Tori/Exostoses Etiology and Pathogenesis PDF

Tori/Exostoses Etiology and Pathogenesis ~ Tori and exostoses are considered to be normal structural variants. Their etiology is multifactorial and poorly defined, although genetics is a dominant factor. The First & The Only Franchise in the Iraq...

Tori/Exostoses Etiology and Pathogenesis ~ Tori and exostoses are considered to be normal structural variants. Their etiology is multifactorial and poorly defined, although genetics is a dominant factor. The First & The Only Franchise in the Iraq 4 The First & The Only Franchise in the Iraq 8  Foliate papillae ~ These bilateral, pinkish soft nodules on the lateral borders of the tongue contain taste buds and minor oral tonsils forming part of Waldeyer’s ring. They lie at the junction of the anterior two-thirds and the posterior third and sometimes become hyperplastic or inflamed and sore. Management No management is required. The First & The Only Franchise in the Iraq 9  ~ Foliate Papillae The First & The Only Franchise in the Iraq 10  Lingual varicosities ~ Dilated tortuous veins are normal along the ventral surface of the tongue and tend to become more prominent with age They lie superficially and raise the covering thin mucosa into soft sessile nodules and generally cause no problems, being only extremely rarely the site of thrombus formation. The First & The Only Franchise in the Iraq 11  ~ The First & The Only Franchise in the Iraq 12  Papillomas These benign lesions have spiky exophytic or rounded cauliflower-like shapes as large as a centimeter or so in diameter. Probably all are caused by human papillomavirus (HPV) even though it cannot be detected in some lesions The First & The Only Franchise in the Iraq 32  Squamous papillomas ~ mainly affect adults and have a distinctive, clinically recognizable, cauliflower-like or branched structure of finger-like processes. Histologically, the papillae consist of stratified squamous epithelium supported by a vascular connective tissue core. Most are keratinized and so appear white Associated with HPV type 6 ,11. The First & The Only Franchise in the Iraq 33 The First & The Only Franchise in the Iraq 34  Infective warts (verruca vulgaris) ~ Lesions caused by autoinoculation from warts on the hands are uncommon but seen particularly in children. The lesions may appear identical to squamous papillomas, be more rounded or even only slightly raised. The First & The Only Franchise in the Iraq 35 The First & The Only Franchise in the Iraq 37  Pigmented lesions of the oral mucosa 1. Focal pigmentation conditions a. Freckle/ephelis j b. Oral/labial melanotic macule c. Oral melanoacanthoma d. Melanocytic nevus e. Malignant melanoma The First & The Only Franchise in the Iraq 6  A freckle (ephelis) A freckle (ephelis) is a hyperpigmented macule commonly observed on the facial and perioral skin. They usually develop during the first decade of life and are more common in light-skinned individuals with blonde or red hair. There is no gender predilection, and the color intensity and frequency of freckles typically decrease after adolescence. The First & The Only Franchise in the Iraq 7  Pathophysiology Freckles are due to an increase in melanin production without an increase in the number of melanocytes and become more pronounced after sun exposure. Freckles are thought to be developmental in origin. Freckles appear as a uniformly tan- or brown colored, oval or round macule, between 1 and 3 mm in size on sun-exposed cutaneous surfaces. Patient Management Treatment is typically not indicated for freckles in childhood or adolescence The First & The Only Franchise in the Iraq 8  Oral/Labial Melanotic Macule Epidemiology A melanotic macule is a benign pigmented lesion that may occur on intraoral mucosal surfaces (oral melanotic macule) or on the lips (labial melanotic macule).They are considered to be the most common oral mucosal lesions of melanocytic origin and are also termed focal melanosis. Oral/labial melanotic macules are present in up to 3% of the population, are typically observed in patients in the fourth and fifth decades, and have a 2:1 female predilection. The First & The Only Franchise in the Iraq 9  Etiology The etiology of oral/labial melanotic macules has not been determined but may represent a reactive or a physiologic process. Pathophysiology Oral/labial melanotic macules are caused by an increased production and deposition of melanin within the basal cell layer, the lamina propria, or both. The First & The Only Franchise in the Iraq 10  Clinical-Pathologic Features Oral/labial melanotic macules are solitary, well circumscribed lesions that are typically less than 1 cm in diameter. Oral melanotic macules may appear on any surface but are most commonly observed on the buccal mucosa, gingiva,and palate. The First & The Only Franchise in the Iraq 11  Histopathological analysis of melanotic macules reveals an increase in melanin in the basal and parabasal layers of normal stratified squamous epithelium without an increase in number of melanocytes. Patient Management Oral/labial melanotic macules are considered benign lesions without malignant potential. Since early malignant melanoma may have a similar clinical appearanceand exhibits a predilection for the maxillary alveolar mucosa and palate, it is strongly advisable to perform an excisional biopsy for any suspected macules. The First & The Only Franchise in the Iraq 12  Oral Melanoacanthoma Epidemiology Oral melanoacanthoma represents a benign melanocytic lesion that is most commonly observed in dark-skin females. Etiology Oral melanoacanthoma is of unknown etiology. Pathophysiology The pathophysiologic mechanism for oral melanoacanthoma is most consistently associated with acute regional trauma or chronic irritation. The First & The Only Franchise in the Iraq 13  Clinical-Pathologic Features Oral melanoacanthoma typically presents as a diffuse, rapidly enlarging area of macular pigmentation that may range in size from a few millimeters to several centimeters Histologically, oral melanoacanthoma is characterized by spongiotic epithelium containing dendritic pigmented melanocytes throughout the lesional epithelium. The First & The Only Franchise in the Iraq 14  Patient Management Treatment of oral melanoacanthoma is typically not indicated after diagnosis has been established. An incisional biopsy is necessary to rule out malignant melanoma as it is considered in the differential diagnosis of melanoacanthoma. The First & The Only Franchise in the Iraq 15  Melanocytic Nevus Epidemiology Melanocytic nevi, commonly referred to as“moles,” represent a group of benign tumors that develop due to melanocytic growth and proliferation. The First & The Only Franchise in the Iraq 16  Etiology In general, melanocytic nevi are acquired lesions with both environmental and genetic factors thought to play a role in the development of cutaneous and oral lesions. Pathophysiology Pigmented nevi are rare causes of focal oral pigmentation. They present as either brown or blue lesions. Unlike ephelides and melanotic macules, which result from an increase in melanin pigment synthesis, nevi