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Oral manifestations of hiv/ aids
- 1. ORAL MANIFESTATIONS OFHIV Presented by Anusha.v MDS
- 2. Contents : • Introduction •Historical review • Virus structure & lifecycle • Routes of transmission • Oral manifestations
- 3. INTRODUCTION • HIV INFECTIONserious disorder affecting immune system • Body’s normal defenses against infection break down • Host is vulnerable to life-threatening infections/ conditions including malignances.
- 4. AIDS most advancedstage of HIV infection • THE PROGRESSION OF HIV TO AIDS IS DEFINED BY CD4 COUNT < 200/Cu.mm OR ABOUT 14% OF CD4- T HELPER CELLS 4
- 5. • AIDS isdefined as a condition indicative of a defect in cell mediated immunity occurring in a person with no known cause for immunodeficiency other than the presence of HIV. • Acquired - not inherited • Immune - attacks the immune system • Deficiency - by destroying certain WBC • Syndrome- a group of symptoms / illnesses that occur as a result of the HIV Infection.
- 6. • Before 1956– patients from Central Africa – reported with strange pneumonia - Gay fever ( GRID) • Extra ordinary out break of Pneumocystis Carinii pneumonia and Kaposi’s Sarcoma in previously fit young men - Los Angeles and NewYork • In 1981, the HIV epidemic has spread beyond gay males, Haitians, and hemophiliacs, and affected many people worldwide. • 1982 – condition began to be referred as AIDS HISTORICAL REVIEW
- 7. • 1st reportof AIDS – by US CDC – in morbidity mortality weekly report • In 1986, the initial cases of AIDS was found in chennai– by Dr. Sunithi solomon
- 8. CDC – 1993- AIDS Definition “The occurrence of one or more group of life- threatening opportunistic infections, malignancies, neurologic diseases and other specific illness in patients with HIV infection or with CD4 counts less than 200/cu mm”
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- 11. PATHOGENESISHIV in blood stream Entrappedin lymphnodes Presence of virus evokes antigenic stimulation Activates CD4 T cells, macrophage TNF ALPHA, IL-6 INCREASED NO OF CD4
- 13. Oral manifestations • Representearliest manifestations • First meeting regarding oral problems – 1986 – European Economic Community in Copenhagen • 1989 - j. pindborg revised • 1989 - WHO collaborative center and EC Clearing house • Revised classification by EC Clearing house - 1992
- 14. Sept 1992 revisedclassification of oral lesions associated with adult HIV INFECTION • GROUP 1 : LESIONS STRONGLY ASSOCIATED WITH HIV INFECTION • CANDIDIASIS : pseudomembranous , erythematous • Oral hairy leukoplakia • Non – hodgkins lymphoma • Kaposi’s sarcoma • Periodontal disease – • linear gingival erythema • Necrotising ulcerative gingivitis • Necrotising ulcerative periodontitis
- 15. • Group 2: lesions less commonly associated with HIV infection • BACTERIAL: M. AVIUM INTERCELLULARE M. TB • MELANOTIC HYPERPIGMENTATION • NECROTISING ULCERATIVE STOMATITIS • SALIVARY GLAND DISEASE – DRY MOUTH UNI/BILATERAL SWELLING OF MAJOR SALIVARY GLANDS • THROMBOCYTOPENIC PURPURA • ULCERATION OTHERWISE NOT SPECIFIED
- 16. • VIRAL : •HSV INFECTION • HPV INDUCED WARTS • CONDYLOMA ACCUMINATUM • FOCAL EPITHELIAL HYPERPLASIA • VERRUCA VULGARIS • VARICELLA ZOSTER VIRUS INFECTION
- 17. • GROUP 3: LESIONS SEEN IN HIV INFECTION BACTERIAL INFECTIONS : • ACTINOMYCES ISRAELLI • E. COLI, KLEBSIELLA PNEUMONIA • CAT SCRATCH DISEASE • EPITHELOID ( BACILLARY) ANGIOMATOSIS DRUG REACTIONS : • ULCERATIVE , • ERYTHEMA MULTIFORME, • LICHENOID, • TOXIC EPIDERMOLYSIS
