BURKITT LYMPHOMA

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

HODGKIN’S AND NON-HODGKIN’S LYMPHOMA

  • Primary tumors of the lymphoid system
  • Cancers involving lymphocytes during maturation or storage in the bone marrow
  1. Hodgkin’s lymphoma
  2. Non-Hodgkin’s lymphoma
  3. Burkitt’s lymphoma

Hodgkin’s Lymphoma

Hodgkin’s disease (HD) is a lymphoid malignancy characterized by the presence of Reed-Sternberg cells of B cell origin. The disease arises usually in single nodal area and successively spreads to contiguous lymph node areas. Extranodal involvement is rare.

Types (Histological)

• Lymphocyte predominant—abundant lymphocytes, few plasma cells, occasional Reed-Sternberg cell, localized involvement of one side of diaphragm and most favorable prognosis.

• Mixed cellularity—lymphocytes, plasma cells, eosino- phils, easily identified Reed-Sternberg cell.

• Nodular sclerosis—sparse lymphocytes, stromal cells, fibrosis and numerous but bizarre Reed-Sternberg cells. It has poor prognosis.

• Lymphocyte depletion—lymphocytes, plasma cells, eosinophils with localized involvement.

ETIOLOGY

  • Unkonown
  • However both genetic and environmental factors including EBV ( Ebstein Barr Virus) play role in pathogenesis.

CLINICAL FEATURES

  • • Age and sex—it is characterized by a bimodal age incidence, peak one in young adults and the second in the 5th decade of life with equal distribution between sexes.
  • First sign – asymptomatic enlargement of a supradiaphragmatic lymph node often in the neck
  • .Symptoms—theinvolvednodesarepainless.Generalized weakness, loss of weight, cough, dyspnea and anorexia are seen. Pain in back and abdomen owing to splenic enlargement, due to pressure of enlarged nodes or involvement of vertebrae.
  • Pel Ebstein fever—characteristic features of this disease are Pel-Ebstein fever, a cyclic spiking of high fever and generalized severe pruritis of unknown etiology.
  • Mediastinal lymph node involvement is common
  • Night sweats, fever, weight loss
  • Rarely produces oral manifestations

Hodgkin’s lymphoma. This high-power photomicrograph shows the characteristic Reed-Sternberg cell (arrow) of Hodgkin ‘s lymphoma, identifiedby its “owl-eye” nucleus.

  1. Radiographic Features
    • Site—it is rarely seen in jaws. The common regions are the posterior maxilla and mandible.
    • Appearance—malignant lymphoma arising in the oral cavity spreads to bone and cause irregular bone loss to the area of the lesion. There are radiolucent areas sepa- rated from each other by normal appearing bone which later become confluent, unless treatment is carried out.
    • Margins—typically,theradiolucentlesionshavediffuse ill defined margins which suggest infiltration of bone.
    • Osteoblastic type—osteoblastic type is uncommon in jaws, but it is seen in the vertebrae and pelvis. In it, there is frank sclerosis with filling of the marrow spaces by bone. It presents as grayness or whiteness which is abnormal. The margins may be well defined and sharp or irregular and trailing off gradually into the normal bone.

Diagnosis

  • Clinicaldiagnosis—discreteenlargementoflymphnode which is rubbery in consistency with some systemic signs.
  • Radiologicalfeatures—thereisfociofradiolucencyseen in the jaw.
  • Laboratorydiagnosis—itischaracterizedbyreplacement of normal lymph node architecture by an admixture of malignant lymphoid cells and non-neoplastic inflammatory cells. Characteristic Reed Sternberg cells are present. Multinucleated giant cells are also present. There is also presence of anemia which is normocytic and normochromic. ESR is raised. There is also raised level of LDH.

MANAGEMENT

Localized disease: The patients with localized disease (IA, IIA) are treated with 3 cycles of chemotherapy (ABVD-doxorubicin, bleomycin, vinblastine and dacarbazine) followed by radiotherapy of involved nodal areas. 

Extensive disease: Patients with B symptoms or extensive disease receive complete course (6-8 cycles) of ABVD chemotherapy.