are due to benign proliferations of melanocytes. The First & The Only Franchise in the Iraq 17  Clinical-Pathologic Features. Intraoral lesions are unusual and form circumscribed brown to black patches, usually flat, approximately 5 or 6 mm across. Palate and gingiva are favoured sites. Histologically, the cluster of naevus cells is seen below the epithelium Patient Management A biopsy is necessary to confirm the diagnosis of oral melanocytic nevi as the clinical presentation resembles other focally pigmented lesions, such as malignant melanoma. The First & The Only Franchise in the Iraq 18  Malignant Melanoma Epidemiology Malignant melanoma is a neoplasm of melanocytic origin with most cases occurring on the skin. incidence of malignant melanoma increases with age, reaching a peak between80 and 84 years. Oral malignant melanoma occurs much less frequently than its cutaneous counterpart. The First & The Only Franchise in the Iraq 19  Etiology Ultraviolet light exposure, fair complexion and sun sensitivity cause cutaneous melanoma, but no aetiological factors are known for mucosal melanoma. Pathophysiology Malignant melanomas may either develop denovo(new) or from a preexisting benign melanocytic lesion The First & The Only Franchise in the Iraq 20  Clinical-Pathologic Features The most frequent sites are the palate and upper alveolar ridge. Early oral melanomas are asymptomatic dark brown or black flat patches. Symptoms only develop in the late stages with nodular growth, pain, ulceration, bleeding or loosening of teeth. The First & The Only Franchise in the Iraq 21  Melanomas grow in a predictable fashion. Initially, the malignant melanocytes grow only within the epithelium,spreading laterally. This preinvasive or in situ stage is called the radial or horizontal growth phase, and lesions at this stage rarely metastasise. Later, the melanocytes extend out of the epithelium into the connective tissue in the vertical growth phase, this stage is associated with metastases. Because of their rapid growth, most oral melanomas are at least a centimetre across before being noticed, and approximately 50% of patients have metastases at presentation, most commonly in cervical lymph nodes. In addition to the regional lymph nodes, metastases can involve the lungs, liver, brain and bones. The First & The Only Franchise in the Iraq 22  Treatment Oral melanomas are highly invasive, metastasise early and have a high mortality. Early diagnosis is critical to survival so that early biopsy of all oral pigmented lesions is essential. Wide excision with, if possible, a 2–5 cm margin (often with a simultaneous neck dissection) followed by radical radiotherapy. The First & The Only Franchise in the Iraq 23 The First & The Only Franchise in the Iraq 24  ↑ 2. Multifocal/diffuse pigmentation conditions a. Physiologic pigmentation b. Drug-induced melanosis c. Smoker’s melanosis d. Post-inflammatory (inflammatory) hyperpigmentation The First & The Only Franchise in the Iraq 25  Multifocal/Diffuse Pigmentation Physiologic Pigmentation Epidemiology Physiologic (“racial”) pigmentation is the most common multifocal or diffuse oral mucosal pigmentation. It is typically observed in dark-skinned individuals, most commonly in African, Asian,or Mediterranean populations without gender predilection. The First & The Only Franchise in the Iraq 26  Etiology The etiology of physiologic pigmentation has not been identified. Pathophysiology The increased pigmentation associated with this condition is attributed to increased melanocytic activity rather than an increase in numbers of melanocytes. Clinical-Pathologic Features Physiologic pigmentation typically affects the gingiva, where it presents as a bilateral, well demarcated, band like brown pigment that usually does not affect the marginal gingiva nor interfere with normal tissue architecture. Microscopically, this condition is characterized by the presence of increased amounts of melanin deposition within the basal cell layer The First & The Only Franchise in the Iraq 27  Patient Management Diagnosis of physiologic pigmentation is typically made based on clinical appearance, and treatment is not indicated for this condition. It may be of esthetic concern to patients, and although procedures such as gingivectomy, laser therapy, and cryotherapy have been used. The First & The Only Franchise in the Iraq 28  Drug-Induced Melanosis Epidemiology Mucosal coloration can be induced by an array of medications. It has been estimated that 10–20% of all cases of acquired melanocytic pigmentation may be induced by drugs. Etiology Several medications have been implicated in drug-induced melanosis such as hormones and oral contraceptives; antipsychotics , antimalarial drugs such as hydroxychloroquine ,chemotherapeutic agents including bleomycin, busulfan, fluorouracil, anti-retroviral agents including zidovudine; anti-fungal drugs such as ketoconazole; and anti-microbial agents including minocycline and tetracycline. The First & The Only Franchise in the Iraq 29  Pathophysiology In some cases, the coloration is true pigmentation resulting from stimulation of melanin synthesis by the drug and/or its metabolites. In other cases, drug precipitates deposit within the lamina propria or submucosa resulting in blue-brown-black mucosal coloration. The First & The Only Franchise in the Iraq 30  Clinical-Pathologic Features Drug-induced pigmentation can affect any mucosal site. Some medications, such as hydroxychloroquine, produce characteristic patterns of mucosal pigmentation; the palate is usually affected in patients taking this drug. Microscopically, basilar hyperpigmentation and melanin incontinence without a concomitant increase in number of melanocytes are characteristics of drug induced melanosis. The First & The Only Franchise in the Iraq 31  Patient Management Diagnosis of drug-induced melanosis can be achieved if a temporal association is made between the use of a medication and development of pigmentation. Biopsy is warranted if a diagnosis of drug-induced,melanosis cannot be appropriately made. Discontinuation of the medication may eventually resolve the pigmentation, which may take weeks to months to achieve. The First & The Only Franchise in the Iraq 32  Smoker’s Melanosis Epidemiology ↓ Smoker’s melanosis is the term used to describe oral mucosal pigmentation that develops secondary to heavy tobacco use. Pathophysiology It has been postulated that melanin production stimulated by tobacco smoke may have a protective role against the harmful agents in the smoke. The First & The Only Franchise in the Iraq 33  Clinical-Pathologic Features Smoker’s melanosis typically presents as diffuse,patchy melanosis affecting the anterior vestibular maxillary and mandibular gingivae, buccal mucosa, labial commissures, lateral tongue, palate, and/or floor of mouth. Histopathologically, this condition is characterized by increased melanin pigmentation of the basal cell layer of the surface epithelium. The First & The Only Franchise in the Iraq 34  Patient Management Diagnosis of smoker’s melanosis is usually established by a positive history of tobacco use correlated