoepithelial cells. Acini may be serous, mucous, or mixed The normal function and health of the
Dr. Mustafa Al-Talqani
L. Mucocele The mucocele is a common lesion of the oral mucosa that results from rupture of a salivary gland duct and spillage of mucin into the surrounding soft tissues. This spillage is often the result of local trauma Unlike the salivary duct cyst, it is not a true cyst since it lacks an epithelial lining
Clinical features Mucoceles typically appear as dome shaped mucosal swellings that can range from few millimeters to several centimeters in size They are most common in children and young adults The spilled mucin below the mucosal
surface often imparts a bluish translucent
mouth depend on normal secretion of the
saliva by the major and minor salivary
glands. Failure of salivary secretion causes
a dry mouth which promotes oral infections. Both the major and minor salivary glands are composed of parenchymal elements which are supported by connective tissue. The parenchyma derived from the oral epithelium consists of terminal secretary units leading into ducts that open into the oral cavity The connective tissue forms a capsule
around the gland and extends into it. The blood and lymph vessels and nerves that supply the gland are contained within the connective tissue The saliva contains various organic and inorganic substances and helps in the mastication, deglutition and digestion of food,
Lac. 7: Salivary Glands Pathology
11. Salivary Duct Cyst (Mucus
Retention Cyst) The salivary duct cyst is a true cyst (epithelium-lined that arises from salivary gland tissue The Rise of such cysts is uncertain
Cyst-like dilatation of salivary ducts also may develop secondary to ductal obstruction (eg mucus plug). which creates increased intraluminal pressure Although some authors refer to such lesions as mucus retention cysts, such lesions probably represent salivary ductal ectasia rather than a true cyst. Clinical features
Salivary duct cysts usually occur in adults and can arise within either the major or minor glands. Cysts of the major glands are most common within the parotid gland, presenting as asymptomatic, slowly growing swellings Intraoral cysts can occur at any minor gland site, but most frequently they develop in the floor of the mouth, buccal mucosa, and lips. They often look like mucoceles and are characterized by a soft, fluctuant swelling Histopathology
The lining of the salivary duct cyst is variable and may consist of cuboidal, columnar, o atrophic squamous epithelium suRRounding thin or mucoid secretions in the lumen
Treatment
Isolated salivary duct cysts are treated by conservative surgical excision. For cysts in the major winds, partial or total removal of the gland may be necessary
Lec. 7: Salivary Glands Pathology
IV. Sialolithiasis (Salivary Calculi: Salivary Stones)
Sialoliths are calcified structures that develop within the salivary ductal system. It is believe that they arise from deposition
of calcium salts around a midas of debris
bue to the swelling, although deeper
mucoceles may be normal in color. The
lesion characteristically is fluctuant, but
some mucoceles feel firmer to palpation
The duration of the lesion can vary from a
few days to several years, however, it may
rupture and release its fluid contents.
The lower lip is the most comMon site for the mucocele, less common sites include the floor of mouth, anterior ventral tongue, buccal mucosa, palate, and retromolar pad.
Histopathology surrounded by a granulation tissue response Treatment
It shows an area of spilled mucin
Sometimes mucoceles rupture and heal by themselves. However, chromic lesions need local surgical excision. To minimize the risk of recurrence, the surgeon should remove any adjacent minor salivary glands.
Dr. Mustafa Al-Talqani
III Runulu
Ranula is a term used for mucoceles that occur in the floor of the mouth, arising from the sublingual gland, which produces a continuous flow of mucus even in the absence of neural stimulation that accounts for such gland's ability to produce a ranula after rupture of one of its multiple ducts. Clinical features
The meestally appears as a blue, dome-shaped, fluctuant swelling in the floor of the mouth. Ranulas are seen most frequently in children and young adults. They tend to be larger than mucoceles, often developing into large masses that fill the floor of the mouth and elevate the tongue The ranula usually is located lateral to the midline, a feature that may help to distinguish it from a midline dermoid cyst. Like coceles, ranulas may rupture and release their contents, only to re-form
Histopathology The microscopic appearance of a raula is similar to that of a mucocele. The spilled mucin elicits a granulation tissue response that typically contains foamy histiocytes. Treatment
Treatment of the ranula consists of removal of the feeding sublingual gland and/or marsupialization Marsupialization exteriorization) entails removal of the roof of the intraoral lesion, which often can be Successful for small, superficial ranulas. However, marsupialization is often unsuccessful for larger ranulas, and removal of the offending gland is the most important consideration in preventing a recurrence.