Long-term cure can be achieved in >90% patients with localized disease and in 50-75% patients with extensive disease.

Non-Hodgkin’s Lymphoma

It is also called as ‘lymphosarcoma’. In this group, there is neoplastic proliferation of lymphoid cells, usually affecting the B-lymphocytes. Unlike Hodgkin’s lymphoma, the disease is frequently widespread at the time of diagnosis, often involving not only the lymph nodes but also bone marrow, spleen and other tissue. Early involvement of bone marrow is typical of this lymphoma.

Types (Histological)

  • Nodular—neoplastic cells tend to aggregate in such a way that large clusters of cells are seen.
  • Diffuse—thereismonotonousdistributionofcellswith no evidence of nodularity or germinal center pattern.
  • Etiology
  • Viral—the etiology is unclear but herpes virus and Epstein barr etiology has been suggested.
  • Immunological—there may be induced immunologic effect permitting a malignant clone to proliferate.
  1. Clinical Features
    • Age and sex—it affects persons of all ages from infants to the elderly. But is commonest in middle age group. Males are affected more commonly than the females.
    • Onset—the onset of symptoms may be insidious. Painless lymph node enlargement of abdominal and mediastinal region are the most common finding. Very often the first group of lymph nodes affected may be cervical, axillary or inguinal.
    • Symptoms—the patient complains of tiredness, loss of weight, fever and sweating. Pain is the main symptom of bone involvement which may present as a patho- logical fracture. Patient may complain of abdominal pain, nausea, vomiting, diarrhea or intestinal obstruc- tion which may occur due to involvement of gastro- intestinal tract. Pressure effect of lymphoma may cause dysphagia, breathlessness, vomiting, intestinal obstruction or ascites and paraplegia.
    • Signs—if liver and spleen are involved, hepato- splenomegaly is present. The growth is fleshy and is prone to ulceration.

The matted, nontender lymph node enlargement in the lateral cervical region represents a common presentation of lymphoma.

Oral manifestations

  • Gingival or mucosal tissue swelling or masses
  • Rapid growth of tumour from non-healing tooth extraction site.
  • Paresthesia or anaesthesia due to nerve invasion

Radiographic Features

• Appearance—asthediseaseprogressessmallradiolucent foci scattered throughout the area may be seen. Subsequent radiographs of the expanding lesion will show that these small foci have coalesced to form large multilocular moth eaten radiolucency with poorly defined margins.

• Margins—lesion blends imperceptibly with adjacent normal bone, in most of the cases.

• Effect on surrounding structures—lesions may cause marked expansion of bone. Erosion and perforation of cortex may occur.

• Maxillary sinus involvement—if the lesion involves maxillary sinus, possible opacification with breached cortical walls and associated paracentral or intracentral mass.

• Teeth—cortices of unerupted tooth buds and lamina dura of adjacent teeth are lost. Teeth may be resorbed.

Diagnosis

  • Clinical diagnosis—bluish color mass of the palate with multiple lymph node involvement may suspect the diagnosis of non-Hodgkin’s lymphoma.
  • Radiological features—expansion of bone with radio- lucency is present.
  • Laboratory diagnosis—blood count usually shows hypersplenism or hemolytic anemia. The reduced WBC and RBC counts are seen along with reduced hemo- globin levels and reticulocytosis. In some cases, there may be slight increase in lymphocytes and thrombo- cytopenia. Moderate degree of anemia will also present when there is considerable bone marrow involvement. Some very aggressive high grade non-Hodgkin’s lymphomas are associated with very high urate levels which can precipitate renal failure.

Treatment

The disease stage is determined after clinical evaluation and investigations.
Treatment of low grade lymphoma: It depends on the stage of the disease and clinical status.