with characteristic physical findings on clinical examination. Cessation of smoking habits results in gradual resolution of the lesions attributed to smoker’s melanosis, typically within a 3-years. The First & The Only Franchise in the Iraq 35  Post-inflammatory (Inflammatory) Hyperpigmentation ↑ Post-inflammatory hyperpigmentation is a condition characterized by pigment deposition in area(s) subjected to inflammation or previous injury that is more commonly observed in dark-complexioned individuals. Inflammatory conditions, such as lichen planus,resulting in increased melanin deposition in affected areas. The First & The Only Franchise in the Iraq 36  3. Pigmentation associated with systemic or genetic disorders a. Adrenal insufficiency (Addison disease) b. Cushing disease c. Human immunodeficiency virus (HIV) – associated pigmentation d. Peutz-Jeghers syndrome The First & The Only Franchise in the Iraq 37  Addison’s disease results from failure of secretion of cortisol and aldosterone by adrenal gland. The disease is usually autoimmune with organ-specific circulating autoantibodies. Tuberculous or fungal adrenal destruction are rare causes, sometimes secondary to HIV infection. Adrenal insuffeciency cause severe disorder of electrolyte and fluid balance and serious clinical effects. The First & The Only Franchise in the Iraq 38  Pigmentation results from compensatory excessive adrenocorticotropic hormone (ACTH) secretion as this peptide hormone has a similar amino acid sequence to melanocyte-stimulating hormone(MSH). Pigmentation is often an early sign and, in the mouth, is patchily distributed on gingivae, buccal mucosa and lips. It is brown or almost black. The skin pigmentation looks similar to suntan. Long-term treatment of Addison’s disease is usually by oral hydrocortisone. The dose of steroid needs to be adjusted to provide additional steroid support in times of stress, infection, other illness, surgery or exercise. Failure to provide sufficient steroid, or untreated disease, may lead to Addisonian crisis(adrenal crisis). The First & The Only Franchise in the Iraq 39 The First & The Only Franchise in the Iraq 40  ~ Typical clinical features of Addison’s disease Lassitude, anorexia, weakness and fatigue Abnormal oral and cutaneous pigmentation Gastrointestinal disturbances, diarrhoea, nausea, vomiting Craving for salt (caused by lack of aldosterone) Loss of weight Low blood pressure Susceptibility to hypotensive crises Associated with chronic mucocutaneous candidosis in polyendocrinopathy syndrome. The First & The Only Franchise in the Iraq 41  ↑ Investigation required for diagnosis of Addison disease : Blood pressure (hypotension). ACTH level raised. ACTH stimulation test (Synacthen test) is abnormal. Low cortisol level. Low aldosterone level. Low sodium ,high potassium levels. The First & The Only Franchise in the Iraq 42  Thrush Thrush a disease recognised by Hippocrates, is also sometimes called the acute pseudomembranous type of candidosis because of the thick white layer of candidal hyphae, dead and dying epithelial and inflammatory cells and debris that covers the mucosa like a membrane. Thrush is common in neonates, caused by lack of an immune response and infection acquired during passage through the birth canal. It is also common in the very elderly and the very debilitated and on the soft palate of asthmatic steroid inhaler users who spray their palate rather than inhale the drug. It may also follow antibiotic treatment The First & The Only Franchise in the Iraq 4  Clinical features Thrush forms soft, friable and creamy coloured plaques on the mucosa and the pseudomembrane can be scraped or wiped off by gauze exposing the erythematous mucosa below. This differentiates thrush from chronic forms of candidosis in which the white surface layer is keratin. The extent of pseudomembrane varies from isolated small flecks to widespread confluent plaques and the buccal mucosa, palate and dorsal tongue are the most commonly affected sites. The First & The Only Franchise in the Iraq 5  Pathology A Gram- or periodic acid-Schiff (PAS)-stained scraping from the pseudomembrane shows large masses of tangled hyphae, detached epithelial cells and neutrophils , and this test is diagnostic. Management The diagnosis is made on clinical features supported by microscopy of a scraping The infection itself is managed by dealing with any identifiable predisposing factors, and this alone may allow thrush to resolve. Topical antifungal like Nystatin suspension used four times daily for at least two weeks is effective. The First & The Only Franchise in the Iraq 6  Acute antibiotic stomatitis - This condition is also known as antibiotic sore mouth and acute atrophic candidosis. It follows overuse or topical oral use of antibiotics, especially broad-spectrum drugs such as tetracycline. These suppress the normal oral flora that competes with Candida in the mouth. Clinically, the whole mucosa is red and sore, but the tongue is typically worst affected and appears smooth, having lost its filiform papillae. Resolution may follow withdrawal of the antibiotic but is accelerated by topical antifungal treatment. The First & The Only Franchise in the Iraq 9  Chronic hyperplastic candidosis The alternative name of candidal leukoplakia reveals the controversial nature of this condition, in which chronic low level candidosis induces a localised zone of epithelial keratosis. Clinical features Adults, typically males of middle age or older, are affected, and most are smokers. The usual sites are the post commissural buccal mucosa and the dorsum of the tongue. The plaque is variable in thickness, often rough or irregular in texture and tightly adherent,It will not rub off. Angular stomatitis may associated. The First & The Only Franchise in the Iraq 14  Pathology The surface epithelium is parakeratotic and contains candidal hyphae. They are often sparse and elicit little or no inflammatory response, just a few neutrophils focally. PAS stain shows the hyphae growing (as in thrush)through the epithelial cells of the keratin layer to the prickle cell layer, but no further. If dysplasia is present on biopsy, the lesion is a leukoplakia with superimposed candidal infection and not chronic hyperplastic candidosis. The First & The Only Franchise in the Iraq 15  Management After confirmation of the diagnosis by histology or a scraping for hyphae, antifungal treatment is provided, but eradication of infection is difficult in this chronic infection. Usually miconazole gel is effective, but may need supplementing with a systemic antifungal drug such as fluconazole for two weeks. If, after all these interventions, the plaque remains, consideration must be given to the fact that it may be a leukoplakia with superimposed candida infection and require follow up as a potentially malignant lesion. The First & The Only Franchise in the Iraq 16  Infections of oral mucosa Bacterial infections Dr.Noor Qasim F.K.H.C.M.S(PhD)OMFM The First & The Only Franchise in the Iraq 1  Tuberculosis Oral tuberculosis is rare and a complication of active pulmonary disease in which the mucosa is infected from the