- 18. FUNGAL ( OTHERTHAN CANDIDIASIS) • CYPTOCOCCUS NEOFORMANS • GEOTRICHUM CANDIDUM • HISTOPLASMA CAPSULATUM • MUCORACEA • ASPERGILLUS FLAVUS NEUROLOGICAL : • FACIAL PALSY • TRIGEMINAL NEURALGIA
- 19. RECURRENT APHTHOUS STOMATITIS VIRALINFECTIONS • CYTOMEGALO VIRUS • MOLLUSCUM CONTAGIOSUM “ Classification & Diagnostic Criteria For Oral Lesions In H.I.V. Infections. EC – Clearing House On Oral Problems Related To H.I.V. Infection & W.H.O. Collaborative Centre On Oral Manifestations Of Immunodeficiency Virus J Oral Pathol Med 1993; 22: 289-91”
- 20. CLASSIFICATION OF OROFACIALLESIONS ASSOCIATED WITH HIV IN PEDIATRIC PATIENTS GROUP 1 – LESIONS COMMONLY ASSOCIATED WITH HIV IN PEDIATRIC PATIENTS • Candidiasis • HSV Infection • Linear gingival erythema • Recurrent aphthous ulcers major /minor /herpetiform
- 21. • GROUP 2– LESIONS LESS COMMONLY ASSOCIATED WITH HIV IN PEDIATRIC PTS • BACTERIAL INFECTIONS OF ORAL TISSUES • PERIODONTAL – NUG , NUP • NUS • SEBORRHEIC DERMATITIS • VIRAL INFECTIONS – CMV , HPV , MOLLUSCUM CONTAGIOSUM , VARICELLA ZOSTER , HERPES ZOSTER , VARICELLA , XEROSTOMIA
- 22. • GROUP 3– LESIONS STRONGLY ASSOCIATED WITH HIV ( RARE IN CHILDREN) • NEOPLASM , KS , NON HODGKIN’S LYMPHOMA OHL , TB RELATED ULCERS • Ramos – Gomez Fj , Flait Zc , Catapanop , Et.Al Classification , Diagnostic Criteria & Treatment Recommendations For Oro Facial Manifestations In Hiv Infected Pediatric Patients. Collaborative Work Group On Oral Manifestations Of Pediatric Hiv Infection. J Clin Pediatric Dent 1999;23:85-96
- 23. GROUP 1 1.ORO PHARYNGEALCANDIDIASIS ( OPC) • One of initial manifestation of HIV • 90% of untreated • 60% - atleast 1 episode per yr with frequent recurrences • Chiefly caused by yeast – c.albicans • Other : c. glabrata, c.dubliniensis • C. tropicalis, c.parapsilosis, c.kruseii • C.novergensis
- 24. • Pseudomembranous :commonest form • characterized by Creamy yellow curd like plaques that can be easily removed with wiping with a cotton gauze or tongue depressor, often leaving a red, raw base. Erythematous Form (atrophic) is characterized by reddish macular lesion . • loss of papillations when involving the tongue dorsum.
- 25. • Angular cheilitisaffects the labial commissures & results in cracking, ulceration & pseudomembrane formation. • Hyperplastic: appear white and hyperplastic • white areas are due to hyperkeratosis • Non scrapable • Confused with hairy leukoplakia.
- 26. • Diagnostic modalities:based on clinical appearance and response to empirical antifungal therapy. • Microscopic Examination : swab - budding yeast cells, pseudohyphae, or filaments • KOH & PAS - improve Visualization of Fungal elements in cytologic specimens. • Culture on Sabouraud dextrose agar medium for 24 to 48 hours
- 27. 2. Oral hairyleukoplakia • 2nd most common hiv associated mucosal lesion • Caused by EBV virus • latently infects 90% of the population worldwide without causing disease. • OHL occurs in pts with CD4+ T cell counts < 400 • Used as a marker of disease activity • affects men more than women
- 28. Clinical features : •Site : lateral borders of tongue, dorsum • Rarely FOM, buccal mucosa • Bilaterally as painless, faint white vertical streaks/ thickened & furrowed areas with shaggy keratotic surface ( hyper keratotic hair like projections) • Vertical striations imparts a corrugated appearance. • Non scrapable lesion • Asymptomatic