Dr. Mustafa Al-Talqani
V. Sialadenitis
Inflammation of the salivary glands (sialadenitis) cat arise from infectious and Don't Infectious causes, including . Viral infection (mumps) Lec. 7: Salivary Glands Pathology
IV. Sialolithiasis (Salivary Calculi:
Salivary Stones)
Sialoliths are calcified structures that
develop within the salivary ductal system. It is believed that they arise from deposition of calcium salts around a nidus of debris within the duct lumen This debris may include inspissated mucus, bacteria, ductal epithelial cells, or foreign bodies
Clinical and radiographic features
The submandibular gland has the greater tendency to form sialoliths because of the long tortuous, upward path of the Wharton duct and the thicker, mucoid secretions of this gland. However, the formation of staloliths in other major and minor salivary glands is distinctly less frequent
Symptoms including episodic pain or
swelling (especially at meal-time) vary depending on the degree of obstruction. The Stone may be palpated if it located toward the terminal portion of the duct. Sialoliths appear radiopaque masses on radiograph. Stones in the terminal portion of the submandibular duct are best seen with an occlusal radiograph. On panoramic or
periapical radiographs, the calcification may
appear superimposed on the mandible and
care must be exercised not to confuse it with
an intra-boat lesion.
Treatment
Small sialoliths of the major glands can be treated conservatively by gentle massage to milk the stone toward the duct orifice Sialogogues (drugs that stimulate saliva Now), moist heat and increased fluid intake niso may promote passage of the stone Larger sialoliths usually removed surgically
Lec. 7: Salivary Glands Pathology
episodes of unilateral or bilateral, non- suppurative parotid swelling, usually beginning between the ages of 3 - 6 years. The exact cause is unknown. The condition usually revolves around the time of puberty
Treatment
The treatment of acute sialadenitis includes appropriate antibiotic therapy and rehydration of the patient to stimulate salivary flow Surgical drainage may be needed if there is abscess formation. The management of chronic sialadenitis depends on the severity of the condition and ranges
from conservative therapy to surgery
VI. Mumps (Epidemic Parotitis) Mumps is a viral infection caused by paramyxovirus and Rubulavirus, The virus can be transmitted through respiratory droplets, saliva, and urine. The incubation period usually is 16 to 18 days. Patients are contagious from 1 day before the clinical appearance of infection to 14 days after its clinical resolution
Mumps most commonly occurs in winter and spring Allergy attack, immunity is long lasting. Childhood mumps is becoming infrequent with the use of immunization. Adult mumps may take special form Clinical features
Prodromal symptoms of fever, headache, malaise, anorexia, and myalgia develop first. The parotid glands are involved most often Discomfort and swelling develop in the tissues surrounding the lower half of the ear Enlargement of the glands usually begins on one side, followed by (within a few days) contralateral involvement,
Lec. 7: Salivary Glands Pathology
1. Positive serological factors (autoantibodies, Rheumatoid factor). 2. Labial salivary gland biopsy exhibiting
focal lymphocyte salutemitis
Dr. Mustafa Al-Talqani
V. Sialadenitis
Inflammation of the salivary glands (sialadenitis) can arise from infectious and noninfectious causes, including
1. Viral infection (mumps)
2. Bacterial infections (mostly Suz) may arise as a result of ductal obstruction or decreased salivary flow allowing Retrograde spread of bacteria throughout
the ductal system 3. Recent surgery (especially abdominal
surgery), because the patient has been kept without food or fluids and has received atropine during the surgery
4. Medications producing xerostomia as a
side effect (atropine) 5. Sjögren syndrome
6. Sarcoidosis
7. Allergy
8. Radiotherapy
Clinical and radiographic features
Acute bacterial sialadenitis is most common in the parotid gland. The affected
gland is swollen and painful and the overlying skin may be erythematous and warm. Low-grade fever and trisemus may be present. A purulent discharge often is observed from the duct orifice when the gland is massage
Ductal obstruction can lead to a chronic sialadenitis. Periodic swelling and pain occur, usually a mealtime. Sialography often shows sialectasia ductal dilatation proximal to the area of obstruction
