FACIAL PAIN & ITS DIAGNOSIS

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:⬇️

Swellings in the angle of Mandible, Floor of Mouth & Palate

Swellings at the angle of Mandible include: ✍🏻👇🏻

🔅Congenital disease

• Branchial Cleft Cyst

🔅Neoplasm

(i) Benign

  • Hemangioma
  • Lymphangioma, Cystic hygroma
  • Pleomorphic adenoma (mixed tumor)
  • Warthin tumor
  • Neurofibroma
  • Angiolipoma
  • Adenoma
  • Hamartoma
  • Lipoma
  • Oncocytoma

(ii) Malignant

  • Mucoepidermoid carcinoma
  • Squamous cell carcinoma
  • Adenoid cystic carcinoma
  • Acinic cell carcinoma
  • Adenocarcinoma
  • Rhabdomyosarcoma
  • Lymphoma, leukemia
  • Metastatic adenopathy

🔅Inflammation/Infection

  1. Parotitis
  2. Parotid Abscess
  3. Tuberculosis
  4. Sarcoidosis
  5. Sjögren disease
  6. HIV

Detailed View🔍

1) Branchial Cleft Cyst:

  • Failure of involution of clefts and pouches lead to cysts, fistulas or sinus tracts.
  • Its a painless fluctuant swelling
  • First branchial cleft cysts are rare usually located at parotid gland or periparotid region.
  • Second branchial cleft cyst – Type II are the most common
  • Typically, second branchial cleft cysts present as a rounded swelling just below the angle of mandible, anterior to the sternocleidomastoid

2) Hemangiomas:

They are the most common benign salivary gland mass. Capillary hemangiomas involve parotids

3) Lymphangiomas

They are congenital malformations of the lymphatic system that may involve the parotid gland (Soft asymptomatic neck mass associated with facial asymmetry)

4) Pleomorphic Adenoma:

Hard painless slow growing mass

5) Warthin Tumor:

Incorporation of heterotopic salivary gland ductal epithelium within intraparotid & periparotid nodes

6) Parotitis & Parotid Abscess:

  • Most common in children
  • Mumps is the most common viral cause of parotitis
  • The condition manifests tender swelling at the angle of Mandible
  • Sialadenitis is most commonly due to bacterial infections caused by Staphylococcus aureus.
  • Premature neonates and immunosuppressed individuals are affected.

Swellings in the floor of Mouth: 👇🏻✍🏻

Ranula presents as a translucent blue, dome-shaped fluctuant swelling & contains viscid, glairy jelly like fluid
  1. Ranula – a type of mucocele found on the floor of the mouth. Present as a swelling of connective tissue consisting of collected Mucin from a ruptured salivary gland by local trauma.
  2. Swellings in the floor of the mouth are more likely to arise from structures above the Mylohyoid muscle. The commonest swellings in the floor of the mouth are denture induced hyperplasia & salivary calculus.
  3. Swellings in the floor of the mouth may inhibit swallowing & speech.
  4. Mandibular tori produce bony hard swelling lingual to the lower premolars.

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: 👇🏻✍🏻

  1. Torus palatinus is an intrinsic bone lesion whereas a dental abscess pointing on the palate (usually from the palatal roots of the 1st & 2nd maxillary molars or from upper lateral incisors) is extrinsic.
  2. Salivary neoplasms
  3. Invasive carcinoma from the maxillary sinus may produce a palatal swelling.
  4. Kaposi’s sarcoma, typical of HIV/AIDS may also present as lump on palate.
  5. Paget’s disease.

Differential diagnosis of palatal swellings: https://www.researchgate.net/figure/Differential-diagnosis-of-palatal-swellings_tbl1_221967546

Dentowesome|@drmehnaz🖊


Image source: Google.com

ANALGESICS AND ANTI-INFLAMMATORY DRUGS(NSAID’s) IN DENTISTRY

💊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:

  1. Opiod/Narcotic/Morphine like
  2. Non-opiod/Non-Narcotic/antipyretic (Aspirin like drugs)

The antipyretic analgesics & NSAID’s are more commonly employed for dental pain because tissue injury and inflammation due to abscess, caries, tooth extraction etc. is major cause of acute dental pain.

🔆 CLASSIFICATION:

Image: 1
Image: 2

🔆 ANALGESIC/NSAID’s IN DENTISTRY:

  • The antipyretic analgesics used mainly for dental pain is Paracetemol.
  • Paracetemol (Acetaminophen) is most frequently used to relieve toothache in Pregnancy. It has week anti-inflammtory effect & causes no teratogenesis in the developing fetus.
  • Pain during invasive dental procedures is alloyed by a local anesthesic before & after is treated with NSAID’s.