- 29. • PROVISIONAL DIAGNOSIS: clinical characteristics • PRESUMPTIVE DIAGNOSIS : HISTOPATHOLOGY • hyperkeratosis & acanthosis leading to corrugations, Koilocytosis, Nuclear beading, chromatin margination • DEFINITIVE DIAGNOSIS : VIRAL DEMONSTRATION • Fluorescent In Situ Hybridisation • IHC, PCR, EM
- 30. 3. KAPOSI SARCOMA •Angiogenic disorder in which multi centric neoplastic proliferation of vascular, spindle cell components occurs in response to circulating growth factors. • Wahman et.al. cofactor model : inf, host, env • Chang et.al., moore et.al. – HHV 8, KSHV • Four types : Classic, • African type • Transplant associated, AIDS related
- 31. AIDS RELATED • seenin 55% homosexual pts • Represents 1st sign of progression of AIDS • Many cutaneous lesions are seen • Oral lesions can occur on any mucosal surface • Mainly on hard palate, maxillary gingiva, • Also – tongue, uvula, tonsils, pharynx • Associated with cervical lymphadenopathy • Salivary gland enlargement
- 32. Multiple Flat, blue/red/purpl e patches Coalesceto form plaques Surface papules / nodules develop Lesion becomes exophytic, ulcerate and bleed Asymptomatic initially • May cause discomfort during speech, eating • on palate, alv . Ridge : resorption - tooth loss • compromise airways Diagnosis : biopsy Patch stage Plaque stage Nodular stage
- 33. NON HODGKINS LYMPHOMA •Second most common neoplasm associated with AIDS • HIV pts are 60 times at risk • Lesions tend to present as large, painful, ulcerated mass on palate, gingival tissues. • Biopsy – for definitive diagnosis
- 34. 4.A. Linear gingivalerythema • As distinctive fiery red band of marginal gingival tissue without ulceration or attachment loss, prone to bleeding • Some times extend beyond the MGJ. • The lesion redness is disproportional to the amount of plaque and persists after removal of plaque • HP : reveals little inflammation • Clinical redness represents vascular reponse with no lymphocytic infiltration.
- 36. 5.B. Necrotising ulcerativegingivitis • Fusospirochaetal infection • Involves primarily free gingiva , crest of gingiva, id papilla • Rarely soft palate, tonsil • Occurs at any age, middle age – common • Stress, immunosuppression, malnutrition, trauma, smoking
- 37. • Painful ,hyperemic gingiva & sharply punched out crater like erosions of id papilla of sudden onset • Ulcerated remanants bleed when touched • Covered by greyish pseudomembrane • Ulcers tend to spread to all margins • Pt c/o inability to eat, fetid odour • Excessive salivation, metallic taste • Systemic manifestations
- 39. 5.C.Necrotising ulcerative periodontitis •characterized by recession and increased attachment loss with shallow probing depths, bleeding, tissue sloughing, loss of id papillae, fetid odor, and moderate pain. • Periods of activity (tissue necrosis and loss) may be followed by • periods of quiescence (healing with no signs of inflammation, but evidence of permanent residual tissue loss)
- 41. • Typical :P. gingivalis, P. intermedia, T.denticola, Actinobacillus actinomycetemcomitans • Atypical bacteria seen in NUP ( HIV PTS) : Bulleidia Extructa, Dialister, fusobacterium, selenomonas, peptostreptococcus, veillonella • Condition may be exacerbated by Candida, herpes like viruses & by an HIV disease–related increased inflammatory cytokine response • Fusobacterium necrophorum plays a major role in progression of NUP to noma.
- 42. • Diagnostic modalities: clinical appearance Measurements of recession, periodontal probing depths, attachment levels, and mobility • Imaging : of areas of NUP involvement may show loss of crestal cortication associated with rapid alveolar bone loss.