  • Asymptomatic patients generally do not require therapy.
  • Symptomatic localized (stage I) disease can be treatedwith radiotherapy.
  • Symptomatic patients with extensive disease (stage III,IV) are treated with chlorambucil or combination chemotherapy (CVP; cyclophosphamide, vincristine, and prednisolone or CHOP; cyclophosphamide, doxorubicin, vincristine and prednisolone).
  • Other newer effective agents are fludarabine, monoclonal antibody (anti-CD20) with or without radionuclides, and lymphoma vaccine.
  • The relapse following therapy is common. Hence, low grade NHL is generally not curable. However, the cure is now possible in some cases with the use of radio- immunotherapy.
  • Treatment of high grade lymphoma:
  • Localized high grade NHL (stage I and non-bulky stage II) is treated with three cycles of chemotherapy (CHOP with monoclonal antibody, anti-CD20) followed by radiotherapy.
  • Extensive disease (bulky stage II, stage III, and stage IV) is treated with six to eight cycles of chemotherapy.
  • Autologous bone marrow transplantation is indicatedin relapsed cases.
  • The cure rate is 60-90% in stage I and II and 30-40% instage III and IV.

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY, ANIL GHOM TEXTBOOK OF ORAL MEDICINE AND GOGLE SLIDE SHARE

INTRINSIC AND EXTRINSIC STAINS

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

CLASSIFICATION OF TOOTH DISCOLORATION

Classification of discoloration

  • Intrinsic discoloration
  • Extrinsic discoloration
  • Combination of both

1.Based on the Etiology of tooth discoloration

Intrinsic stains

  • Pre-eruptive causes– Disease
    i. Alkaptonuria
  • iiHematological disorders
    iii. Disease of enamel and dentin
  • iv. Liver diseases.– Medications
    i. Tetracycline stains and other antibiotic use
  • ii. Fluorosis stain.
  • Posteruptive causes of discoloration– Pulpal changes
    – Trauma
    – Dentin hypercalcification
    – Dental caries
    – Restorative materials and operative procedures – Aging
    – Functional and parafunctional changes.

Extrinsic stains
• Daily acquired stains

– Plaque
– Food and beverages – Tobacco use
– Poor oral hygiene
– Swimmer’s calculus
– Gingival hemorrhage.  

  • Chemicals
    – Chlorhexidine
  • – Metallic stains.

2.Classification of extrinsic stains (Nathoo in 1997)

  • •  N1 type dental stain (direct dental stain): Here colored materials bind to the tooth surface to cause discoloration. Tooth has same color, as that of chromogen.
  • •  N 2 type dental stain (direct dental stain): Here chromogen changes color after binding to the tooth.
  • •   N3 type dental stain (indirect dental stain): In this type prechromogen (colorless) binds to the tooth and undergoes a chemical reaction to cause a stain.

3.Different Types of Stains according to Color:

BLACK COLOR-

It usually results due to contact with certain metallic elements such as silver, iron and lead.It may appear as thin line running approximately 1 mm or so above the gingival margin, it may occur on both the facial and lingual surfaces of teeth.Stain is firmly attached to the surface but remains extrinsic, thus it may be removed by brush and abrasives. But, it recurs later on.

Green stain

It usually occurs as thick deposit involving the cervical one-third of facial surface of maxillary incisors of young children. It affects boys more frequently than girls.

It is associated with poor oral hygiene and decalcification is sometimes present in enamel, underlying the deposit. It occurs due to chromogenic bacteria or fungi or it may be caused by bacterial action on remnants of enamel cuticle. It is extrinsic and may be removed by simple brushing and abrasive.

Orange stain

It occurs infrequently and usually involve both facial and lingual surfaces of the incisors. It is easily removed than green stain and its cause is unknown but it is believed to be the result of chromogenic bacteria. It is associated with poor oral hygiene and removed with the help of brush and abrasives.

Brown stain

It can be seen in non-smokers and is usually lighter brown than that of tobacco and form a tenacious, but delicate film on surface of the teeth. It is usually seen more commonly on lingual surface of lower incisors and buccal surface of maxillary molar teeth. It is formed due to altered salivary mucins which have undergone change through the action of bacterial enzymes.

REFERENCE- NISHA GARG TEXTBOOK OF ENDODONTICS AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE

NATAL AND NEONATAL TEETH

NATAL AND NEONATAL TEETH

It is also called as ‘congenital teeth’, ‘fetal deciduous teeth’, ‘dentition proceox’ and ‘natal and neonatal teeth’. There is premature eruption of teeth or teeth like structures that are present at birth.