sputum. Open active tuberculosis is now rare and tend to be seen in elderly men with pulmonary infection and a chronic cough that has progressed unrecognised, those who have neglected treatment or are immunosuppressed. They are likely to show typical signs of pulmonary infection: chest pain, malaise, weight loss and haemoptysis. The First & The Only Franchise in the Iraq 2  The typical lesion is an ulcer on the mid dorsum of the tongue; the lip or other parts of the mouth are infrequently affected. The ulcer is typically angular or stellate, with overhanging edges and a pale floor, but can be ragged and irregular. It is painless in its early stages, and regional lymph nodes are usually unaffected. A second typical presentation is a non- healing extraction socket. The First & The Only Franchise in the Iraq 3  Pathology Typical non-caseating tuberculous granulomas containing occasional Langhans type giant cells are seen in the floor of the ulcers. Mycobacteria are sometimes identifiable in the oral lesion by using special stain(Ziehl Neelsen stain). Management Diagnosis is confirmed by biopsy, chest radiography and a specimen of sputum. Oral lesions clear up rapidly if vigorous multidrug chemotherapy is given for the pulmonary infection. No local treatment is needed. The First & The Only Franchise in the Iraq 4  Syphilis Congenital syphilis Congenital syphilis arises when an infected mother transmits the infection with treponema pallidum spirochates to her child in uterus. The classical triad of interstitial keratitis of the cornea, sensorineural hearing loss and dental anomalies(Hutchinson incisiors and mulbery molars) is diagnostic. The First & The Only Franchise in the Iraq 5  Primary syphilis An oral chancre appears 2–8 weeks after infection and may form on the lip, tip of the tongue or, rarely, other oral sites. It consists initially of a firm nodule about a centimetre across. The surface breaks down after a few days, leaving a rounded ulcer with raised indurated edges. Chancres are usually solitary, and multiple lesions suggest immunosuppression. A chancre is typically painless, but regional lymph nodes are enlarged, rubbery and discrete. The First & The Only Franchise in the Iraq 6  Secondary syphilis The secondary stage develops 1–4 months after infection. It typically causes mild fever with malaise, headache, sore throat and generalised lymphadenopathy, soon followed by a rash and stomatitis. Oral lesions, which rarely appear without the rash, mainly affect the tonsils, lateral borders of the tongue and lips. They are usually flat ulcers covered by greyish membrane and may be irregularly linear (snail’s track ulcers) or coalesce to form well-defined rounded areas (mucous patches). The First & The Only Franchise in the Iraq 7  Tertiary syphilis Late-stage syphilis develops in patients approximately 3 or more years The characteristic oral lesion is the gumma, usually of the palate, tongue or tonsils. This starts as a swelling a few to several centimetres in diameter sometimes with a yellowish centre that undergoes necrosis, leaving a painless indolent deep ulcer. Leukoplakia of the tongue may develop during this late stage. Definitive diagnosis and treatment must be provided by specialists. Clinical diagnosis and biopsy diagnosis with confirmation of Treponema by immunohistochemistry and serological tests The First & The Only Franchise in the Iraq 8  Thank you The First & The Only Franchise in the Iraq 9  Oral Mucosal Ulceration Dr.NOOR QASIM F.K.H.C.M.S (PhD ) OMFM i The First & The Only Franchise in the Iraq 1  ulcers ↑ An ulcer is a break in the continuity of the epithelium, exposing the connective tissue to the oral environment. Ulcers may have sharp well-defined borders or ragged margins, but all are covered by a grey- yellow fibrin slough. Ulcers have a superficial bacterial contamination by oral flora, but the tissue below very rarely becomes infected. The rapid turnover of oral epithelium allows uncomplicated ulcers to heal rapidly. The First & The Only Franchise in the Iraq 2  Main causes of mucosal ulcers ↑ 1- Systemic disease (bigs) incudes: A- blood disorders (anemia –haematinic deficiency-leukemia) B- infections(viral-bacterial –fungal ) C- gastrointestinal disease(crohn disease-celiac disease-ulcerative colitis) D-skin diseases(lichen planus-immune blistering disease) 2- Malignant neoplasms 3- Local causes and trauma(mechanical-chemical –thermal-radiation) 4- Aphthae(RAS) 5- Drugs The First & The Only Franchise in the Iraq 3  Although histological examination and specific laboratory tests are often mandatory, a careful clinical examination, associated with thorough history taking, can provide insights into the nature of an oral ulcer. Important clinical features in investigating a patient affected by ulcer(s) of the mouth range from: Number of ulcers, single as for oral cancer or multiple as for herpetic infection Specific localization, as for aphthae which prefer non keratinized mucosa or chronic traumatic ulcer, in relation with rough surface. Duration, acute ulceration usually due to viral infection or chronic as neoplasm, traumatic or tuberculosis. The First & The Only Franchise in the Iraq 4  Presence of a blister preceding the ulcer, a feature of immune-mediated conditions(bulla) or viral infection (vesicle) Presence of other mucosal or cutaneous changes, as for lichen planus, blistering lesions on skin. Gastrointestinal symptoms as pain ,diarrhoea or constipation. Ulcers should always be examined for induration (firmness on palpation), which may be indicative of malignancy. Unless the cause is undoubtedly local, general physical examination is also indicated, looking especially for mucocutaneous lesions, lymphadenopathy or fever. The First & The Only Franchise in the Iraq 5  Systemic disease associated with ulceration (Aphthous like ulcer ALU) A-Blood disorder ~ Anemia and haematinic deficiency The role of iron metabolism in the maintenance of the structure of the oral mucosa has been the subject of much investigation. It is certainly the case that iron deficiency, even when relatively mild in clinical terms, can result in generalized oral epithelial atrophy and loss of the papillary pattern of the tongue mucosa. It seems that other deficiencies that might affect iron metabolism and erythrocyte production, such as folate and vitamin B12 deficiencies, may also contribute to this destabilization of the oral epithelium. The First & The Only Franchise in the Iraq 6  Oral ulcers in cases of leukemia are secondary to anemia ,haematinic deficiency or due to chemotherapy and radiotherapy (mucositis). In leukemia the patient also will complain from malaise, generalized weakness,pallor,purpura and lymphadenopathy. Investigation required include: Complete blood count (CBC) Haematinics (ferritin,folate,vit B12 )and zinc Blood film in suspected cases of leukemia The First & The Only Franchise in the Iraq 7  B-infections(viral-bacterial –fungal ) Viral infection :Human herpes virus infections include (HSV-1,varicella virus –EBV –CMV) and HIV infection. Bacterial infections like Syphilis and Tuberculosis. Fungal infections like deep mycosis