Tag: Oral Pathology

BURKITT LYMPHOMA

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It is also called as ‘African jaw lymphoma’. It is a lymphoreticular cell malignancy. In the African form jaw involvement is 75% and in cases of the American form, abdomen involvement is more common. It is a B-cell neoplasm.

Etiology

• Epstein-Barrvirus(EBV)which also causes nasopharyn- geal carcinoma and infectious mononucleosis is considered to be the etiological factor. There are higher EBV antibody levels in patients of Burkitt’s lymphoma.

Clinical Features

  • Age and sex—peak incidence is in children between 6to 9 years. Males are affected more commonly than the females, with a ratio of 2:1.
  • Site distribution—more are found in maxilla than in mandible, where it may spread rapidly to the floor of the orbit. Almost always occurs in molar area. In the African form, more than one quadrant is involved while in the American form, only one quadrant is involved.
  • Onsetandprogress—the most important hall mark of this tumor is the fast growth with a tumor doubling time of less than 24 hours.
  • Symptoms—the most common presenting features are swelling of the jaws, abdomen and paraplegia. It is painless.
  • Sign—peripheral lymphadenopathy is common.
  • Prognosis—it is rapidly fatal in the absence of treatment,with death occurring within 6 months.

Oral Manifestations

  • • Onset and extent—it begins generally as a rapidly growing tumor mass of the jaws, destroying the bone with extension to involve maxillary, ethmoid and sphenoid sinus as well as orbit.
  • Symptoms—loosening or mobility of permanent teeth.There is gross distortion of the face due to swelling. Paresthesia and anesthesia of inferior alveolar canal or other sensory facial nerves are common.
  • Signs—gingiva and mucosa adjacent to the affected teeth become swollen, ulcerated and necrotic. As the tumor mass increases, the teeth are pushed out of their sockets. Swelling of the jaw occurs and it may cause facial asymmetry. They are capable of blocking nasal passages, displacing orbital contents and eroding through skin. There is derangement of arch and occlusion. There may be large quantity of mass protruding into the mouth, on the surface of which may be seen rootless, developing permanent teeth.
  • Spread—once the tumor perforate the bone, it is initially confined by the periosteum, but subsequently it spreads to the soft tissues of the oral cavity and face where rapid tumor growth soon obliterates the entire face and skin becomes tense and shiny.

Histology

Shows characteristic starry sky appearance.

  1. Radiographic Features
    • Motheaten appearance—small radiolucent foci scattered throughout the affected area. These small foci coalesce and form a multilocular moth eaten appearance.
    • Sunray appearance—if periosteum is elevated, it will produce sunray appearance.
    • Margins—margins are ill defined and non-corticated.
    • Shape—they expand rapidly and are ballooned shaped.
    • Teeth—Lesions are osteolytic with loss of lamina dura about the erupted teeth and crypts of developing teeth are enlarged.
    • Effect ons urrounding structures—they expand very rapidly and breach its outer cortical limits.
  1. Diagnosis
  2. • Clinical diagnosis—swelling of the jaw and abdomen with peripheral lymphadenopathy can give clue to the diagnosis.

• Radiological diagnosis—moth eaten appearance is seen with loss of lamina dura around the teeth.

• Laboratorydiagnosis—monotonous sea of un differentiated monomorphic lymphoreticular cells, usually showing abundant mitotic activity. There is also hyperchro- matosis and loss of cohesiveness. Characteristic ‘starry sky’ appearance is seen.

Management

• Cytotoxicdrugs—cytotoxicdrugs like cyclophosphamide 40 mg/kg in single IV administration and repeated about 2 weeks later. Vincristine and methotrexate have been successful in some cases.

• Multiagent chemotherapy—combination of drugs such as cyclophosphamide, vincristine and methotrexate give better results than any single drug. Majority of patients show dramatic response to the therapy. The swelling regresses and the displaced teeth return to their normal position within 1 to 2 weeks.

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE

INTRINSIC AND EXTRINSIC STAINS

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Intrinsic Stains

Pre-eruptive Causes

These are incorporated into the deeper layers of enamel and dentin during odontogenesis and alter the development and appearance of the enamel and dentin

.Alkaptonuria: Dark brown pigmentation of primary teeth is commonly seen in alkaptonuria. It is an autosomal recessive disorder resulting into complete oxidation of tyrosine and phenylalanine causing increased level of homogentisic acid.

