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ulceration that affects the mucous membranes Incidence ranges from 20-60% Prevalence tends to be higher in professional persons and those in upper socio-economic groups Also known as canker sores & recurrent aphthous stomatitis APHTHOUS ULCERS etiology & pathogenesis Cause is unknown Etiologic factors: Immunologic factors Microbiologic factors Nutritional factors Other factors: hormonal alterations, stress, trauma & food allergies

APHTHOUS ULCERS etiologic factors: immunologic The most promising avenue of investigation Aphthous ulcers result from a focal immune dysfunction in which T lymphocytes play a significant role Causative agent Endogenous antigen autoimmune Exogenous antigen hyperimmune

APHTHOUS ULCERS etiologic factors: microbiologic After several studies, this theory has been discarded

APHTHOUS ULCERS etiologic factors: nutritional Deficiencies of vitamin B12, folic acid & iron Correction of the above deficiencies has produced improvement or cures APHTHOUS ULCERS etiologic factors: others Hormonal alterations Stress Trauma Food allergies: nuts, chocolate & gluten

None of these is seriously regarded as being important in the primary causation But can have triggering role APHTHOUS ULCERS clinical features Three forms of aphthous ulcers Minor aphthous ulcers Major aphthous ulcers Herpetiform aphthous ulcers

All are believed to be part of the same disease spectrum with a common etiology Differences are essentially clinical & correspond to degree of severity APHTHOUS ULCERS clinical features

All forms present as painful recurrent ulcers Occasionally, patient have prodromal symptoms: tingling or burning prior to the appearance of the lesions Ulcers are not preceded by vesicles

Rarely appear: gingiva & hard palate APHTHOUS ULCERS clinical features Appear on : Vestibular & buccal mucosa Tongue Soft palate Fauces Floor of the mouth MINOR APHTHOUS ULCERS clinical features Most commonly encountered form Appear as single, painful, oval ulcers Less than 0.5 cm in size Covered by a yellow fibrinous membrane Surrounded by an erythematous halo Lesion lasts 7-10 days MINOR APHTHOUS ULCERS clinical features Heals without scar formation When the lateral or ventral surfaces of the tongue are affected, pain tends to be out of proportion to the size of the lesion Multiple oral aphthae may occasionally be seen Recurrences vary from one person to another Periods of freedom from this disease may range from a matter of weeks to as long as years MINOR APHTHOUS ULCERS

MINOR APHTHOUS ULCER MINOR APHTHOUS ULCER MAJOR APHTHOUS ULCERS clinical features Was referred to as periadenitis mucosa necrotica recurrens (PMNR) or Suttons disease Regarded as the most severe expression of aphthous stomatitis Lesions are larger & more painful Persist longer than minor aphthae MAJOR APHTHOUS ULCERS clinical features Appear crateriform because of the depth of inflammation Heal with scar Lesions may take as long as 6 weeks to heal as soon as one lesion disappears, another one starts MAJOR APHTHOUS ULCERS clinical features In patients who experience an unremitting course with significant pain and discomfort, systemic health may be compromised because of difficulty in eating and psychologic stress MAJOR APHTHOUS ULCERS MAJOR APHTHOUS ULCER HERPETIFORM APHTHOUS ULCERS- clinical features Unlike herpetic infection, this form are not preceded by vesicles Exhibit no virus-infected cells HERPETIFORM APHTHOUS ULCERS-clinical features clinically presents as recurrent crops of small ulcers

Although movable mucosa is predominantly affected, palate & gingiva may be involved Pain may be considerable Healing occurs in 1-2 weeks HERPETIFORM APHTHOUS ULCERS HERPETIFORM APHTHOUS ULCER APHTHOUS ULCERS histopathology It is generally accepted that important clues to the etiology and pathogenesis may be found during the early stages , therefore biopsies are unnecessary and rarely done APHTHOUS ULCERS differential diagnosis Diagnosis is generally based on history & clinical appearance Secondary recurrent oral herpes is often confused with aphthous ulcers but can be distinguished from it, because the latter is not precede by a vesicle APHTHOUS ULCERS treatment In patients with occasional or few minor aphthous ulcers usually no treatment is needed because of minor discomfort For patients who are affected severely, some form of treatment can provide significant control but not necessarily cure Because of its immunologic defect related factor, treatment includes drugs that can regulate the immune response APHTHOUS ULCERS treatment Chemotherapeutic agents used: Systemic steroids Topical steroids antibiotics