Juvenile recurrent parotitis is the second most common inflammatory salivary disorder of children world-wide (following mumps). It is characterized by recurring
Dr. Mustafa Al-Taqani
The most frequent oral manifestation is
redness and enlargement of Steriset and Wharton salivary gland duct openings. In addition, involvement of the sublingual glands may produce bilateral enlargement of the floor of the mouth. The second most common finding is epididymo-orchitis, which occurs in about 25% of post-pubertal males The testicle
exhibits rapid swelling, with significant pain
and tenderness Permanent sterility is rare
sub-fertility may develop. Less commonly, oophoritis and mastitis can be seen in post pubertal females. In addition, spontaneous abortion occurs in approximately 25% of women who contract mumps during the first trimester of pregnancy. Treatment
The treatment of mumps is palliative in nature (bed rest, avoid sour food and drink, non-aspirin analgesics and antipyretics) VII. Sjögren
Syndrome Sjögren syndrome is a chronic, systemic autoimmune disorder that involves the salivary and lacrimal glands, resulting in xerostomia dry mouth) and xerophthalmia (dry eyes) It also can affect various other body tissues: the skin is often dry, as are the nasal and vaginal mucosae the cause of Sjogren syndrome is unknown. Although it is not a hereditary disease per se, there is evidence of a genetic influence
Clinical features
Sjögren syndrome is not a rare condition with a 9 I female-to-male ratio. American College of Rheumatology has proposed three criteria for classification
Dr. Mustafa Al-Talcan
is the most frequent) Submandibular gland is less commonly affected, but the frequency of malignancy in this gland is Lec. 7: Salivary Glands Pathology
1. Positive serological factors (autoantibodies, Rheumatoid factor).
2. Labial salivary gland biopsy exhibiting
focal lymphocytic sialadenitis 3. Dryness of eyes for certain levels. Xerostomia is the main oral symptom. The patients may complain of difficulty in swallowing, altered taste, or difficulty in wearing dentures The tongue often becomes fissured and exhibits atrophy of the papillae. The mucosa is red and tender. The patient is more susceptible to develop dental decay (especially cervical caries), About one-half of patients have diffuse enlargement of the major salivary glands.
Histopathology The basic microscopic finding is a lymphocytic infiltration of the salivary elands Biopsy of the minor salivary glands of the lower lip sometimes is paid as a diagnostic test for Sjogren's syndrome.
Treatment The treatment of the patient with Sjögren syndrome is most supportive. Artificial tears, artificial saliva, sugarless gum, sialadenitis, and daily fluoride applications can be helpful
Salivary Gland Tumors
Tumors of the salivary glands constitute an important area in the field of oral and maxillofacial pathology. Both major and minor glands can be affected. The most common site for salivary gland tumors is the parotid gland (pleomorphic adenoma is the most common tumor) Fortunately, a relatively low percentage of parotid tumors are malignant (mucoepidermoid carcinoma
Lec. 7: Salivary Glands Pathology
grotesque proportions. It is mostly unilateral, but bilateral tumors have been reponed (synchronous or metachronous). The palate (posterior lateral aspect) is the most common site for minor salivary gland mixed tumors, presenting as smocith- surfaced, dome-shaped, immovable masses The upper lip is the next common site.
Histopathology The tumor is composed of variable
Dr. Mustafa Al-Talgani
is the most frequent) Submandibular
gland is less commonly affected but the frequency of malignancy in this gland is much greater than that of the parotid gland. Tumors of the sublingual gland are rare However, vast majority of sublingual gland tumors are malignant. Minor salivary glands are the second most common site for salivary neoplasia, unfortunately, relatively high proportions of these have been malignant
Generally, salivary gland tumors may arise from epithelial mesenchymal or
mixed origin
VIIL Pleomorphic Adenoma (Benign Mixed Tumor
The pleomorphic adenoma is the most common salivary neoplasm. Pleomorphic adenomas are derived from a mixture of ductal and myoepithelial elements, hence the term "mixed tumor A remarkable microscopic diversity can exist from one tumor to the next as well as in different areas of the same tumor, hence the term "pleomorphie".
Clinical features
Pleomorphic adenoma is typically a well circumscribed, encapsulated tumor 1 appears as a painless slowly growing, firm mass. It is most common in young and middle-aged adults.