💊 NSAID’s use during Pregnancy: (The devastating effects to the infant) 👇🏻

Image: 3

🔆Use of OPIOIDS in Dental Pain:

  • Less used than analgesics
  • Mostly codeine is used for dental patients because other opioids cause dullness & short lasting pain.
  • Other alternative Opioid Analgesics used are – Tramadol, Pentazocine.

💊MORPHINE – Depressant actions‼️

🔻Adverse effects:
  1. Sedation, mental clouding, lethargy, nausea, vomitting, diarrhoea.
  2. Respiratory depression, blurring of vision.
  3. Allergic conditions, rashes, urticaria, itching, swelling.
  4. May develop tolerance & dependance.
🔻Contraindications:
  1. Urinary retention – infants & elderly
  2. Asthma patients
  3. Hypotensive states
  4. Hypovolaemic states

💊NSAID’s :

  1. Analgesic, antipyretic, anti-inflammatory effect.
  2. Effectively relieves inflammatory tissue, injury related pain, signs of inflammation like pain, tenderness, swelling are suspected.
  3. Cellular metabolism is increased & due to increased Glucose utilization there is decrease in blood sugar.
  4. Has teratolytic & mild-antiseptic properties
  5. Irritates gastric mucosa
  6. Interferes with platelet aggregation & bleeding time prolonged.
🔻Adverse effects:
  • Nausea, vomiting, diarrhoea, blood loss in stools.
  • Haemolysis in G6PD deficient patients.
  • Nephrotoxicity & hepatotoxicity in long term use.
  • Allergic reactions – rashes, urticaria, photosensitivity.
  • Pregnancy & Infancy – Refer Image 3
🔻Contraindications:
  • Nursing and pregnancy
  • Serious bleeding
  • Allergy/Asthma/Angioedema
  • Impaired renal function
  • Drug (anticoagulant)

Dr. Mehnaz Memon🖊


References:

  1. Flowcharts: Classification of Drugs with DOC by Vikas Seth (Third Edition)
  2. KD TripathiEssentials of Medical Pharmacology 7th Edition; Internet

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

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

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

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

BECHET’S SYNDROME

  • Behçets disease (BD) was initially described by the Turkish dermatologist Hulusi Behçet as a triad of symptoms including 

                        1. Recurring oral ulcers, 

                         2.Recurring genital ulcers, and 

                         3.Eye involvement.

ETIOLOGY

  • The cause of BD is unknown, 
    • but immune dysregulation, 
    • including circulating immune complexes, 
    • autoimmunity, cytokines, and 
    • heat shock proteins, 
    • major factor in the pathogenesis of BD.

CLINICAL MANIFESTATIONS

  • Highest incidence is in young adults between the ages of 25 and 40.
  • The most common site of involvement is oral mucosa. 
  • The genital area is the second most common site of involvement and presents as ulcers
  • The eye lesions consist of uveitis, retinal vasculitis, vascular occlusion, optic atrophy, and conjunctivitis. 
  • Blindness is a common complication of the disease, and periodic evaluation by an ophthalmologist is necessary.

  • Positive pathergy is defined as  an inflammatory reaction  forming within 24 hours of a needle puncture scratch, or saline injection.
  • A positive pathergy test, which is performed by placing a 20 gauge needle 5 mm into the skin of the forearm. The test is positive if an indurated papule or pustule greater than 2 mm in diameter forms within 48 hours.

ORAL MANIFESTATIONS

  • The most common single site of involvement is the oral mucosa. 
  • Recurring oral ulcers appear in over 90% of patients; these lesions cannot be distinguished from RAS .
  • Some patients experience mild recurring oral lesions; others have the deep large scarring lesions characteristic of major RAS.
  • These lesions may appear anywhere on the oral or pharyngeal mucosa.

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

  • Sweet Syndrome : oral ulcers, conjunctivitis, episcleritis, Inflamed tender skin papules or nodules.
  • Erythema Multiforme: erosions, target(iris) lesions.
  • Pemphigoid: bullae, erosions.
  • Pemphigus : erosions, flaccid skin bullae.
  • Reiter syndrome: ulcers, conjunctivitis,
  • Herpes simplex virus
  • Lupus erythematosus

TREATMENT

The management of Behçet’s syndrome depends on the severity and the sites of involvement.

  • Azathioprine combined with prednisone has been shown to reduce ocular disease as well as oral and genital involvement.
  • Pentoxifylline, which has fewer side effects than do immunosuppressive drugs or systemic steroids, has also been reperted to be effective in decreasing disease activity, particularly of oral and genital lesions.
  • Dapsone, colchicines and thalidomide have also been reported to be effective to treat mucosal lesions of Behcet’s disease.