Other drugs

APHTHOUS ULCERS treatment / systemic steroids Appropriate for severe disease Should not be use unless the clinician as experience in this treatment area/ working with a knowledgeable consultant Should know the effects & side effects of systemic steroids therapy APHTHOUS ULCERS treatment / systemic steroids Effects: Anti-inflammation Immunosuppression Gluconeogenesis from protein & fat Altered fat metabolism Fluid retention from Na resorption & K excretion Potentiation of vasopressors Increased gastric secretions Suppression of pituitary-adrenal axis CNS effects Ocular effects Side effects: Therapeutic Aggravation of Tb & other infections, delayed wound healing Aggravation of diabetes, muscle weakness & osteoporosis Buffalo hump, hyperlipidemia Moon face, weight gain

Blood pressure elevation, aggravation of congestion, heart failure Aggravation of peptic ulcer Adrenal atrophy Psychologic changes Cataracts, glaucoma

APHTHOUS ULCERS treatment / systemic steroids For immediate control of severe case, a lo to moderate dose of prednisone over a short period of time is recommended A typical regimen: 20-40 mg daily for 1 week Followed by another week at half the initial dose Prednisone should be taken in one bolus in the morning APHTHOUS ULCERS treatment / systemic steroids A slow steroid taper is not necessary if the treatment lasts for less than 4 weeks In patients requiring higher dosage prolonged, or maintenance therapy, an alternate-day regimen may be used after initial daily therapy

APHTHOUS ULCERS treatment / topical steroids If used judiciously, can be effective and safe in mild to moderate condition Creams & gels: Orabase APHTHOUS ULCERS treatment / topical steroids Side effects : Systemic Suppression of pituitary-adrenal axis

Iatrogenic Cushings syndrome

Local (skin) Striae Atrophy Hypopigmentation Telangiectasia Induced acne Folliculitis candidiasis

APHTHOUS ULCERS treatment / antibiotics Tetracycline oral suspension Used to eliminate secondary bacterial infection of the ulcers Combination of tetracycline oral suspension, nystatin oral suspension anddephenhydramine hydrchloride ( Benadryl) provides more clinical benefits Oral rinse containing chlorhexidine gluconate .12% ( Peridex, Orahex) APHTHOUS ULCERS treatment / other drugs Vitamin A derivatives Anti-inflammatory drugs Sulfones sulfonamides

BEHCETS SYNDROME A multisystem disease in which recurrent oral aphthae are a consistent feature System involve are: GIT, cardiovascular, ocular, CNS, articular, pulmonary, dermal Oral manifestations are relatively minor, involvement of other sites , esp. the eyes & CNS can be quite serious

BEHCETS SYNDROME etiology Cause is basically unknown Underlying disease mechanism may likely be immuno-dysfunction in which vasculitis has a part Genetic predisposition to the frequent presence of HLA-B15 within the group BEHCETS SYNDROME clinical features Typically affect the oral cavity, eyes & genitalia Recurrent arthritis of the wrists, ankles and knees Cardiovascular manifestations results fro vasculitis and thrombosis CNS manifestations are in the form of headaches, but infarcts have been reported BEHCETS SYNDROME clinical features Presence of pustular erythema nodosum-like skin lesions Relapsing polychondritis ( e.g. auricular cartilage & nasal cartilage) in association with Bechets stigmata Behcets stigmata known as MAGIC syndrome Mouth & genital ulcers with Inflamed Cartilage BEHCETS SYNDROME clinical features Oral manifestations are identical to the ulcers of aphthous stomatitis, minor, and with the same distribution Ocular changes such as uveitis, conunctivitis and retinitis Genital lesions are ulcerative in nature & may cause significant pain & discomfort BEHCETS SYNDROME clinical features Painful ulcerative lesions may also occur around the anus