Natal teeth are the teeth which are present at the time of birth and neonatal teeth are the teeth which are present within 30 days after the birth.

Etiology

Hereditary—superficial position of tooth germ.

Hormonal influence—eruption accelerated by febrileincident or hormonal stimulation.

Classification

  • Mature—they are fully developed in shape and comparable in morphology to the primary teeth. Prognosis is relatively good.
  • Immature—their structure and development is incomplete. Poor prognosis of teeth.

Clinical features

  • Appearance—teeth may be conical or may be normal in size and shape and opaque yellow-brownish in color.
  • Signs—they are hypermobile because of their limited root development. Within relatively short time, premature erupted tooth will become stabilized and other teeth of the arch are erupted. Teeth appear to be attached to a small mass of soft tissue.
  • Significance—some teeth are so much mobile that there is danger of displacement and possible aspiration and in this case, removal is indicated.
  • Riga fede ulcer—there is ulceration of the ventral surface of the tongue caused by the sharp incisal edges. It leads to interference with proper suckling and feeding and thus the neonate is at risk of nutritional deficiency.
  • Associated syndromes—it may associate with syndromes like Ellis-van Creveld syndrome and cleft palate.

Management

  • Extraction—extraction of the teeth should be carried out if it is causing inconvenience during suckling, interference with breastfeeding and causing traumatic injury.
  • NOTE- Extraction should be done after 10th postpartum day due to the inability of the clotting but nowadays, it is no longer considered because of prophylactic administration of vitamin K as a standard procedure in most of the hospitals.
  • Rounding of sharp angle—the other option that may be used is rounding of the sharp angle of incisal edges of teeth.
  • Retaining the tooth—if not necessary, tooth should not be removed.The preferable approach, however, is to leave the tooth in place and to explain to the parents the desirability of maintaining this tooth in the mouth because of its importance in the growth and uncomplicated eruption of the adjacent teeth.
  • A retained natal or neonatal tooth may cause difficulty for a mother who wishes to breast-feed her infant. If breast-feeding is too painful for the mother initially, the use of a breast pump and bottling of the milk are recommended. However, the infant may be conditioned not to “bite” during suckling in a relatively short time if the mother persists with breast-feeding. It seems that the infant senses the mother’s discomfort and learns to avoid causing it.

REFERENCE- MC DONALD TEXTBOOK OF PEDODONTICS AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE

SUPERNUMERARY TEETH

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

FORENSIC ODONTOLOGY PART-2

LIP PRINTS

The wrinkles and grooves visible on the lips have been named by Tsuchihashi as ‘sulci labiorum rubrorum’. The imprint produced by these grooves is termed as ‘lip print’, the examination of which is referred to as ‘cheiloscopy’.

Tsuchihashi proposed a classification dividing the pattern of grooves into six types:
Type I: Clear-cut vertical grooves that run across the entire lip
Type I’: Similar to type I, but do not cover the entire lip Type II: Branched grooves
Type III: Intersected grooves
Type IV: Reticular grooves
Type V: Grooves that cannot be morphologically differentiated.

     

  • A combination of these grooves may be found in any given set of lips.
  • To simplify recording, the lips are divided into quadrants similar to the dentition- a horizontal line dividing the upper and lower lip and a vertical line and a vertical dividing right and left sides. By noting the type of groove in each quadrants, the individual’s lip print pattern may be recorded. Thus classification, thus, enabled differentiation of lip print patterns between any two individuals.
  • Lip prints are usually left at crime scenes, and can provide a direct link to the suspect. 
  • Although invisible, these prints can be lifted using materials such as aluminium powder and magnetic powder
  • Ball states that the vermillion border has minor salivary glands, and the edges of the lips has sebaceous glands, with sweat glands in between. 
  •  One may therefore, assume that secretions of oils and moisture from these enable development of ‘latent’ lip prints, analogous to latent fingerprints, in most crime scenes where close contact between the victims and culprit has occurred.