Herpes infection Syphilis ulcer T.B ulcer The First & The Only Franchise in the Iraq 8  C- gastrointestinal disease(inflammatory bowel disease IBD and celiac disease): -Inflammatory bowel disease (IBD) The inflammatory bowel diseases are lifelong conditions resulting from aberrant inflammation of the mucosal lining of the gastrointestinal tract. The two main categories are Crohn's disease, which may affect the gut anywhere from mouth to anus, and ulcerative colitis, which is predominantly within the colon. The First & The Only Franchise in the Iraq 9  ~ Crohn’s disease is an inflammatory bowel disease of unknown etiology Granulomatous inflammation affects the ileocaecal region, causing thickening and ulceration(non caseating granuloma). Oral ulceration caused by malabsorption anemia and haematinic deficiency. The First & The Only Franchise in the Iraq 10  Typical orofacial features of Oral Crohn’s disease Diffuse soft or tense swelling of the lips, or mucosal thickening Cobblestone thickening of the buccal mucosa Gingivae may be erythematous and swollen Sometimes, painful mucosal ulcers, linear in sulci or resembling aphthae Mucosal tags in sulcuses Glossitis due to iron, folate or vitamin B12 deficiency can result from malabsorption Orofacial granulomatosis (OFG)shares many features The First & The Only Franchise in the Iraq 11  ULCERATIVE COLITIS Ulcerative colitis is an inflammatory disease of the large intestine causing ulceration and fibrosis There is no direct oral involvement, but the oral condition of pyostomatitis vegetans is closely associated. Oral ulcers caused by anemia and haematinic deficiency secondary to malabsorption. The First & The Only Franchise in the Iraq 12  Coeliac disease (gluten-sensitive enteropathy) ~ Coeliac disease is a permanent intolerance to gliadin—the protein component of wheat. It is a lifelong inflammatory condition of the gastrointestinal tract that affects the small intestine causing villous atrophy. Malabsorption, as a result of coeliac disease, may result in a haematinic deficiency, particularly of iron and folic acid. The First & The Only Franchise in the Iraq 13  Oral manifestations of coeliac disease Oral ulceration—RAS Glossitis Angular cheilitis Enamel hypoplasia of permeant teeth ,short stature and failure to thrive in children IgA anti-gliadin, IgA anti-reticulin, and IgA endomysial autoantibodies are blood tests that can be used as a first-line investigation in those people suspected of having coeliac disease in addition to CBC and haematinics. The First & The Only Franchise in the Iraq 14  If history of the patient revealed any gastrointestinal symptoms investigation includes : Complete blood count Haematinics (folate , ferritin , serum Vit B12 ) and zinc Referral of the patient to Gastroenterologist for further evaluation The First & The Only Franchise in the Iraq 15  V D-skin diseases(lichen planus-immune blistering disease) - Lichen planus Lichen planus is a very common chronic inflammatory disease of skin and mucous membranes. Immune blistering disease includes mainly pemphigus vulgaris – pemphigoid-Epidermolysis bullosa. The First & The Only Franchise in the Iraq 16  2- Malignant Ulcer A single, indurated ulcer is a common presentation of oral cancer and must be carefully differentiated from traumatic or tuberculous ulcers. A range of neoplasms may present with ulcers, most commonly these are carcinomas, but Kaposi sarcoma, lymphomas and other neoplasms may be seen. *carcinoma is cancer that forms in epithelial tissue. *Sarcoma is cancer that develop in mesenchymal cells(muscles,tendons.blood vessels, bone). The First & The Only Franchise in the Iraq 17  3-Local causes and trauma(mechanical-chemical –thermal-radiation-self induced) Traumatic ulcers are usually caused by biting, denture trauma ,hot food, chemical trauma by dental materials or by aspirin(aspirin burn) ,chemotherapy and radiotherapy and arise at trauma-prone sites such as lip, buccal mucosa or adjacent to a denture flange. They are tender, have a yellowish-grey floor of fibrin slough and red irregular margins. Traumatic ulcers heal in days after elimination of the cause. If they persist for more than 10 days without reduction in size and symptoms, or there is any other cause for suspicion as to the cause, biopsy should be carried out to exclude other diseases. The First & The Only Franchise in the Iraq 18  4-Aphthae(Recurrent aphthous stomatitis RAS): Recurrent aphthous stomatitis (RAS), or “canker sores,” is a common oral mucosal disease affecting 10–20% of the general population. characterized by recurring ulcers of the oral mucosa usually manifesting first in childhood or adolescence in patients with no other systemic diseases. RAS may present in three main forms based on its clinical appearance: Minor, major,herpetiform. The First & The Only Franchise in the Iraq 19  Possible etiological factors for recurrent aphthae Genetic predisposition Exaggerated response to trauma Infections Immunological abnormalities Gastrointestinal disorders Haematological deficiencies Hormonal disturbances Stress The First & The Only Franchise in the Iraq 20  Minor aphthae: The most common type Non-keratinized mucosa affected Ulcers are shallow, rounded, 3–7 mm across, with an erythematous margin and yellowish floor One or several ulcers may be present Individual minor aphthae persist for 7–10 days, then heal without scarring. The First & The Only Franchise in the Iraq 21  Major aphthae Uncommon Ulcers frequently several centimetres across Sometimes mimic a malignant ulcer Ulcers persist for several weeks Masticatory mucosa, such as the dorsum of the tongue or occasionally the gingivae, may be involved Scarring may follow healing The First & The Only Franchise in the Iraq 22  Herpetiform aphthae Uncommon Non-keratinized mucosa affected Ulcers are 1–2 mm across Dozens or hundreds may be present May coalesce to form irregular ulcers Widespread bright erythema round the ulcers ulcers may last for approximately 7–14 days, The First & The Only Franchise in the Iraq 23  5-Drugs Drugs may induce ulcers by producing a local burn or by a variety of mechanisms. Cytotoxic drugs (e.g. methotrexate), NSAIDs and nicorandil (a potassium channel activator used in cardiac disorders) or others may be the cause. The First & The Only Franchise in the Iraq 24  Management Treat the underlying cause. Remove etiological factors. ↑ Ensure any possible traumatic element is removed (e.g. a denture flange). Prescribe a chlorhexidine 0.2% aqueous mouthwash. Maintain good oral hygiene. A benzydamine mouthwash or spray, as topical analgesic. Corticosteroid creams, gels and inhalers. Patients should not eat or drink for 30 min after using the corticosteroid, in order to prolong contact with the lesion. Systemic corticosteroids in sever cases( In patients using potent topical corticosteroids for more than a month it is prudent to add an antifungal, since candidosis may arise) The First & The Only Franchise in the Iraq 25  Most important immunological diseases with oral involvement 1-Lichen Planus and lichenoid reaction / 2-Vesicullobullous diseases (pemphigus vulgaris ,pemphigoid) 