Inflammatory bowel disease & neurological problems BEHCETS SYNDROME histopathology T-lymphocytes are very prominent Infiltration of neutrophils appear within the vessel representing leukocytoclastic vasculitis BEHCETS SYNDROME diagnosis Diagnosis is based on clinical signs & symptoms described above Biopsy & laboratory tests will produce non-specific results BEHCETS SYNDROME treatment Systemic steroids Immunosuppressive drugs Chlorambucil Azathioprine

Dapsone, cyclosporine & interferon REITERS SYNDROME etiology Cause is unknown Abnormal immune response to microbial antigen regarded as a likely mechanism for the multiple manifestations of this syndrome REITERS SYNDROME clinical features Major components are: Arthritis Non-gonococcal urethritis Conjuctivitis or uveitis

Urethritis precedes the appearance of other lesions REITERS SYNDROME clinical features Mucocutaneous lesions seen in 50% of patients with this syndrome Maculopapular lesions may occur on the genitalia Oral lesions are relatively painless aphthous-like ulcers occurring anywhere in the oral cavity Tongue lesions is similar to that of georaphic tongue REITERS SYNDROME clinical features Occur predominantly in white males in their third decade Duration of the disease varies from weeks to months Recurrences are not uncommon REITERS SYNDROME diagnosis Upon the recognition of various signs and symptoms No specific laboratory tests REITERS SYNDROME treatment Non-steroidal anti-inflammatory agents Antibiotics can be added to the treatment regimen ERYTHEMA MULTIFORME etiology & pathogenesis Basic cause is unknown Hypersensitivity reaction is suspected Evidence shows that the disease mechanism may be related to antigenantibody complexes that are targeted for small vessels of the upper dermis & submucosa

ERYTHEMA MULTIFORME etiology & pathogenesis Precipitating factors can be identified in 50% of the cases Infections drugs

Other factors which trigger EM Malignancy Vaccination Autoimmune disease Radiotherapy

ERYTHEMA MULTIFORME etiology & pathogenesis Infections frequently reported include Herpes simples ( HSV types I & II) TB Histoplasmosis

Various types of drugs that precipitate EM: Barbiturates sulfonamides

ERYTHEMA MULTIFORME clinical features Usually an acute self-limiting process that affects the skin &/or mucous membranes 25-50% of the patients with cutaneous EM will have oral manifestations May be chronic in nature or recurrent acute type In recurrent cases, prodromal symptoms are experienced prior to any eruptions

ERYTHEMA MULTIFORME clinical features Young adults are mostly affected Often develop in the spring or fall & may have recurrence seasonally Include multiple & varied clinical appearances that are associated with cutaneous manifestations ( multiforme) ERYTHEMA MULTIFORME clinical features Target or iris lesion is the classic skin lesion of EM It is consists of concentric erythematous rings separated by rings of nearnormal color The skin in the center of these lesions may be erythematous or tan, representing resolution ERYTHEMA MULTIFORME target or iris lesion in the skin ERYTHEMA MULTIFORME target lesion on the palmar skin ERYTHEMA MULTIFORME clinical features Typically, the extremities are involved Usually in symmetric distribution Other types of skin manifestations include: Macules Papules Vesicles Bullae Urticarial plaques

ERYTHEMA MULTIFORME clinical features

Orally, EM characteristically presents as an ulcerative disease Varying from a few aphthous-type lesions to multiple, superficial, widespread ulcers Areas involved are the lips, buccal mucosa, palate & tongue ERYTHEMA MULTIFORME on the lower lip ERYTHEMA MULTIFORME oral lesions: lower lip ERYTHEMA MULTIFORME oral lesions: gingiva ERYTHEMA MULTIFORME clinical features Recurrent oral lesions may appear as multiple painful ulcers similar to the initial episode As less asymptomatic erythematous patches with limited ulceration Symptoms range from mild discomfort to severe pain ERYTHEMA MULTIFORME clinical features Patient experience considerable apprehension because of occasional explotive onset Systemic signs & symptoms are: Headache Slightly elevated temperature lymphadenopathy ERYTHEMA MULTIFORME clinical features Stevens-Johnson syndrome- a major variant of EM Intense involvement of the mouth, eyes, skin, genitalia & occasionally the esophagus & respiratory tract may be seen

