Category: Oral Medicine And Radiology

Pleomorphic Adenoma (Mixed Tumour)

Dr. Kriti Jain1 Comment

Name suggested by Willis.
Most common neoplasm of salivary gland tumor.
Benign neoplasm- consisting of cells exhibiting the
ability to differentiate to epithelial (ductal and
nonductal) cells and mesenchymal (chondroid,
myxoid, osseous) cells.
Other names:

  1. Branchioma,
  2. enclavoma,
  3. teratoma,
  4. cyindroma,
  5. myxochondrocarcinoma.

Salivary gland tumor origin: EPITHELIAL

 Shows cytogenic abnormalities in chomosomes- 12q13-15.
 Putative pleomorphic adenoma gene(PLAG1) has been
mapped to chromosomes 8q12

Histogenesis:-

  • Currently, numerous theories centre around the myoepithelial cell and the reserve cell in the intercalated duct.
  • Ultrastructural studies have confirmed the presence of both ductal and myoepithelial cells in pleomorphic adenomas.
  • It follows that possibly either or both may play active roles in the histogenesis of the tumour.
  1. Hubner and his associates:- have postulated that the myoepithelial cell is responsible for the morphological diversity of the tumour, including the production of the fibrous, mucinous, chondroid and osseous areas.
  2. Regezi and Batsakis:- postulated that the intercalated duct reserve cell can differentiate into ductal and myoepithelial cells, and the latter, in turn, can undergo mesenchymal metaplasia, since they inherently have smooth muscle-like properties. Further differentiation into other mesenchymal cells then can occur.
  3. Batsakis:- has discussed salivary gland tumourigenesis, and while still implicating the intercalated duct reserve cell as the histogenetical precursor of the pleomorphic adenoma, stated that the role of the myoepithelial cell is still uncertain and that it may be either an active or a passive participant histogenetically.
  4. Finally, Dardick and his associates have questioned the role of both ductal reserve and myoepithelial cells. They stated that a neoplastically altered epithelial cell with the potential for multidirectional differentiation might be histogenetically responsible for pleomorphic adenoma.

CLINICAL FEATURES:-

Most common tumor.
 Rate of occurance: 60-70%- parotid glands
40-60%- submandibular glands
40-70%- minor salivary glands
seldomly- sublingual glands
 Age: 30-50 years
 Sex: female> male – 3:1 – 4:1
 In parotid- presents in the lower lobe of the superior lobe
as a mass over the angle of the mandible, below and infront
of the ear.

Clinical presentation: painless, slow growing, firm
mass, initially small in size and begins to increase in
size.
Initially movable but with continued growth become
more nodular and less movable.
Recurrent tumor- multinodular, fixed on palpation.
Palate – intraorally common site.
Seldom ulcerated- unless secondarily traumatized.

 

Slowly growing tumor of
The parotid gland.

HISTOPATHOLOGY:-

 HALLMARK: Morphologic Diversity.
 Charecterized by- Variable, Diverse, Structural & histologic
patterns.
 It demonstrate glandular epithelium and mesenchyme like
tissue and the proportion of each component varies widely.
 Typically a well-circumscribed encapsulated tumor
 The epithelium often forms ducts and cystic structures or may
occur as islands or sheets of cells , anastomosing cords and foci
of Keratinizing squamous cells and spindle cells .

  • Foote and Frazell (1954) categorized PA into:
    a) Primarilly myxoid (36%)
    b) Myxoid and cellular component in equal proportions
    (30%)
    c) Predominantly cellular (22%)
    d) Extremely cellular (12%)

Myoepithelial cells are major component of PA.
 Have variable morphology- sometimes appearing as
angular or spindled, some with eccentric nucleus
resembling plasma cells.
 Are responsible for characteristic mesenchyme like
changes.
 Vacuolar degeneration of myoepithelial cells can produce a
chondroid appearance.
 the stroma exhibits areas of an eosinophilic hyalinized change,
fat or osteoid also is seen.