- 43. GROUP II A) Mycobacterialinfections • MAC, M.TB • Approx 1/3rd of AIDS-related deaths worldwide are due to TB • increased reactivation of latent TB infections as well as higher primary rates of TB • Pulmonary TB is the most common • Extrapulmonary disease affecting the liver, spleen,or kidney may occur in patients with CD4 < 100 cells/mm3
- 44. ORAL MANIFESTATIONS : •Primary TB : gingiva, tooth extraction sockets, buccal folds • Sec. TB : tongue, palate, lips, alveolar mucosa & jaw bones • present as ulcers or nodules, vesicles, fissures,, plaques, granulomas and verrucous proliferations. • single or multiple, painful or painless
- 45. • Ulcer –irregular, ragged, undermined edges, minimal induration , with yellowish granular base • Tongue : lateral border, ant. Dorsum, base of tongue • Painful, grayish-yellow, firm well demarcated • Palate : Small granulomas or ulcerations • Lips : shallow granulating ulcers • TB OSTEOMYELITIS • TB SIALADENITIS
- 47. B) MELANOTIC HYPERPIGMENTATION •HIV pts hyperpigmentation of oral mucosa , skin, nails occurs suddenly Due to • Direct result of HIV infection • Adrenocortical destruction due to several infections associated with hiv • Medication intake : ketoconazole, zidovudine
- 48. C) NECROTISING ULCERATIVESTOMATITIS • NUG, NUP, NUS – different clinical stages of same disease ( robinson et.al) • Collectively – necrotising gingivostomatitis • NUS is an outcome of NUG/P progressing beyond mucogingival demarcation • Sometimes arise on mucosa seperately • NUS involves mainly soft tissues, may extend into underlying bone causing massive tissue destruction. • If NUS extends from oral mucosa to involve facial skin, it will result in noma
- 49. Hiv infects lc cells Depletion of lccells Decreased local immune response Increased susceptibility to infections NPD, NUS STIMULATES CYTOTOXIC T- CELL RESPONSE PATHOGENESIS
- 50. D)UNI/BILATERAL SWELLING OFMAJOR SALIVARY GLANDS • HIV-associated lymphoepithelial lesions which are known as hiv associated salivary gland lesions ( HIV SGD) • Hyperplastic reactive lymphadenopathy, • Benign lymphoepithelial cysts, • Malignant : lymphoma, ks • benign neoplasms • Bacterial , mycobacterial , and viral infections
- 51. • Diffuse InfiltrativeLymphocytosis Syndrome (Dils) • In 3% of hiv pts multiple lymphoepithelial cysts proliferate in parotid gland • Painful enlargement of gland • Lesion involves entire parotid parenchyma, so presents as localised mass • Not moveable, Tender on palpation • Tense , due fluid accumulation in multiple cysts • Reduced salivary gland function : xerostomia, sicca symptoms
- 52. • In HIV+ve, CT scan showing multiple hypodense areas is suggestive of DILS . Histopathology : • Characterized by persistent infiltration of CD8 cells that have the ability to destroy HIV-infected cells • lymphocytic infiltration involving the salivary glands (~ to Sjogren syndrome) • Differentiation : DILS also involves lungs, kidney, git • Sj autoab’s will be absent in pts with DILS
- 53. • Fine-needle aspiratescan be useful in differential diagnosis of salivary gland masses • Confirmatory - histopathologic diagnosis • If ct shows a defined mass, then superficial parotidectomy • If no defined mass is seen in ct then incisional biopsy • Immunohistochemical analysis from a biopsy are essential to determine the nature of the salivary gland enlargement.
- 54. E) THROMBOCYTOPENIC PURPURA •HIV related immune thrombocytopenic purpura • Immune mediated destruction • Circulating immune complexes are non specifically deposited on platelet membrane, resulting in reticuloendothelial clearance. • Us studies , HIV directly infects megakaryocytes , leading to impaired production
- 55. • Thrombotic thrombocytopenicpurpura is also seen in HIV pts. • Other causes of thrombocytopenia in HIV : • Infections / neoplastic conditions involving bone marrow • Any medication causing myelosuppression
- 56. F) ULCERATIONS NOTOTHERWISE SPECIFIED • single or multiple, well-circumscribed, extremely painful • often with a pseudomembrane, > 0.5 cm to 2/ 3 cm • may have a recurrent pattern/ not • may last for several weeks, healing with scarring. • Typically found on nonkeratinized epithelial mucosa
- 57. • In immune-suppressedpatients ulcers are deeper and devoid of the classic erythematous halo at ulcer margin • Biopsy should be obtained for lesions lasting > 3 weeks
- 58. G) VIRAL 1)HSV :In HIV pts presents • as an erythematous pruritus that develops into painful vesicles and ulcerates over a brief period, accompanied by painful regional lymphadenopathy. • HSV infection may involve all oral mucosa • Both keratinised & non keratinised • can be more prolonged and severe than in HIV-ve
- 59. 2) HUMAN PAPILLOMAVIRUS • 120 strains , 25 – oral lesions • Epitheliotrophic, it contains epithelial growth factors • Induce distinct squamous cell proliferation • VERRUCA VULGARIS – CUTANEOUS HPV 2, 57 • CONDYLOMA ACCUMINATA – HPV 6 & 11 • FOCAL EPITHELIAL HYPERPLASIA – HPV 13 & 32
- 60. • VERRUCA VULGARIS( COMMON WART) • cutaneous lesion, less common on mucos memb • Numerous finger like projections • Resulting in lesion with rough, verrucous, cauliflower like surface • Well circumscribed, pendculated/sessile • Contagious, capable of spreading to other parts
- 61. • CONDYLOMA ACCUMINATUM( veneral wart) • Soft, pink nodules which proliferate & coalesce rapidly to form diffuse papillomatous clusters of varying size • Occurs on moist, intertriginous areas • Seen on tongue, commissures • Also present on other mucosal surfaces
- 62. • FOCAL EPITHELIALHYPERPLASIA • Most contagious oral papillary lesion • Well circumscribed numerous soft, flat,sessile, non papillomatous papules are distributed throughout oral mucosa • Site : labial, buccal, lingual mucosa, Gingiva, tonsil • Differs from other HPV infections : extreme acanthosis, hyperplasia, but minimal production of surface projections • Mucosa is 8-10 times thicker than normal.