3-Erythema multiforme 4-Behcet disease 5-Lupus erythematosus 6-Systemic sclerosis(scleroderma) 7-Sjogren Syndrome (will be included in salivary gland disease) The First & The Only Franchise in the Iraq 4  Desquamative gingivitis Desquamative gingivitis is a clinical description, not a diagnosis. Its meaning is inflamed gingiva with peeling of the surface epithelium, and the most common causes are lichen planus, mucous membrane pemphigoid or pemphigus. The gingivae appear smooth, from matt dull red to shiny bright red and translucent due to the thinness of the atrophic epithelium. When lichen planus is the cause, there may be white flecks on the red background. Peeling or blistering may be seen as bullae or small tags of epithelium at the margins of zones of epithelial separation. The appearances are strikingly different from simple marginal gingivitis. The correct underlying diagnosis should be confirmed by biopsy The First & The Only Franchise in the Iraq 5  1-Lichen planus(oral lichen planus OLP) Lichen planus is a very common chronic inflammatory disease of skin and mucous membranes found in 1%– 2% of the population. It mainly affects patients of middle age or older and is slightly more common in females. Aetiology and pathogenesis The aetiology of lichen planus remains unknown.In contrast, the pathogenesis is relatively well understood. Basal cells in epidermis and mucosal epithelium are destroyed by an immunologically mediated process in which cytotoxic T cells (CD8+), and smaller numbers of helper T cells, migrate into the basal layers and destroy the basal cells. The First & The Only Franchise in the Iraq 6  Clinical manifestations OLP classically presents in a bilateral, symmetrical pattern with the buccal mucosa (bilaterally) being the most typical site of involvement. Other common sites of involvement include the tongue ,gingiva ,labial mucosa, and vermilion of the lower lip. Clinically, thereare six clinical subtypes of OLP that can be seen individually or in combination: reticular, plaque like, atrophic, erosive, papular, and bullous. The most common of these are the reticular, erosive, and plaque-like subtypes, and these variants can coexist within the same patient The First & The Only Franchise in the Iraq 7  Lp of vermillion Reticular type Mixed LP patterns Erosive type Plaque type Papular type The First & The Only Franchise in the Iraq 8  Skin(Cutaneous) lichen planus In this disease the skin lesions take the form of dusky pink papules that may occur in any site, but are most commonly found on the flexor surfaces of the wrists , on the genital skin, on the abdomen and lumbar regions, and on the ankles and shins. Fine white striations overlie the papules. These are the so-called Wickham's striae that are characteristic of the condition. The First & The Only Franchise in the Iraq 9  Lichen planus: typical histological features · White lesions (striae) Hyperkeratosis or parakeratosis Apoptotic degeneration of the basal cell layer Compact, band-like lymphoplasmacytic (predominantlyT cell) infiltrate cells hugging the epithelial-connective tissue interface CD8 lymphocytes predominate in the epithelium Atrophic lesions Severe thinning and flattening of the epithelium Minimal or no keratin Marked destruction of basal cells Compact band-like, subepithelial inflammatory infiltrate hugging the epithelial-connective tissue The First & The Only Franchise in the Iraq 10  Lichenoid Reaction This term is given to lichen planus-like lesions caused by a known trigger, usually a drug. Lichenoid reactions cannot be confidently distinguished from lichen planus either clinically or histologically. Lichenoid drug reactions A very wide range of drugs can cause lichenoid reactions of the skin, mucous membranes or both , and a complete drug history is mandatory in all patients thought to suffer from lichen planus The cause of drug reactions is unclear. It is possible that the drug itself becomes bound to the epithelial cells and elicits an antigen-specific response. It is also possible that the drug is metabolised idiosyncratically in the epithelium of susceptible patients, triggering the immune reaction. The First & The Only Franchise in the Iraq 11  Systemic drug groups commonly implicated in oral lichenoid drug eruptions Nonsteroidal anti-inflammatory drugs (NSAIDs) Angiotensin-converting enzyme (ACE) inhibitors Oral hypoglycaemics Diuretics Antimalarials Gold Penicillamine The First & The Only Franchise in the Iraq 12  Topical lichenoid reactions:Restoration reactions Topical lichenoid reactions to restorative materials are usually triggered by amalgam but may be to polymeric materials. The clinical appearances are similar or identical to lichen planus or lupus erythematosus, but lesions are localised to the mucosa in contact with, not just close to, restorations. For this reason, most develop on the posterior buccal mucosa or posterior ventral tongue. The First & The Only Franchise in the Iraq 13  Management There is no treatment for the underlying disease process,treatment is symptomatic to manage any flare up in severity and complications. Asymptomatic striae and keratotic lesions usually require no treatment. Atrophic and ulcerated lesions are painful, are sensitive to acid, spicy or irritant foods and can make eating difficult. Reassurance and education, Patients need to understand that lesions will persist for many years, but that symptoms can be managed Chlorhexidine mouthwash Topical low-potency steroids Topical medium-potency steroids Systemic steroids The First & The Only Franchise in the Iraq 14  Monitoring for complications is critical. Candidal infection is frequent because of increased keratinisation and steroid treatment. A sudden exacerbation of symptoms or a switch from keratotic to atrophic or ulcerated form may well indicate superimposed candidosis. A scraping for hyphae is diagnostic, and antifungal treatment alone is likely to allow the lichen planus to return to its less symptomatic state. The First & The Only Franchise in the Iraq 15  2-Vesicullobullous diseases 28 A-pemphigus Vulgaris g Pemphigus vulgaris is an uncommon autoimmune disease causing vesicles or bullae on skin and mucous membranes. r Aetiology da Pemphigus vulgaris is a classical autoimmune disease. Autoantibodies are directed against desmoglein 1 or 3, two proteins of the desmosomes that hold epithelial cells together I Sesome - Di protein ↑ The First & The Only Franchise in the Iraq 16  lethal because it caused sepsis. * previously Clinical Features Females aged 40–60 years are predominantly affected, and those of Indian and Jewish origin are predisposed. Blisters first appear in the mouth in two-thirds of patients and then develop widely on the skin. Blisters on the skin have a tough layer of keratin as their roof and often persist for some time, filled with clear fluid, before bursting. Blisters in the mouth usually develop on the non-keratinised lining mucosa, and their roofs disintegrate quickly, leaving very painful erosions or superficial ulcers with ragged edges The First & The Only Franchise in the Iraq 17  Histopathology Loss of intercellular adherence of