 

DIFFIRENTIAL DIAGNOSIS:-

 Polymorphous low grade adenocarcinoma, PLGA
 Adenoid cystic carcinoma, AdCC
 Epithelial myoepithelial carcinoma, EMC
 Squamous cell carcinoma, SCC
 Mucoepidermoid carcinoma, MEC

TREATMENT:-

 Surgical excision
 Superficial parotidectomy with preservation of the facial nerve
 Local enucleation should be avoided – resulting in seeding of
the tumor bed.
 Deep lobe of the parotid- total parotidectomy is usually
necessary also with preservation of the facial nerve.

 Submandibular tumors – Total removal of the gland with the
tumor.
 Malignant degeneration is a potential complication, resulting in
a carcinoma ex pleomorphic adenoma.
 The risk of malignant transformation is probably small, but it
may occur in as many as 5% of all cases.

REFERENCES:-

1.Shafers- 8e

2.Nevill’s-3rd e

3.Maji Jose

4.GOOGLE Images

Calcifying Odontogenic Cyst (COC)

Dr. Kriti Jain1 Comment

DEF:-Calcifying odontogenic cyst (COC), previously known as Gorlin cyst, is a rare, well-circumscribed, solid or cystic lesion derived from odontogenic epithelium that resembles follicular ameloblastoma but contains ‘ghost cells’ and spherical calcifications.

Other Names:-

1.Keratinizing and/or Calcifying Epithelial Odontogenic Cyst,

2.Gorlin Cyst

3.Cystic Keratinizing Tumour

4.Dentinogenic Ghost Cell Tumour

5.Odontogenic ghost cell cyst 

  • It Has many features of odontogenic tumor, therefore it is placed in the category of tumors in the latest WHO classification of odontogenic cysts and tumors.
  • In the latest WHO publication on odontogenic tumours (Prætorius and Ledesma-Montes, 2005) it was classified as a benign odontogenic tumour and was renamed calcifying  cystic odontogenic tumour (CCOT).
  • CLINICAL FEATURES:-
  1. Age : Wide range, peak in 2nd decade.
  2. Sex : Equal.
  3. Site : Anterior segment of both jaws
  • Calcifying odontogenic cysts that are associated with odontomas tend to occur in younger patients, with a mean age of 17 years.

  • PATHOGENESIS:-
  • COC is a unicystic process and develops from the reduced dental epithelium or remnants of dental lamina.
  • The cyst lining has the potential to induce formation of dentinoid or even odontoma in adjacent CT wall.
  • CLASSIFICATION OF THE ODONTOGENIC GHOST  CELL LESIONS:-
  1. Group 1 : ‘Simple’ cysts Calcifying odontogenic cyst (COC)
  2. Group 2 : Cysts associated with odontogenic hamartomas or benign neoplasms: calcifying cystic odontogenic tumours (CCOT).
  3. Group 3 : Solid benign odontogenic neoplasms with similar cell morphology to that in the COC, and with dentinoid Formation
  4. .Group 4 : Malignant odontogenic neoplasms with features similar to those of the dentinogenic ghost cell tumour Ghost cell odontogenic carcinoma.
  • SIGNS & SYMPTOMS:-
  1. Swelling is the commonest complaint, seldom associated with pain.
  2. Intraosseous lesions can cause hard bony expansion and resulting facial asymmetry.
  3. Displacement of teeth can also occur.
  • RADIOLOGICAL FEATURES:-
  1. Intraosseous lesions produce well defined lucency which  is usually unilocular.
  2. Irregular calcified masses of varying sizes may be seen within the lucency.
  3. Displacement of root/roots with or without root resorption and expansion of  cortical plates also seen.

*Radiograph of a calcifying odontogenic cyst with well-demarcated  margins extending from the right to the left premolar regions of the  mandible. Numerous calcifications are present, some suggestive of  small denticles.

  • HISTOLOGICAL FEATURES:-
  1. Lining is usually thin about 6 – 8 cell thick, may be thickened in other areas.
  2. Lining shows characteristic odontogenic features with reversely polarized basal cell layer.
  3. TYPICALLY – GHOST CELLS may be seen in thicker areas of lining.
  4. Ghost cells are enlarged, ballooned, ovoid, eosinophilic cells with well

defined cell boundaries.

5.Some times many cells may fuse.

6.They represent abnormal keratinization and frequently calcify.

7.Tubular dentinoid and even complex odontome may be found in connective tissue wall close to epithelial lining.