Systemic signs & symptoms are more pronounced Cutaneous & mucosal lesions are more extensive ERYTHEMA MULTIFORME clinical features: stevens-johnson Lips my become encrusted Oral lesions may cause exquisite pain Superficial ulceration, often preceded by a bullae is common to all affected sites Ocular inflammation ( conjunctivitis & uveitis) may lead to scarring & blindness in some patients ERYTHEMA MULTIFORME ocular lesion ERYTHEMA MULTIFORME histopathology No specific or consistent microscopic pattern Dermal vessels shown to have IgM complement and fibrin in their walls- this support an immune-complex vasculitis cause of EM ERYTHEMA MULTIFORME differential diagnosis Target or iris skin lesion is present, clinical diagnosis is straightforward If skin lesion is absent, it has to be compared with primary HSV infections, aphthous ulcers, pemphigus vulgaris, bullous pemphigoid & erosive lichen planus ERYTHEMA MULTIFORME diagnosis To diagnose EM, the ff. should be present: General lack of systemic symptoms Favored oral location of lips, buccal mucosa, tongue, & palate Larger sized ulcers- not precede by vesicles

Presence of target skin lesions History of recent drug ingestion or infection

ERYTHEMA MULTIFORME treatment Symptomatic treatment for mild affected patients Topical corticosteroids with anti-fungals

In severe cases, moderate dose of systemic corticosteroids may be used to shorten the course of the disease & abort recurrences or reduce its intensity ERYTHEMA MULTIFORME treatment Supportive measures to provide patients with substantial benefits: Oral irrigation Adequate fluid intake Use of antipyretics

LUPUS ERYTHEMATOSUS Encompasses three (3) recognized subsets: Systemic (acute) LE Subacute cutaneous LE Discoid (chronic) LE- which may have oral manifestations

LUPUS ERYTHEMATOSUS Systemic lupus erythematosus (SLE) is of greatest importance because of profound impact it has on many organ system LUPUS ERYTHEMATOSUS Discoid lupus erythematosus (DLE) is the least aggressive form, affecting predominantly the skin and rarely progressing to a more severe form It may be of great cosmetic significance because of its predilection for the face LUPUS ERYTHEMATOSUS

Subacute cutaneous lupus erythematosus (SCLE) lies intermediate between SLE and DLE Skin lesions of mild to moderate severity Mild systemic involvement Appearance of some abnormal autoantibodies

LUPUS ERYTHEMATOSUS etiology & pathogenesis Result from an autoimmune process that may be influenced by genetic or viral factors Both humoral & cell-mediated arms of the immune system are involved LUPUS ERYTHEMATOSUS clinical features- DLE Characteristically seen in middle age, especially women Lesions frequently appear solely on the skin, most commonly on the face & scalp Oral & vermillion lesions are also frequently seen but usually accompany cutaneous lesions LUPUS ERYTHEMATOSUS clinical features- DLE On the skin, lesions appear as disk-shaped erythematous plaques with hyperpigmented margins As the lesions expand peripherally, the center heals, with the formation of scar & formation of pigment Involvement of hair follicles results in permanent hair loss (alopecia) LUPUS ERYTHEMATOSUS clinical features- DLE Mucous membrane lesions appear in 25% of the patients with cutaneous DLE Most frequently affected are: buccal mucosa, gingiva, & vermilion Lesions appear as erythematous plaques or erosions