suprabasal prickle cells (acantholysis) Formation of clefts immediately superficial to the basal cells Extension of clefts to form intraepithelial vesicles Rupture of vesicles and bullae to form ulcers High titre of circulating antibodies to desmogleins Binding of antibodies to desmosomes detectable by immunofluorescence staining Epithelial cells that have lost their attachment become rounded and fall into the bullae and can be seen in a smear of the fluid, in which they are known as acantholytic or Tzanck cells. Epithelialdel Attachemea cell vi!!! ↑ O - The antibodies are of IgG class and fix complement. Fishnet Apearance. - & - chicken wireapearance. Immunofluorscence pf PV The First & The Only Franchise in the Iraq 18  Management The diagnosis must be confirmed as early as possible. When skin blisters are present, the picture is distinctive. When oral ulcers suggest the disease but no blisters have been noticed, gently stroking the weakened epithelium of mucosa or skin can sometimes cause a vesicle or bulla to appear (Nikolsky’s sign). Diagnosis requires biopsy and immunofluorescence findings. Treatment is with systemic steroids, usually prednisolone starting at around 80–100 mg/day, plus azathioprine as a steroid sparing drug. Treatment must continue, reducing the dose after initial response, until all blisters are healed. The First & The Only Franchise in the Iraq 19  B –Mucous membrane pemphigoid Diseases of the pemphigoid group are uncommon chronic autoimmune diseases causing bullae and painful erosions as a result of separation of epithelium from the connective tissue. Aetiology In mucous membrane pemphigoid, the autoantibodies are directed against several basement membrane components(hemidesmosome), mostly against the BP180 antigen or less frequently integrins, laminin and type VII collagen. The antibodies are of IgG class and fix complement. Binding to the basement membrane causes complement activation, attracting and activating neutrophils to degrade the basement membrane. The result is that the epithelium falls off the connective tissue on the slightest trauma The First & The Only Franchise in the Iraq 20  bolus is above > - pemphigous > - if basemerrane ein u The First & The Only Franchise in the Iraq 21  Clinical Features Mucous membrane pemphigoid affects mostly women and has onset between the ages of 50 and 80 years. Blisters develop on the oral mucosa and in the eye(symblepharon), and less frequently in the genital area, pharynx, nose, pharynx and oesophagus. Desquamative gingivitis is a common manifestation and occasionally the only intraoral sign in mild disease. The First & The Only Franchise in the Iraq 22  Histologically, there is loss of attachment and separation of the full thickness of the epithelium from the connective tissue at basement membrane level. The roof of a bulla is formed by intact full thickness epithelium. The First & The Only Franchise in the Iraq 23  Diagnosis and management In addition to the typical presentation, Nikolsky’s sign is typically positive. The diagnosis is confirmed by biopsy and immunofluorescence microscopy Depend on severity of the disease treatments ranges from topical mild,moderate potency corticosteroids, systemic steroid and immunomodulators. The First & The Only Franchise in the Iraq 24  3-Erythema multiforme This mucocutaneous hypersensitivity reaction affects the mouth in many cases and, in patients presenting to dentists, oral lesions may be the only sign. Most patients are aged between 20 and 40 years, with a slight male predominance. Two forms are recognised. In the minor form only skin is involved and this is a relatively mild self-limiting condition. In the major form there are florid lesions on skin and oral, nasal and genital mucosae. There is acute onset, sometimes preceded by vague arthralgia or slight fever for a day in the major form. Then the characteristic ‘target’ lesions appear, initially on arms and legs and spreading centrally Triggers for erythema multiforme Herpes simplex infection, usually a cold sore Genital recurrent herpes Mycoplasmal pneumonia Varicella zoster infections Rarely drugs, penicillins The First & The Only Franchise in the Iraq 25  Erythema multiforme: typical clinical features Adolescents or young adults, particularly males, mainly affected Lips frequently grossly swollen, split, crusted and bleeding Widespread irregular fibrin-covered erosions and erythema in the mouth Conjunctivitis may be associated Cutaneous target lesions or erythematous patches Attacks may recur at intervals of several months Recurrent but usually ultimately self-limiting The First & The Only Franchise in the Iraq 26  Management A short reducing dose of prednisolone starting at around 60 mg/day for 3 days, tapering off over a week, is frequently given but has no good evidence base. Chlorhexidine will prevent secondary mucosal infection and maintain gingival health while tooth brushing is impossible. Eye lesions require specialist treatment. The First & The Only Franchise in the Iraq 27  6-Systemic sclerosis (scleroderma) Systemic sclerosis is an uncommon connective tissue disease characterised by widespread subcutaneous and submucous fibrosis. Although the most obvious feature is the progressive stiffening of the skin, the gastrointestinal tract, lungs, heart and kidneys can also be affected. Clinically, women between the ages of 30 and 50 years are predominantly affected. Raynaud’s phenomenon is the most common early manifestation, often associated with arthralgia. The First & The Only Franchise in the Iraq 34  The head and neck region is involved in more than threequarters of patients and, in a minority, symptoms start there. Narrowing of the eyes and taut, mask-like limitation of movement can give rise to a characteristic appearance (Mona Lisa face). The lips may be constricted (fish mouth) or become pursed with radiating furrows. Occasionally, involvement of the periarticular tissues of the temporomandibular joint together with the microstomia may greatly limit opening of the mouth Involvement of the oral submucosa may cause the tongue to become stiff and narrowed (chicken tongue). Oesophageal stiffness causes dysphagia and allows gastric reflux and teeth erosion. The First & The Only Franchise in the Iraq 35  Clinical features Limitation of opening Limited oral access from microstomia Prominent gingival recession in a minority Coup de sabre linear scars of face and tongue Widening of periodontal ligament radiographically in7% cases Dental erosion from gastric reflux Mandibular resorption at angle and ramus Dry mouth Risk of Sjögren’s syndrome The First & The Only Franchise in the Iraq 36  Histologically, there is great thickening of the subepithelial connective tissue, degeneration of muscle fibres and atrophy of minor glands(including salivary gland leads to hyposalivation). No specific treatment is available. Immunosuppressive drugs are ineffective. Penicillamine may be given to depress fibrous proliferation but can cause loss of taste, oral ulceration, lichenoid reactions and other complication. The First & The Only Franchise in the Iraq 37  Primary herpetic gingivostomatitis