Histological features of a calcifying odontogenic cyst with clusters  of fusiform ghost cells and focal calcifications, lying in a stratified  squamous epithelium.
In this calcifying odontogenic cyst, there are sheets of ghost cells  and a focal area in which there has been induction of a strip of  dysplastic dentine (dentinoid).
  • DIFFERENTIAL DIAGNOSIS:-

Based on radiographic appearance, following lesions must be included in the provisional diagnosis –

  1. Ameloblastoma
  2. CEOT
  3. AOT
  4. Ameloblastic fibro odontoma

References :-

1.Shafers- 8e

2.Neville -3e

3.Google-Slideshare

ABFRACTION

bmeghna4082Leave a comment
  1. It is also called as ‘stress lesion’. It is the loss of tooth structure that results from flexure which is caused by occlusal stresses. The magnitude of tooth tissue loss depends on the size, duration, direction, frequency and location of the forces.
  1. Causes and mechanism

• Occlusal restoration—some suggested that occlusal restoration may lead to weakening of tooth ability to resist the stresses of occlusion leading to abfraction.

• Predisposing factors—factors, such as erosion and abrasion may play a significant role in tooth tissue loss.

Clinical features

  • Location—itusuallyaffectsbuccal/labialcervicalareas of teeth. Commonly affects single teeth with excursive interferences or eccentric occlusal loads.
  • Appearance—itappearsasdeep,narrowV-shapednotch. The lesion is typically wedge shaped with sharp line angles, but occlusal abfraction may present as circular invaginations.

REFERENCE- ANIL GHOM TEXTBOOK OF ORAL MEDICINE [2nd ed]

EROSION

bmeghna40822 Comments

It is the loss of tooth substance by chemical process that does not involve known bacterial action. Dissolution of mineralized tooth structure occurs due to contact with acids. Erosion is a chemical process in which the tooth surface is removed in the absence of plaque.

Types (depending upon etiology)

  • Intrinsic—erosionthatoccurduetointrinsiccausese.g. gastroesophageal reflux, vomiting.
  • Extrinsic—erosionoccurringfromextrinsicsourcese.g. acidic beverages, citrus fruits.Etiology
  • • Local acidosis—it is seen in periodontal tissue from damage due to traumatogenic occlusion.
  • • Chronic vomiting—complete loss of enamel on lingual surfaces of teeth through dissolution by gastric hydrochloric acid. Vomiting can also occur in alcoholics, peptic ulcer, gastritis, pregnancy and drug side effect.
  • • Acidic foods and beverages—Large quantities of highly acidic carbonated beverages or lemon juice can produce erosion. Most of the fruits and fruits juices have a low pH and can cause erosion. Frequent consumption of carbonated drinks, which are acidic in nature, may result in the erosion of teeth.
  • • Anorexia nervosa—it induces chronic vomiting often after bouts of uncontrolled eating that is interspersed between periods of starvation, because of inner rejection of food.
  • • Occupational—workersinvolvinginmanufacturingof lead batteries, sanitary cleaners or soft drinks can develop erosion.
  • • Poorly monitored pH swimming pool—in cases of poorly monitored pH swimming can also cause erosion of the teeth.
  • • Medication—medication like chewable vitamin C and aspirin tablet may lead to erosion of teeth.
  • Clinical features

• Sites—It occurs most frequently on labial and buccal surfaces of teeth; some times, may occur on proximal surfaces of teeth. Usually confined to gingival thirds of labial surface of anterior teeth. Erosion may involve several teeth of dentition. From extrinsic source, it causes erosion on labial and buccal surface and from intrinsic source, it causes erosion on lingual or palatal source.