Usually present are delicate, white, keratotic striae radiating from the periphery of the lesions LUPUS ERYTHEMATOSUS chronic DLE LUPUS ERYTHEMATOSUS LE on the mucosa of hard palate LUPUS ERYTHEMATOSUS LE on the buccal mucosa LUPUS ERYTHEMATOSUS clinical features- DLE Diagnosis of oral lesions may not be evident on the basis on clinical appearance, but it is often suspected in the presence of skin lesions Progression to SLE is very unlikely although the potential does exist LUPUS ERYTHEMATOSUS clinical features- SCLE Skin lesions are annular or papulosquamous in nature Lesion persist for weeks to months and heal without a scar Oral lesions are those similar to DLE Mild systemic symptoms in the form of musculoskeletal complains as well as serologic abnormalities are frequently seen LUPUS ERYTHEMATOSUS clinical features- SCLE Circulating antibodies to cytoplasmic components may be found in affected patients One is known as anti-Ro or Sjogrens syndrome A antibody (SS-A) since it may also be found in the serum of patients with Sjogrens syndrome anti-La (SS-B)- an auto-antibody

LUPUS ERYTHEMATOSUS clinical features-SCLE Long term prognosis is believed to be good, with progressive to SLE an unlikely event

LUPUS ERYTHEMATOSUS clinical features- SLE Skin and mucosal lesion are relatively mild Patient complaints are dominated by multiple system involvement Numerous auto-antibodies directed against nuclear & cytoplasmic antigens are found in patients with SLE These antibodies when complexed to their corresponding antigens either in serum or in the target organ resulting in a wide variety of clinical signs & symptoms LUPUS ERYTHEMATOSUS clinical features- SLE Skin involvement results in an erythematous rash, seen over the malar processes and bridge of the nose resulting to butterfly appearance Other affected areas are: face, trunk and hands Disk-shaped lesions are non-scarring may flare as systemic involvement progresses LUPUS ERYTHEMATOSUS clinical features-SLE Oral lesions are similar to that of DLE Ulceration Erythema Keratosis

Areas frequently involved are: Vermilion Buccal mucosa Gingiva palate LUPUS ERYTHEMATOSUS clinical features-SLE

Systemic symptoms: initial Fever Weight loss Malaise

Will progress into involving many organs: Joints Kidneys Heart lungs

LUPUS ERYTHEMATOSUS clinical features- SLE The inflammatory of the various involved tissues result in a wide array of signs & symptoms Kidney- glomerulopathy- most important & the most common cause of death for patient with SLE LUPUS ERYTHEMATOSUS diagnosis Serologic tests for autoantibodies are positive in patients with SLE The ANA test is the most reliable & relatively specific for SLE Another serologic test for SLE is the LE test , but less sensitive & less specific LUPUS ERYTHEMATOSUS histopathology The most important microscopic feature diagnostically is the interface change, since it appears that the basal layer is the primary target in the skin & mucous membrane LUPUS ERYTHEMATOSUS differential diagnosis

Lesions similar with erosive lichen planus, but lupus lesions are less symmetrical in distribution Keratotic striae in LE are more delicate & subtle than that of lichen planus LUPUS ERYTHEMATOSUS differential diagnosis The presence of characteristic skin lesions or systemic signs & symptoms may help diagnose LE Biopsy & direct immunofluorescent testing should help confirm the clinical impression Negative serologic tests for autoantibodies would rule out systemic involvement LUPUS ERYTHEMATOSUS treatment DLE is usually treated with topical steroids High-potency creams can be used intra-orally but should be used with caution on the facial skin because of secondary cutaneous changes

LUPUS ERYTHEMATOSUS treatment Systemic steroids may be utilized in the treatment of SLE and SCLE Prednisone combined with immunosuppressive agends Anti-malarials, non-steroidal anti-inflammatories, dapsone, & retinoids DRUG REACTIONS etiology & pathogenesis Although the skin is more commonly involved in adverse reactions to drugs Oral mucosa ay occasionally be the target organ or maybe the sole site of involvement (or part of a skin reaction) Drugs Known to Cause Adverse Reactions Anti-malarials Aspirins