- 63. 3) VARICELLA ZOSTER: •Acute ubiquitous extremely contagious disease occuring in children, young adults • Maculopapular rash, vesicular eruptions which begins on trunk, spreads centrifugally ( face & extremities) • Occurs in successive crops. • Skin lesions rupture , form superficial crusting , heals by desquamation • Can occur anywhere on oral mucosa • Vesicles rupture to form eroded ulcers with red margins.
- 64. • HERPES ZOSTER •In HIV latent VZV is reactivated by Immunocompromised state • Lymphomas like Hodgkins , T Cell Leukemia • Prodrome : Deep aching / burning pain • Dermatomatic/ zosteriform distribution of vesicles • Unilateral, clustered distribution of vesicles, ulcers • Thoracic > lumbar> craniofacial areas • V1 is most commonly involved
- 65. • Post herpeticneuralgia : • Pain that persists for 30/120 days after onset of rash. • Occurs at any age • More common in elderly pts • Cli. Features: persistent pain, hyperesthesia, parasthesia, allodynia for months or yrs after zoster lesions have healed.
- 66. Diagnostic modalities : •History, clinical examination • h/p : tzanck cells ( multinucleated giant cells) • Fluorescent antibody staining • Culture, serology
- 67. Group : 3 lesionsseen in HIV
- 68. ACTINOMYCOSIS • Actinomyces –filamentous bacteria • living as commensal organisms in the human oral cavity and respiratory and digestive tracts • Becoming invasive when, through a mucosal lesion, they gain access to the subcutaneous tissue. • Infection is always endogenous. Doesnot occur by person to person contact.
- 69. • Presents asa chronic, fluctuant mass • Located at the border of the mandible • Pain is rare, slight fever • Initially, the mass may be surrounded by induration or erythema; later, it may become tender to palpation, on account of a central necrosis process • Becoming progressively larger within weeks or months
- 70. • Mass breaksdown and abscess, sinuses are formed • Discharging pus contain typical yellow sulphur granules • Skin overlying abscess is purplish,red indurated has appearance of wood. • Infection may extend into adjoining soft tissue as well as bone • Leads actinomycotic osteomyelitis
- 72. Epitheloid (bacillary) angiomatosis •Vascular proliferation that ~ ks • First described in 1983 in HIV pts • Occurs when CD4 count < 100/cumm • Rarely seen in immunocompetent pts • Mucocutaneous disorder • Lesions – vascular papules that grow to form nodules • Diagnosis : hp • Which demonstrate presence of causative bacteria
- 73. Drug reactions • Ulcerative •Erythema multiforme • Lichenoid reactions • Toxic epidermolysis
- 74. 4)Fungal other thancandidiasis • cryptococcus neoformans • Geotrichum • Histoplasma • Mucoracea • Aspergillus flavus
- 75. Cryptococcosis: • Cryptococcus neoformans •Meningoencephalitis • Symptoms include headache, nausea, irritability, and diminished cognitive function • physical findings include cranial nerve palsies, hyperreflexia, and papilledema. • Rarely, intraoral ulcerations may occur in mucosal tissues with dissemination of cryptococcosis
- 76. • Histoplasmosis • Primaryinfection – self limiting pulmonary infection. • Heals with fibrosis, calcification • In HIV PTS progressive disseminated form • Predilection for RE SYSTEM • Involves liver, spleen, lymphnodes, bone marrow • Oral histoplasmosis in HIV occurs alone/ as a part of disseminated infection.