  • Appearance—it is usually a smooth lesion which exhibits no chalkiness.
  • Symptoms—loss of enamel often causes hypersensitivity in teeth and may also trigger secondary dentin formation.
  • Signs—lossoftoothsubstanceismanifestedbyshallow, broad, smooth, highly polished and scooped out depression on enamel surface adjacent to cementoenamel junction. When erosion affects the palatal surfaces of upper maxillary teeth, there is often a central area of exposed dentine surrounded by a border of unaffected enamel. In most cases, it results in little more than a loss of normal enamel contour, but in severe cases, dentin or pulp may be damaged.
  • Pink spot—there may be pink spot on tooth which is attributable to the reduced thickness of enamel and dentin making the pink hue of pulp visible.
  • Cupping—erosive lesions cause ‘cupping’ in dentin.
  • Radiographic features
  • • It appears as radiolucent defect in the crown margins may be well defined or diffuse.
  • Management
  • Dietcontrol—inapatientwherelossoftoothsurfaceis essentially caused by erosive fluids, advise regarding diet and use of sugar free chewing gum.
  • Fluoride mouthwash—prescription of a fluoride mouthwash is certainly indicated here.
  • Brushinghabits—brushinghabitsshouldbemodified.
  • Restoration—restoration of the defect, usually by glassinomer cement.
  • Systemic management—for systemic management ofvomiting, patient should be referred to the physician.

REFERENCE- ANIL GHOM TEXTBOOK OF ORAL MEDICINE [2nd ed]

ABRASION

bmeghna40823 Comments

Abrasion is the pathological wearing away of tooth substance through some abnormal mechanical process. Abrasion usually occurs on the facial surface of the crown and the exposed root surfaces of teeth, but under certain circumstances it may be seen elsewhere such as on incisal or on proximal surfaces.

  1. Etiology
    • Abrasivedentifrices—useofabrasivedentifricescanleadto abrasion of the incisal surface.
    • Habitual—Habitualpipesmokermaydevelopabrasion on the incisal edges of lower and upper anterior teeth. In some cases habitual opening of bobby pins may lead to abrasion.
    • Horizontal tooth brushing—horizontal tooth brushing may lead to abrasion of the cervical area of teeth.
    • Occupational—itoccurswhenobjectsandinstrumentare habitually held between the teeth by people during working. Holding nails or pins between teeth e.g. in carpenters, shoemakers or tailors.
    • Dentalflossortoothpicksinjury—improperuseofdental floss and tooth picks.
    • Ritual abrasion—it is mainly seen in Africa.Clinical featuresTooth brush injury
      • Sites—itusuallyoccursonexposedsurfacesofrootsofteeth. It is more commonly seen on left side of right handed persons and vice versa.

• Mechanism—it occurs due to back and forth movement of brush with heavy pressure causing bristles to assume wedge shaped arrangement between crown and root.

• Appearance—in horizontal brushing there is usually a ‘V’ shaped or ‘wedge’ shaped ditch on the root at cementoenamel junction . It is limited coronally by enamel.

• Symptoms—patient develops sensitivity as dentin becomes exposed.

• Signs—the angle formed in the depth of the lesion as well as that of enamel edge is a sharp one. Cervical lesions caused purely by abrasion have sharply defined margins and a smooth, hard surface. The lesion may become more rounded and shallow, if there is an element of erosion present.

• Dentinal features—exposed dentin appears highly polished  Exposure of dentinal tubules and consequent irritation of the odontoblastic processes stimulates secondary dentin formation which is sufficient to protect the pulp from clinical exposure.

Dental floss or tooth pick injury
• Site—Cervical portion of proximal surfaces ,just above the gingival margin, is affected. Grooves on distal surface are deeper than on mesial surface

Radiographic features

Tooth brush injury

  • Location—radiolucent defect at the cervical level of teeth.
  • Shape—well defined semilunar shape ,with borders of increasing density.
  • Pulp—pulp chamber may be partially or fully sclerosed in severely affected teeth.Dental floss injury
    • Appearance—narrow semilunar grooves in theinterproximal surfaces of teeth near cervical area.
  • Management

• Modified teeth cleaning habits—modification of teeth cleaning habits will be indicated.

• Removal of cause—elimination of causative agent should be carried out.

• Restoration—restoration should be done for esthetics purpose and to prevent further tooth wear.

REFERENCE- ANIL GHOM TEXTBOOK OF ORAL MEDICINE [2nd ed]

ATTRITION

bmeghna40821 Comment
  1. It is the physiologic wearing away of teeth because of tooth- to-tooth contact, as in mastication. It plays an important physiological role as it helps to maintain an advantageous crown-root ratio and gains intercoronal space of 1 cm, which facilitates third molar eruption. Attrition can be considered pathological when it cause functional, esthetics and dental sensitivity problems.

Types

• Physiological attrition—attrition which occurs due to normal aging process, due to mastication.