Barbiturates Chlorpromazine Cimetidine Codeine Erythromycin Gold compounds Indomethacin Ketoconazole Local anesthetics Meprobamate Methlydopa Oxyprenolol hydrochloride Penicillin Phenytoin Retinoids Streptomycin Sulfonamides Tetracycline Drug Reactions pathogenesis Immunologic mechanism Non-immunologic mechanism Drug Reaction pathogenesis

Immunologic Mechanism

Triggered an antigenic component on drug molecule ( allergic reaction) Depend on the following factors: immunogenecity of the drug frequency of exposure the route of administration innate reactivity of the patients immune system

Drug Reaction pathogenesis

Non-immunologic Mechanism Do not stimulate an immune response in the patient Are not antibody-dependent Drugs directly affecting the mast cells, causing the release of chemical mediators Reactions may be overdoe, toxicity or side effects Drug Reaction clinical features Cutaneous manifestations Oral manifestations Drug Reaction clinical features

Cutaneous manifestations Varied depending upon many factors: Type of drug Drug dosage Individual patient differences

Changes: (appear rapidly)

Anaphylaxis Angioedema Urticaria Drug Reaction clinical features

Acquired Angioedema IgE-mediated allergic reactions Precipitated by drug or foods (nuts or shellfish) Substances act as sensitizing agent that elicit IgE production Drug Reaction clinical features

Hereditary Angioedema Produces the similar clinical changes as that of acquired type Inherited through autosomal dominant trait having deficiency of the inhibitor of the first component of compemen, C1 esterase Drug Reaction clinical features

Angioedema Either acquired or hereditary Appear soft, diffuse, painless swelling Usually affecting the lips, neck or face No color change Condition subsides after 1-2 days which may recur at a later date Emergency treatment may be required to prevent respiratory distress or glottic or laryngeal involvement Drug Reaction clinical features

Other cutaneous manifestations

Urticaria Maculopapular rash Erythema Vesicles Ulcers Target lesions (EM) Drug Reaction clinical features Oral manifestations Erythematous, vesicular or ulcerative May mimic lichen planus ( lichenoid drug reations) Widespread of ulcers typical or EM are often representative of a drug reaction Drug Reactions histopathology Non-specific: spongiosis, necrotic keratinocytes, lymphoid infiltrates, eosinophils Biopsy may be helpful but not diagnostic Drug Reaction diagnosis Diagnosis requires a high index of suspicion and careful history taking Recent use of drug

Withdrawal of suspected drug should result in improvement Drug Reaction treatment Important measure in management is identification & withdrawal of the causative agents Antihistamines Corticosteroids (occasionally)

Contact Allergy etiology & pathogenesis Antigenic stimulation of vast array of foreign substances Immune response is cell-mediated Sensitization phase: Langerhans cell recognize the foreign antigen & present them it the Tlymphocytes Local lymphocytes secrete chemical mediators producing allergic reactions

Contact Allergy clinical features Lesions directly adjacent to the causativ agent Presenting lesions ranges from erythematous to ulcerative Frequently seen in skin, uncommon intraorally Contact Allergy clinical features Materials containing agents known to cause oral contact allergic reactions: Toothpaste Mouthwash, mouthrinse Candy Chewing gum Topical antimicrobials Topical steroids Iodine Essential oils Denture base materials Cinnamon white , lichenoid, red or ulcerative lesions

Contact Allergy histopathology Epithelium & connective tissue sho inflammatory changes Spongiosis & vesiculation is also seen Dilated blood vessels Eosinophils may be seen Contact Allergy diagnosis Careful history taking is essential Establish a cause & effect relationship may not be possible Biopsy may be helpful but non-conclusive Patch testing may be helpful but may give a false-positive or false-negative result Contact Allergy treatment Elimination of the offending agent or material Healing should take place in 1- 2 weeks Topical steroids may hasten the healing process Wegeners Granulomatosis Inflammatory condition of unknown origin Wegeners Granulomatosis clinical features Triad of upper respiratory tract, lung and kidney involvement Occasionally, only 2 of 3 sites are affected