Hematological disorders

• Erythroblastosis fetalis: It is a blood disorder of neonates due to Rh incompatibility. In this, stain does not involve teeth or portions of teeth developing after cessation of hemolysis shortly after birth. Stain is usually green, brown or bluish in color.

• Congenital porphyria: It is an inborn error of por- phyrin metabolism, characterized by overproduction of uroporphyrin. Deciduous and permanent teeth may show a red or brownish discoloration. Under ultraviolet light, teeth show red fluorescence.

• Sickle cell anemia: It is inherited blood dyscrasia characterized by increased hemolysis of red blood cells. In sickle cell anemia infrequently the stains of the teeth are similar to those of erythroblastosis fetalis, but discoloration is more severe, involves both dentitions and does not resolve with time.

Amelogenesis imperfecta: It comprises of a group of conditions, that demonstrate developmental alteration in the structure of the enamel in the absence of a systemic disorders. Amelogenesis imperfecta (AI) has been classified mainly into hypoplastic, hypocalcified and hypomaturation type.

Fluorosis: In fluorosis, staining is due to excessive fluoride uptake during development of enamel. Excess fluoride induces a metabolic change in ameloblast and the resultant enamel has a defective matrix and an irregular, hypomineralized structure 

  • Vitamin D deficiency results in characteristic white patch hypoplasia in teeth.
  • Vitamin C deficiency together with vitamin A deficiency during formative periods of dentition resulting in pitting type appearance of teeth.
  • Childhood illnesses during odontogenesis, such as exanthematous fevers, malnutrition, metabolic disorder, etc. also affect teeth.
  1. Dentinogenesis imperfecta : It is an autosomal dominant development disturbance of the dentin which occurs along or in conjunction with amelogenesis imperfecta. Color of teeth in dentinogenesis imperfecta (DI) varies from gray to brownish violet to yellowish brown with a characteristic usual translucent or opalescent hue.
  2. Tetracycline and minocycline: Unsightly dis- coloration of both dentitions results from excessive intake of tetracycline and minocycline during the development of teeth. Chelation of tetracycline molecule with calcium in hydroxyapatite crystals forms tetracycline orthophosphate which is responsible for discolored teeth.

Posteruptive Causes

  • Pulpal changes: Pulp necrosis usually results from bacterial, mechanical or chemical irritation to pulp. In this disintegration products enter dentinal tubules and cause discoloration.
  • Trauma: Accidental injury to tooth can cause pulpal and enamel degenerative changes that may alter color of teeth.Pulpal hemorrhage leads to grayish discoloration and nonvital appearance. Injury causes hemorrhage which results in lysis of RBCs and liberation of iron sulfide which enter dentinal tubules and discolor surrounding tooth.
  • Dentin hypercalcification: Dentin hypercalcification results when there are excessive irregular elements in the pulp chamber and canal walls. It causes decrease in translucency and yellowish or yellow brown discoloration of the teeth.
  • Dental caries: In general, teeth present a discolored appearance around areas of bacterial stagnation and leaking restorations.
  • Restorative materials and dental procedures: Discoloration can also result from the use of endodontic sealers and restorative materials.
  • Aging: Color changes in teeth with age result from surface and subsurface changes. Age related discoloration are because of:– Enamel changes: Both thinning and texture changes occur in enamel.

– Dentin deposition: Secondary and tertiary dentin deposits, pulp stones cause changes in the color of teeth.

• Functional and parafunctional changes: Tooth wear may give a darker appearance to the teeth because of loss of tooth surface and exposure of dentin which is yellower and is susceptible to color changes by absorption of oral fluids and deposition of reparative dentin.

Extrinsic Stains

Daily Acquired Stains

Plaque: Pellicle and plaque on tooth surface gives rise to yellowish appearance of teeth.

Food and beverages: Tea, coffee, red wine, curry and colas if taken in excess cause discoloration.

Tobacco use results in brown to black appearance of teeth.

Poor oral hygiene manifests as:

  • –  Green stain
  • –  Brown stain
  • –  Orange stain.

Swimmer’s calculus:
– It is yellow to dark brown stain present on facial andlingual surfaces of anterior teeth. It occurs due toprolonged exposure to pool water.

Gingival hemorrhage.