DISADVANTAGE

  • A major disadvantage of lip print investigation pertains to uncertainty about the permanence of lip patterns. While they are believed to remain unchanged throughout one’s life, 
  • Sivapathasundharam B and coworkers doubted this, as major trauma to the lips resulting in scarring, pathosis, surgical treatment  rendered to correct the pathosis, affect the size and shape of the lip, thereby may alter the pattern and morphology of the grooves.

REFERENCE-SHAFER’S TEXTBOOK OF ORAL PATHOLOGY 8TH EDITION

FORENSIC ODONTOLOGY PART 1


Forensic Odontology defined by the Federation Dentaire International (FDI) as ‘that branch of dentistry which, in the interest of justice, deals with the proper handling and examination of dental evidence, and with the proper evaluation and presentation of dental findings’.

Scope of Forensic Odontology

• Record preparation—the correct handling and exami- nation and the proper preparation and presentation of dental evidence in both civil and criminal legal procedures.

• Identification—personal identification, either individually or in context of mass disasters.

• Age assessment—to calculate the age of patient.
• Bite mark investigation—investigation of criminal cases where bite marks are involved and the interpretation of

• Humanabuse—recognitionofdomestic,andchildabuse.

• Lipprint—comparisonandidentificationoflipprint.

• Legalaspect—legalaspectofdentaltraumatology.

A vital role the forensic dentist plays is in criminal investigation.

  • Crime investigation includes the investigation of 
  • BITE MARKS
  • LIP PRINTS
  • CHILD ABUSE

BITE MARKS

McDonald (1974) has defined bitemark as “a mark caused by the teeth either alone or in combination with other mouth parts”.

Bite marks may be caused by humans or animals; they may be on tissue, food items, or other objects. 

CLASSIFICATION OF BITE MARKS

Cameron and Sims classification

  1. Depending on biting agent

a. Human : Children, Adults

b. Animals : Mammals, Reptiles, Fish

c. Mechanical : Full denture, belt marks etc

  1. Depending on material bitten 

a. Skin : Human, Animal

b.  Perishable items : Food items like cheese,  apple etc.

c. Non- perishable items : Unanimated objects such as pipes, pens, pencils.


WEBSTER’S CLASSIFICATION

Type I – food item fractures readily with limited depth of tooth penetration e.g. hard chocolate.

Type II – food item fractures with considerable penetration of teeth e.g. bite marks in apple & firm fruits.
Type III – Complete or near complete penetration of the food item with slide marks e.g cheese

FACTORS AFFECTING BITE MARK INJURIES

  • Inherent skin factor
  • Age
  • Sex
  • Time
  • Vascularity

CHARACTERISITCS OF HUMAN BITE MARK FOR IDENTIFICATION

  • Human bite mark characteristics include an elliptical or ovoid pattern containing tooth and arch marks.
  • Simplest form of a bite mark consists of tooth marks produced by antagonistic teeth.
  • An arch mark may indicate the presence of 4 to 5 teeth marks reflecting the shape of their incisal or occlusal surfaces.
  • Class features: differentiate between tooth type
  • Incisors- rectangular
  • Canines- triangular
  • Premolars + molars – spherical/point shaped
  • Depends on attrition
  • Other significant findings to identify a bite mark to give the identify of the suspect are :
  • Presence or absence of each tooth
  • Peculiar shape of each tooth
  • Mesiodistal dimensions
  • Arch form and size
  • Relationship between the upper and the lower jaws
  • Any unusual features, such as rotation, fractured teeth, supernumerary teeth, microdontia, diastema etc.  

BITE MARK INVESTIGATION

  • The guidelines for bite marks analysis are given by American Board of Forensic Odontology (ABFO) and careful use of these helps in enhancing the quality of the investigation and conclusions. The collection of evidence regarding the bite marks falls in following categories :

1. Description of the bite marks

  1. Demographic data
  2. Location of bite marks
  3. Shape Color
  4. Type of injury (Abrasion, Ecchymosis, Laceration, Petechial hemorrhage and Incision) 

2. Collection of evidence from victim

3. Collection of evidence from suspect

REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY AND SLIDE SHARE

CHARACTERISTICS OF A DIGITAL IMAGE

Image Characteristics

  • Contrast Resolution
  • Spatial Resolution
  • Detector Latitude
  • Detector Sensitivity
  • Signal to noise ratio

CONTRAST RESOLUTION

  • Contrast resolution is the ability to distinguish different densities in the radiographic image. 
  • Current digital detectors capture data at 8-, 10-, 12-, or 16-bit depths. 
  • The bit depth is a power of 2. 