REFERENCE- BURKET TEXTBOOK OF ORAL MEDICINE AND SHAFER’S TEXTBOOK OF ORAL PATHOLOGY {8TH EDITION}

Systemic lupus erythematosus{SLE}

  • SLE is a multisystem autoimmune inflammatory disorder of unknown etiology.
  • Main feature is the formation of antibodies to DNA, which may initiate immune complex reactions, in particular a vasculitis. 
  • Female to male ratio of 9:1
  • More common in persons of non-European descent.
  • Etiology
  • Geneticpredisposition—relativeofpatientshavehigher incidences of auto-antibodies, immune deficiency and connective tissue disease. This tendency is greatest among identical twins.
    • Immunological abnormality possibly mediated by viral infection—immune complex consisting chiefly of nucleic acid and antibody account for majority of the tissue changes.
    • Autoimmune disease—as these patients develop antibodies to many of their own cells.
    • Endocrine—thereishighincidenceinfemalesinpreg- nancy. This finding suggestive of increased estrogen level.
    • Biochemicalincreaseinexcretionofmetabolicproducts, particularly tyrosine and phenylalanine, in certain SLEpatient.
  • CLINICAL MANIFESTATIONS
  • Lupus is known as “the great mimic.”
  •  Skin lesions of lupus can be classified 
    • lupus-specific (having diagnostic clinical or histopathologic features) 
    • nonspecific lesions.
  • Three subtypes of lupus-specific 
    • Acute
    • subacute 
    • chronic. 
  • Acute cutaneous lupus occurs in 30 to 50% of patients and is classically represented by the butterfly rash-mask-shaped erythematous eruption involving the malar areas and bridge of the nose
  • Chronic cutaneous lupus occurs in 15 to 20% of cases and affects the skin of the face or scalp in about 80% of cases.
  • The least common subtype, subacute cutaneous lupus, occurs in 10 to 15% of patients and includes papulo­squamous (psoriasiform) and annular-polycystic eruptions, usually on the trunk and arms.
  • Nonspecific but suggestive skin manifestations of lupus are common and include 
    • alopecia (both scarring following discoid lesions and non-scarring)
    • Photosensitivity
    • Raynaud’s phenomenon
    • Urticaria
    • Erythema
    • Telangiectases
    • cutaneous vasculitis.

  • ORAL MANIFESTATIONS
  • Two predominant types of oral lesions are
    •  discoid lesions 
    • ulcerations.
  • Oral ulcerations associated with SLE  they occur with increased frequency on the palate and in the oropharynx and are characteristically painless.
  • Histologically, they are characterized by lymphocytic infiltrate at the base of the ulcer and in the perivascular distribution, which is similar to that observed in discoid lesions.
  • Discoid oral lesions, appear as whitish striae frequently radiating from the central erythematous area, giving a so-called “brush border.”
  • Buccal mucosa, gingiva, and labial mucosa are the most commonly affected intraoral sites.
  • Direct immunofluorescent staining for immunoglobulins and complement C3 factor is a useful aid to diagnosis. Granular deposition of IgM, IgG, and C3 along the basement membrane is characteristic

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.

  1. Differential Diagnosis
    • Lichenplanus—homogenouspicture,nodarkerythema and no telangiectasia. Mucosal changes are usually extensive and symmetrical.
    • Lichenoidreaction—historyofdrugisalwaysthere.
    • Ectopic geographic tongue—systemic manifestation present is lupus erythematous, which is absent in ectopicgeographic tongue.
    • Psoriasis—Auspitz’s’signispositive.
    • Electrogalvanic lesion—dissimilar restorations are seenin oral cavity.
    • Leukoplakiaanderythroplakia—lesionstendtomaintainsame appearance and there are no skin changes.
    • Geographic stomatitis—no skin changes, mucosal lesionschange location rapidly.
    • Benign mucous membrane pemphigoid—no systemiccomplain and serology test to be done.
  • TREATMENT
  • Corticosteriods are the cornerstone of therapy
  • A pulse i.v cyclophosphamide regimen for remission induction followed by quarterly infusions
  • Recently, mycophenolate mofetil and azathioprine
  • NSAIDs for arthritis relief
  • Antimalarial like hydroxychloroquinine – effective in cutaneous lupus 
  • DENTAL MANAGEMENT
  • Recommended prophylactic antibiotics if ANC count falls below 500 – 1000 cells/mm3
  • Adrenal supression –
  • Adenocorticotropic hormone supression test is used to evalute
  • Current guidelines – Replacement therapy with hydrocortisone is unnecessary

REFERENCE- ANIL GHOM TEXTBOOK OF ORAL MEDICINE; BURKIT TEXTBOOK OF ORAL MEDICINE AND GOOGLE[SLIDE SHARE]