Chemicals

• Chlorhexidine stain: The stains produced by use of chlorhexidine are yellowish brown to brownish in nature.

Metallic stains: These are caused by metals and metallic salts introduced into oral cavity in metal containing dust inhaled by industry workers or through orally administered drugs.

Stains caused by different metals

• Copper dust—green stain
• Iron dust—brown stain
• Mercury—greenish black stain • Nickel—green stain
• Silver—black stain.

Reference- Nisha garg textbook of endosontics and Anil Ghom textbook of oral medicine

SUPERNUMERARY TEETH

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A supernumerary tooth is an additional tooth to the normal set of teeth. It may closely resemble the teeth of the group to which it belongs, i.e, molars, premolars or anterior teeth, or it may bear little resemblance in size or shape to the teeth with which it is associated.

It is also called as ‘hyperdontia’. It is defined as any tooth or tooth substance in the excess of the usual configuration of twenty deciduous or thirty two permanent teeth.

Pathogenesis and etiology

  • The various factors which are responsible for formation of supernumerary teeth as follows:
  • Phylogenetic reversion theory—this theory is nowadaysdiscarded.
  • Dichotomy theory—this theory states that tooth bud issplit to form two different tooth,
  • Hyperactivity of dental lamina—a supernumerary toothdevelops from 3rd tooth bud arising from dental lamina near the permanent tooth bud.
  • Hereditary—it is inherited as an autosomal dominant trait, when associated with syndromes. It is inherited as an autosomal recessive trait when associated with only supernumerary teeth. Supernumerary teeth are most commonly found in relative of affected children than in general population.

Four different morphological types of supernumerary teeth have been described:

• Conical
• Tuberculate
• Supplemental
• Odontome

Conical. This small peg-shaped conical supernumerary tooth is most commonly found in the permanent dentition. It develops with root formation ahead of or at an equivalent stage to that of permanent incisors and usually presents as a mesiodens. The conical supernumerary can result in rotation or displacement of the permanent incisor, but rarely delays eruption.

Tuberculate. The tuberculate type of supernumerary possesses have more than one cusp or tubercle. It is frequently described as barrel-shaped and may be invaginated. Root formation is delayed compared to that of the permanent incisors. Tuberculate supernu- meraries are often paired and are commonly located on the palatal aspect of the central incisors. They rarely erupt and are frequently associated with delayed eruption of the incisors.

Supplemental. The supplemental supernumerary refers to a duplication of teeth in the normal series and is found at the end of a tooth series. The most common supplemental tooth is the permanent maxillary lateral incisor, but supplemental premolars and molars also occur. The majority of supernumeraries found in the primary dentition are of the supplemental type and seldom remain impacted.

Odontome. The term ‘odontoma’ refers to any tumour of odontogenic origin. Odontoma represents a hamartomatous malformation rather than a neoplasm. The lesion is composed of more than one type of tissue and consequently has been called a composite odontoma. Two separate types have been described, the diffuse mass of dental tissue which is totally disorganized is known as a complex composite odontoma; whereas, the malformation which bears some superficial anatomical similarity to a normal tooth is referred to as a compound composite odontoma.

According to location
• Mesiodens—it is located at or near the midline in the incisal region of maxilla between central incisors . It is a small tooth with cone shaped crown and short root. It may cause retarded eruption, displacement or resorption of adjacent root. It frequently causes improper alignment.

• Distomolar—it is found in molar region frequently located distal to 3rd molar. Generally, these teeth are smaller than normal 2nd and 3rd molar, crown morphology is highly abnormal.

• Paramolar—it is supernumerary molar, usually small and rudimentary and is situated buccally or lingually to one of the maxillary molars or interproximally between 1st, 2nd and 3rd maxillary molars.

• Peridens—supernumerary teeth that erupt ectopically, either buccally or lingually to the normal arch are referred as peridens.

Radiographic features

When it is needed—if abnormal clinical signs are present you can go for OPG examination, IOPA, occlusal radiographic examination.

Significance—radiograph will aid in determining the location and number of unerupted teeth. It can also used to see if there is any cyst formation.

Appearance—theirradiographicpictureischaracteristic of teeth.

Management

• Surgical extraction—it depends on potential effect on normal dentition, their position, number and complications that may result from surgical removal. If required, they should be extracted.

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY 8TH ED AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE TEXTBOOK OF ORAL MEDICINE