Highlights (You will learn) ⬇️
1. Trigeminal Neuralgia
2. Post-herpetic Neuralgia
3. Giant-cell Arteritis
4. Other causes of facial pain
5. Approach to facial pain diagnosis
LINK:⬇️
1. Trigeminal Neuralgia
2. Post-herpetic Neuralgia
3. Giant-cell Arteritis
4. Other causes of facial pain
5. Approach to facial pain diagnosis
LINK:⬇️
• Swellings at the angle of Mandible include: ✍🏻👇🏻
• Branchial Cleft Cyst
(i) Benign
(ii) Malignant
• Swellings in the floor of Mouth: 👇🏻✍🏻
Differential diagnosis of swellings of the floor of the mouth or neck (Jham et al., 2007): https://www.researchgate.net/figure/Differential-diagnosis-of-swellings-of-the-floor-of-the-mouth-or-neck-Jham-et-al-2007_tbl1_287206404
• Swellings on the Palate: 👇🏻✍🏻
Differential diagnosis of palatal swellings: https://www.researchgate.net/figure/Differential-diagnosis-of-palatal-swellings_tbl1_221967546
Dentowesome|@drmehnaz🖊
Image source: Google.com
💊Analgesic is a drug that selectively relieves pain by acting in the CNS or on the peripheral pain mechanisms without significantly altering consciousness.
💊They are divided into 2 groups:
Dr. Mehnaz Memon🖊
References:
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
Oral Manifestations
Histology
Shows characteristic starry sky appearance.
• 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 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
Posteruptive Causes
– 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:
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
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.
DISADVANTAGE
REFERENCE-SHAFER’S TEXTBOOK OF ORAL PATHOLOGY 8TH EDITION
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.
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
a. Human : Children, Adults
b. Animals : Mammals, Reptiles, Fish
c. Mechanical : Full denture, belt marks etc
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
CHARACTERISITCS OF HUMAN BITE MARK FOR IDENTIFICATION
BITE MARK INVESTIGATION
1. Description of the bite marks
2. Collection of evidence from victim
3. Collection of evidence from suspect
REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY AND SLIDE SHARE
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.
REFERENCE- SHAFER’S TEXTBOOK OF ORAL PATHOLOGY [8TH ED} AND ANIL GHOM TEXTBOOK OF ORAL MEDICINE
1. Recurring oral ulcers,
2.Recurring genital ulcers, and
3.Eye involvement.
ETIOLOGY
CLINICAL MANIFESTATIONS
ORAL MANIFESTATIONS
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.
Laboratory Findings
The patients usually have a mild leukocytosis, an elevated erythrocyte sedimentation rate, and pyuria.
DIFFERENTIAL DIAGNOSIS
TREATMENT
The management of Behçet’s syndrome depends on the severity and the sites of involvement.
REFERENCE- BURKET TEXTBOOK OF ORAL MEDICINE AND SHAFER’S TEXTBOOK OF ORAL PATHOLOGY {8TH EDITION}
Diagnosis
• Clinical diagnosis—skin lesion with lesion present on oral mucosa which is atrophic and erythematous will suspect lupus erythematous. Oral and nasopharyngeal ulceration is major diagnostic criteria for SLE.
Laboratory diagnosis—L.E. cell inclusion phenomenon with surrounding pale nuclear mass apparently devoid of lymphocytes. Anemia, leukopenia and thrombocyto- penia, with sedimentation rate increased. Serum gamma globulin increased and Coomb’s test is positive.
Positive lupus band test—it shows deposition of IgG,IgM or complement component in skin.
REFERENCE- ANIL GHOM TEXTBOOK OF ORAL MEDICINE; BURKIT TEXTBOOK OF ORAL MEDICINE AND GOOGLE[SLIDE SHARE]