Lesions may present in the oral cavity & skin & other organ system Basic process common to all foci is necrotizing vasculitis with granuloma formation

Wegeners Granulomatosis clinical features Rare disease of middle age Initial presentation often occur with head & neck Sinusitis, rhinorrhea, nasal stuffiness & epistaxis seen w/ or w/o fever arthralgia & weight loss

In majority of the cases, nasal or sinus ( maxillary) involvement is seen & is often seen in the course of the disease Wegeners Granulomatosis clinical features Destructive lesions are typically ulcerated Necrosis & perforation of nasal septum Perforation of hard palate is uncommon

Intraorally, red granular gingival lesions Generalized & results in relatively uniform enlargement

Wegeners Granulomatosis clinical features Most patients have kidney involvement Focal necrotizing glomerulitis Renal failure is the final outcome

Inflammatory lung lesions Intensify from slight to severe May lead to respiratory failure

Wegeners Granulomatosis histopathology Basic pathologic process is granuloatous with necrotizing vasculitis Presence of acute & chronic inflammatory cells Affected small vessels show a mononuclear infiltrate within their walls

Wegeners Granulomatosis diagnosis Depend upon the finding of granulomatous vasculitis in biopsy tissue of URT, evidence of lung involvemen or kidney lesions Anti-neutrophil cytoplasmic antibodies (ANCA) Negative culture & tissue identification of microorganisms would help rule out infectious processes Immunohistochemical staining could be used to rule out neoplasm Wegeners Granulomatosis treatment Cytotoxic agent Cyclophosphamide Corticosteroids

Remissions seen 75% of cases Midline Granuloma Diagnosis made exclusion of other granulomatous & necrotizing midfacial lesions Represents an atypical or unrecognized lymphoma Midline Granuloma etiology Unknown etiology Hyper-immune response to an unidentified antigen Lymphoid neoplasia from chronic immune stimulation has been suggested Midline Granuloma clinical features Unifocal destructive process in the midline of the oronasal region Lesions appear as aggressive necrotic ulcers that are progressive & nonhealing

Extension through soft tissue, cartilage & bone is typical Perforation of the nasal septum & hard palate is characteristic Midline Granuloma clinical features Without treatment, the inflammatory process eventually consumes the patient Because of continuous erosion into vital structures especially blood vessels: death has been a typical outcome Midline Granuloma histopathology Appear like acute & chronic inflammation in partially necrotic tissue Several biopsies are required to confirm the diagnosis Midline Granuloma differential diagnosis Wegeners granulomatosis Infectious disease Bacterial infection ( TB) Deep fungal diseases

Neoplasm Poorly differentiated squamous cell carcinoma, sarcomas & lymphomas

Midline Granulomat treatment

Treatment of choice High dose of local radiation Optimistic prognosis

Corticosteroids Chronic Granulomatous Disease

Inherited condition Resulting clinical defect: altered neutrophil macrophage function Cells have the capacity to phagocyte microorganism but lack the ability to kill certain bacteria & fungi Chronic Granulomatous Disease- clinical features Manifestations appear during childhood Predominantly occur in males Affect different organs: lymph nodes, lung, liver, spleen, bone & skin Recurrent & persistent Oral lesions: multiple ulcers Recurrent & persistent

Chronic Granulomatous Disease- histopathology Granular nodular Granulomas may exhibit central lesions Chronic Granulomatous Disease- diagnosis Clinical features & tissue samples Neutrophil function tests confirm the diagnosis Differential diagnosis: Crohns disease, TB, histoplasmosis, blastomycosis, tularemia Chronic Granulomatous Disease - treatment Use of specific antimicrobial agents Neutropenia Rare blood dyscrasia of unknown cause Manifests as severe cyclic depletions of neutrophils from blood and marrow, with mean cycle of periodicity of about 21 days Signs & symptoms: fever, malaise, oral ulcers, cervical lymphadenopathy & infections may appear neutropenic episodes

Patients are prone to exaggeration of periodontal disease No definitive treatment