- 77. • Oral :nodular / ulcerative/ vegetative lesions • Ulcerated areas covered by pseudomembrane • Indurated margins • Dissemination of histoplasmosis to the oral mucosa may occur primarily on the gingival, tongue, palate, and buccal mucosa. • Gingival lesions will appear as diffuse granulomatous inflammation with progressive alveolar bone erosion and loosening of teeth
- 78. ASPERGILLOSIS • Aspergillus sporeis found in decaying vegetation and in the immunocompromised host may cause acute invasive pulmonary aspergillosis. • Aspergillus species have also been isolated from the air and environmental surfaces of hospital settings • Hospitalized immunosuppressed individuals may be at increased risk.
- 79. • Invade bloodvessels causing thrombosis and infarction of the perivascular tissues. • Less commonly Aspergillus invades the sinuses and can progress through the underlying soft tissue and bone to cause palatal and oral lesions, typically described as black or yellow necrotic lesions of the soft tissue
- 80. Recurrent aphthous stomatitis •Most commonly reported type of ulcers in HIV +ve pts • Etiology remains undetermined • Ulcers appear clinically as painful, round-to-oval, yellow or white, & are surrounded by a halo of erythema. • HIV-positive patients usually experience increased frequency and severity of typical minor aphthous ulcers
- 82. CYTO MEGALO VIRUS: • May cause oral ulceration in HIV-positive pts with • disseminated cytomegalovirus (CMV) disease • Ulcers may occur anywhere in the oral cavity • Resemble MAU in size. • Instead of an erythematous margin, CMV ulcers appear necrotic with a white halo. • Deep tissue biopsy with biopsy punch or scalpel is used to confirm diagnosis • .
- 83. • large intracellularinclusion bodies are characteristic of infection. • Patients may develop CMV retinitis, esophagitis, colitis, pneumonitis, and neurological disease
- 84. Molluscum contagiosum • Infectionof skin caused by pox virus • Shiny, white, skin coloured dome shaped papules that often demonstrate a central depressed crater. • In pts with AIDS numerous lesions may be present • No tendency to undergo spontaneous resolution • Hp : large intracytoplasmic inclusions are seen • Molluscum bodies
- 86. CONCLUSION • Dentists playan important role in managing the oral health of patients with HIV disease • Knowledge of HIV oral lesion clinical appearance, lesion symptoms and behavior, various treatment approaches, and anticipated response to treatment are important for oral disease control and oral health maintenance
- 87. REFERENCES • Lauren LPatton, Oral Lesions Associated With Human Immunodeficiency Virus Disease. Dent Clin N Am 57 (2013) 673- 698 • Nicholas G Mosca, Alicia Rose Hathorn , HIV Positive Patients : Dental Managent Considerations. Dent Clin N Am 50 (2006) 635-657 • Charles E Barr, Michael Glick , Diagnosis And Management Of Oral & Cutaneous Lesions In HIV -1 Disease. Dent Clin N Am 10 (1998)25-45
- 88. • Burkets OralMedicine , 11th Edition, Bc Decker Inc Hamilton 2008 • Robert E Marx, Diane Stern Oral And Maxillofacial Pathology: A Rationale For diagnosis & Treatment. 1st edition, Quintessence.2003 • R Rajendran B Sivapathasundharam Shafer’s Textbook Of Oral Pathology. 5th Edition, Elsevier, 2008
- 89. HIV does notmake people dangerous to know, so you can shake their hands and give them a hug: Heaven knows they need it !!
Editor's Notes
- #4 AIDS CAUSED BY HIV….
- #14 European – listed out 3o lesions
- #24 Mc occurs in 3 forms in hiv : opc, vv, eso….candida are normal inhabitants…1/3rd in normal, 2/3rd in aids
- #27 Only apparent azole refractory strains warrant antifungal sensitivity testing.
- #28 1985 – greenspan……type of human herpes virus
- #29 Asymp….becomes symp when super infected with candida.
- #31 1872…..ARE, MIHSK
- #33 Dd : ecchymosis, vascular lesions, low grade mucoepidermoid ca
- #37 Vincents, trench mouth…in 1999 am ac of perio reclass nug nup as necrotising perio disease….
- #46 OSTEO : difficulty in eating, trismus, paraesthesia of lower lip, lymphadenopathy , Loosening of teeth
- #53 44-fold increased risk of developing lymphoma
- #60 SQ PAPILLOMA- 6, 11