• Pathological attrition—it occurs due to certain abnor- malities in occlusion, chewing pattern or due to some structural defects in teeth.

Etiological factors for pathological attrition

• Abnormal occlusion
• Developmental—malocclusion and crowning of teeth, may lead to traumatic contact during chewing, which may lead to more tooth wear.
• Acquired—due to extraction of teeth. Extraction causes increased occlusal load on the remaining teeth, as the chewing force for the individual remains constant.

• Premature contact in case of edge-to-edge contact,pathological attrition can also occur.
• Abnormal chewing habits parafunctional chewing habit like bruxism and chronic persistent chewing of coarse and abrasive food or other substances like tobacco.
• Occupation in certain occupations, workers are exposed to an atmosphere of abrasive dust and cannot avoid it getting into mouth.
• Structural defect in defects like amelogenesis imperfecta and dentinogenesis imperfecta, hardness of enamel and dentin is reduced and such teeth become more prone to attrition.

Clinical features

• Sex—men usually exhibit more severe attrition than women due to greater masticatory forces.

• Sites—it may be seen in deciduous as well as permanent dentition. It occurs only on occlusal, incisal and proximal surfaces of teeth. Severe attrition is seldomly seen in primary teeth, as they are not retained for any great period. Palabal cusps of maxillary teeth and buccal cusps of mandibular posterior teeth show most wear.

• Appearance – the first clinical manifestation of attrition is the appearance of small polished facet on a cusp tip or ridge and slight flattening of an incisal edge.

Physiologic attrition

  • Physiological tooth surface loss results in a reduction, in both vertical tooth height and horizontal tooth width .Physiological attrition showing wearing of the occlusal surface of the molar teeth.
  • Contact points—due to slight mobility of teeth in their socket (which is a manifestation of resiliency of periodontal ligament) similar facets occur at contact points.
  • Color of teeth when the dentin gets exposed, it generally becomes discolored i.e. brown in color.
  • Signs—there is gradual reduction in cusp height and consequent flattening of occlusal inclined plane. There is shortening of the length of dental arch, due to reduction in the mesiodistal diameter of teeth. Secondary dentin deposition occurs.

• Pathologicalattrition

Severe tooth loss—in pathological attrition severe tooth loss is seen .

Dentoalveolar compensation—if attrition affecting the occlusal surfaces of teeth has occurred, then reduction in occlusal face height (vertical dimension of occlusion) and increase in the freeway space could be anticipated. This may be further complicated by forward posturing of mandible. It is often observed, however, that despite overall tooth surface loss, the freeway space and the resting facial height appear to remain unaltered primarily because of dentoalveolar compensation. This is important with respect to patient assessment. If restoration of worn teeth is being planned then the extent of dentoalveolar compen- sation would appear to determine the dentist’s strategy; defining the need to carry out measures such as crown lengthening, to ensure the same vertical dimension of occlusion and freeway space.

Radiographic features

• Crown—smoothwearingofincisalandocclusalsurfaces of involved teeth is evident by shortened crown image

• Pulp—sclerosisofpulpchamberandcanalsisseendue to deposition of secondary dentin which narrows the pulp canals.

• Periodontal ligament—widening of periodontal ligament space and hypercementosis.

• Alveolar bone—some loss of alveolar bone.

Management

  • Modifying factors—treatment of patient depends upon degree of wear relative to the age of patient, etiology, symptoms and patient’s desire.
  • Habit breaking appliance—the provision of one of three different sorts of splints could be considered. A soft bite guard can help in breaking a bruxist habit or simply will protect the teeth during the bruxist habit. A localized occlusal interference splint is designed to break the bruxist habit and can be worn easily during the day. A stabilization splint reduces bruxism by providing an ideal occlusion: it also enables the clinician to locate and record centric relation. In case of bruxism, use of night guards may be effective in reducing attrition.
  • Correctivemethod—correctionofmalocclusion,stoppage of tobacco chewing habit and restriction of diet to non coarse food are useful in avoiding attrition.
  • Managementofsensitivityandesthetics—non-cariousloss of tooth tissue may require treatment for sensitivity, esthetics, function and space loss in the vertical dimension.

REFERENCE- ANIL GHOM TEXTBOOK OF ORAL MEDICINE [2nd ed]