Spatial Resolution

  • Spatial resolution is the capacity for distinguishing fine detail. 
  • The theoretical limit of resolution is a function of picture element (pixel) size for digital imaging systems.

DSCN6702

Film based IOPA – 20 lp / mm.

Digital receptors 7 lp / mm.

Film  >  CCD  >  PSP 

Detector Latitude

It is the ability of the image receptor to capture a range of x-ray exposures as different densities.

  • The latitude ofCCD and CMOS detectors is similar to film

Photostimulable phosphor receptors have larger latitudes and have a linear response to five orders of magnitude of x-ray exposure.

Detector  Sensitivity

  • Sensitivity of a detector is its ability to respond to small amounts of radiation. Intraoral film sensitivity is classified according to speed.
  • High resolution CCD and CMOS systems achieve less dose reduction than lower resolution PSP systems. CCD and PSP systems or extraoral imaging require exposures similar to those needed for 200-speed screen-film systems.

REFERENCE-WHITE AND PHAROAH 5TH EDITION

REITER’S SYNDROME

Reiter’s syndrome is associated with urethritis, balanitis, conjunctivitis, and mucocutaneous lesions.

 It is a disease of unknown aetiology, although there is evidence of an infec- tious origin.

It is one of the most common complications of non-specific urethritis and it clinically mimicks gonorrhoea, although the urethral discharge is negative for Neisseria.

CLINICAL FEATURES

>Reiter’s syndrome is more prevalent in young adult men, usually between 20 and 30 years of age. 

>The male-to-female ratio is 9:1. 

>There is a typical tetrad of manifestations: non- gonococcal urethritis, arthritis, conjunctivitis, and mucocutaneous lesions. 

>Urethritis may be the first sign. The urethral discharge is usually associated with itching and burning sensation. 

>The arthritis is often bilaterally symmetrical and usually polyarticular.

 >Conjunctivitis is often so mild as to be overlooked. 

>The skin lesions are similar to those seen in keratoderma blennorrhagica and consist of red or yellow keratotic macules or papules which eventually desquamate.

Oral Manifestations

Sites—it is seen on the buccal mucosa, lips and gingiva.

Oral lesions appear as painless, red, slightly elevated areas, some- times granular or even vesicular, with a white circinate border on the buccal mucosa, lips, and gingiva. 

The palatal lesions appear as small, bright red purpuric spots, which darken and coalesce, while the lesions on the tongue closely resemble ‘geographic’ tongue.

Laboratory Findings

The patients usually have a mild leukocytosis, an elevated erythrocyte sedimentation rate, and pyuria.

  • Differential Diagnosis
  • • Geographic tongue and stomatitis—no skin changes, no visceral lesions are seen.
  • • Pustularpsoriasis—Auspitz’ssignpresent.
    • Behcet’ssyndrome—nourethritis,aphthaewithredhalo.
  • • Stevens-Johnson syndrome—acute appearance, moresevere clinical course, no arthritis or urethritis.
    • Benign mucosal pemphigoid—blister formation, nourethritis, found in older patients.
Histologic Features
The microscopic findings are not diagnostic. They consist of parakeratosis, acanthosis, and polymorphonuclear leukocyte infiltration of epithelium, sometimes with mi- croabscess formation similar to psoriasis. The connective tissue shows a lymphocyte and plasma cell infiltrate.
  • Management
  • • Spontaneous remission—many patients undergo spontaneous remission.• Antibiotics—incasesymptomaticpatient,doxycycline or minocycline may be given.
  • • Analgesics—nonsteroidalanti-inflammatorydrugsare given to manage arthritis.
  • • Immunosuppressiveagents—immunosuppressiveagents like azathioprine and methotrexate are given in cases of most resistant cases.

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