Primary infection (systemic infection in a non-immune individual) is caused by Herpes simplex virus, usually type 1(HSV 1). Clinical features The great majority of primary infections are subclinical or completely asymptomatic. Only 1% of those infected develop any symptoms, and these are often minimal. Most patients with clinical infection are children aged younger than 6 years. The First & The Only Franchise in the Iraq 5  Clinical features: In clinical disease, vesicles develop on the oral mucosa approximately 1 week after transmission. The hard palate, gingiva and dorsum of the tongue are favoured sites. The vesicles are dome-shaped, tense and filled with clear fluid and increase from 1 mm in diameter to 2–3 mm. There are usually tens or more than 100 tiny vesicles. Rupture of vesicles after a day or two leaves circular, sharply defined, shallow ulcers with yellowish or greyish floors and red margins. A degree of fever and systemic upset with enlarged cervical lymph nodes. This can be severe, particularly in adults. Oral lesions usually resolve within a week to 10 days The First & The Only Franchise in the Iraq 6 The First & The Only Franchise in the Iraq 7  Pathology: Viral infection of epithelial cell produces intraepithelial vesicles. HSV-infected epithelial cells exhibit acantholysis, and nuclear enlargement (termed ballooning degeneration). The acantholytic cells called Tzanck cells (this term referred to free-floating epithelial cells in any intraepithelial vesicle and is non-specific for herpes). The First & The Only Franchise in the Iraq 8  Diagnosis The clinical picture is usually distinctive (clinical diagnosis). A smear showing virus-damaged cells provides additional diagnostic evidence. Treatment Because the disease is ultimately self-limiting, supportive treatment may be all that is required. Bed rest, soft bland diet, drinking through a straw and paracetamol elixir are effective. Chlorhexidine mouthwash is sometimes used in an attempt to reduce pain by controlling secondary infection of ulcers. It also helps maintain gingival health while tooth brushing is impossible. Treatment with antiviral drugs is highly effective, but only if administered during the first 48 hours or so after vesicles apparent(aciclovir suspension 200 mg /5ml five times daily for five days) The First & The Only Franchise in the Iraq 9  Herpes labialis Herpes labialis is a secondary infection, that is an infection in an immune individual following reactivation of latent virus. Reactivation of latent virus to produce a herpes labialis lesion (‘cold sore’) happens in up to 30% of the population. Triggering factors include the common cold, other febrile infections, exposure to ultraviolet light, menstruation, emotional stress, local trauma, hypothermia, dental treatment and immunosuppression, but often none is identified. The First & The Only Franchise in the Iraq 10  Clinically, changes follow a consistent course with prodromal paraesthesia or burning sensations, then erythema at the site of the attack. Vesicles form after an hour or two, usually in clusters along the mucocutaneous junction of the lips. The vesicles enlarge, coalesce and weep exudate. After 2 or 3 days they rupture and crust over, and finally heal, usually without scarring The First & The Only Franchise in the Iraq 11  Treatment aciclovir, 5% cream, is available without prescription and may be effective if applied before vesicles appear, when premonitory sensations are felt. Penciclovir, on prescription, applied every 2 hours is more effective. These agents must be dabbed and not rubbed onto the lesions to avoid spreading the infectious exudate more widely. If recurrence is intraorally, it’s on hard palate and gingiva. The First & The Only Franchise in the Iraq 12  Herpetic whitlow Both primary and secondary herpetic infections are contagious. Herpetic whitlow is a skin infection in a host after inoculation from another infected site. Children with a primary infection may transfer the infection by finger sucking. Before gloves became routine in dentistry it was an uncommon occupational hazard for dental surgeons and their assistants. The First & The Only Franchise in the Iraq 13  Chicken pox Chicken pox is caused by infection with varicella-zoster virus in a non-immune host, usually a child younger than 12 years. After a 2-week incubation period, there is malaise, nausea, fever, sore throat and the rash appears on the face and trunk producing intensely itchy blisters that break down into ulcers. The oral lesions usually appear before the rash and appear like herpes simplex vesicles except that they tend to occur on the buccal mucosa and palate. Diagnosis is clinical Treatment is mostly supportive, with aciclovir or related drugs if the diagnosis is made early enough. The First & The Only Franchise in the Iraq 14  Herpes zoster of trigeminal nerve The varicella-zoster virus causes chickenpox in the nonimmune, mainly children , while reactivation of the latent virus in nerves causes zoster (shingles), mainly in the elderly. Clinical features Zoster usually affects adults of middle age or older. The first signs are pain and irritation or tenderness in the dermatome supplied by the nerve in which the virus has become latent in. After 2–3 days the pain is felt in the skin and a vesicular rash develops, sharply limited to the dermatome. Facial rash or stomatitis is therefore limited at the midline. The First & The Only Franchise in the Iraq 15 The First & The Only Franchise in the Iraq 16  In its prodromal phase the acute neuralgic pain of trigeminal nerve zoster is a classic mimic of pulpitis, and patients may well present for dental treatment. If no dental cause is evident, this possibility should be considered. This has given rise to the myth that dental extractions can precipitate facial zoster. Pathology The varicella-zoster virus produces epithelial lesions similar to those of herpes simplex The First & The Only Franchise in the Iraq 17  Treatment Mild attacks may require only analgesia and topical soothing cream. Facial infections are usually treated because of the risk of scarring and higher risk of complications. Oral aciclovir, 5 mg/kg, every 8 hours for 5 days is effective. The dose is doubled in the immunocompromised. The drug must be given at the earliest opportunity for maximum effect, ideally within 72 hours, and complemented with analgesics. Addition of prednisolone speeds recovery and reduces the incidence of post- herpetic neuralgia The First & The Only Franchise in the Iraq 18  Ramsay Hunt Syndrome Ramsay Hunt syndrome is reactivated zoster infection in the facial nerve. Virus is latent in the geniculate ganglion, which houses both sensory and motor fibers. On reactivation, patients develop facial paralysis, loss of taste on one side of the anterior tongue and vesicles on the tongue, hard palate and in the external auditory canal. It must be differentiated from Bell’s palsy. Treatment is as for zoster of the trigeminal nerve, but the chances of full recovery are lower than for Bell’s palsy The First & The Only Franchise in the Iraq 19  F The First & The Only Franchise in the Iraq 20