Parotid and submandibular glands are commonly affected major glands. Most pleomorphic adenomas of the parotid gland occur in the superficial lobe and present as a swelling overlying the mandibular ramus in front of the car. Facial nerve palsy and pain are rare. If neglected, the lesion can grow to
Dr. Mustafa Al-Talqani
IS. Monomorphic Adenoma
The term monomorphic adenoma originally was used to describe a group of benign salivary gland tumors demonstrating a more uniform histopathologic patter than ihe common pleomorphic adenoma. A variety of tumors were included under the broad heading of monomorphic adenoma, including:
1. Warthin tumor
amounts of epithelial elements and the
2. Canalicular adenoma mesenchyme-like component. The tumor 3. Basal cell adenoma
shows a great variation in appearance.
The epithelium often finns ducts and cystic structures which may contain an eosinophilic coagulum) or may occur as islands or sheets of cells. Myoepithelial cells often make up a large percentage the tumor cells and have a variable morphology The stroma is highly characteristic and
4. Oncocytoma Because of its ambiguous nature, the term monomorphic adenoma probably should be avoided, and cach of the tumors mentioned should be referred to by its more
specific name.
X. Warthin Tumor (Papillary Cystadenoma Lymphomatosum)
variable, presenting as myxomatous, chondroid or hyalinized background At times, for osteoid also is seen. Treatment
Warthin tumor is a benign neoplasm that occurs almost exclusively in the parotid gland. It represents the second most common benign parotid tumor.
The pathogenesis of Warthin tumor is uncertain There is a strong association between the development of this tumor and smoking Smokers have an eightfold greater risk for Warthin tumor than do nonsmokers Clinical features
Pleomorphic adenomas are treated by
surgical incision, along with preservation of the facial nerve. With adequate surgery the prognosis is excellent. The recurrence is possible The risk of malignant transformation is a
potential complication resulting in a carcinoma ex pleomorphic adenoma. This risk increases with the duration of the tumor.
Warthin tumor appears as a slowly growing, painless, nodular mass of the parotid gland. It may be firm or fluctuant to palpation. One unique feature is the tendency of Warthin tumor to occur bilaterally, Warthin tumor most often occurs in older adults, with peak prevalence in the sixth and seventh decades of life Early studies demonstrated a strong male predilection Recently, a more balanced sex ratio is seen, which can be attributed to more equal prevalence of smoking in women over the past decades.
involvement). Most patients are aware of the lesion for less or more than 1 year Histopathology
As its name implies, mucoepidermoid carcinoma is composed of a mixture of mucus-producing cells and squamous (epidermoid) cells. In addition, a third type of cell the intermediate cell-is typically present and is believed to be a progenitor of
Histopathology The Warthin tumor has one of the most
distinctive histopathologic patterns of any tumor in the body. The tumor is composed of a mixture of ductal epithelium and a lymphoid stroma. The epithelium forms a double row cells surrounding cystic spaces. The inner layer consists of tall columnar cells with centrally placed nuclei, The outer layer consists of cuboidal or polygonal cells with more vesicular nuclei The epithelium is supported by a lymphoid stroma that frequently shows germinal center formation Treatment
Surgical removal, these tumors are well encapsulated and seldom to recur.
XI. Mucoepidermoid Carcinoma
Mucoepidermoid carcinoma is the most common salivary gland malignancy. The mucoepidermoid carcinoma is most common in the parotid gland The minor glands constitute the second most common site, especially the palate. Clinical features
The tumor occurs over a wide age range extending from the second to seventh decades of life. It usually starts as asymptomatic swelling followed by pain and facial nerve palsy (in case of parotid
both the mucous and the epidermoid cells. Traditionally, mucoepidermoid carcinomas have been categorized into three histopathologic grades based on the following:
1. Amount of cyst formation
2. Degree of cytologic atypia
3. Relative numbers of mucous epidermoid, and intermediate cells. Low-grade tumors show prominent cyst formation, minimal cellular atypia, and a relatively high proportion of mucous cells
High-grade tumors consist of solid islands of squamous and intermediate cells which can demonstrate pleomorphism and
mitotic activity Intermediate-grade tumors show features that fall between those of the low grade and high-grade neoplasms.
Treatment
Wide surgical excision; the tumor may
recur
E mustafab.altalgani@uokufa.edu.ig
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