Periodontal management of HIV patients


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AIDS is a lethal viral infection caused by human immunodeficiency virus (HIV) and is characterized by severe depletion of T4 lymphocytes with associated opportunistic infections.
Oral and perioral lesions are common in patients infected with human immune deficiency virus (HIV), are often the presenting feature, and may predict deterioration in general health and a poor prognosis.
Due to multiple oral conditions and periodontal involvement, periodontists are in a unique position to recognize possible HIV infection in its early stage and to be involved in the oral care of these patients.

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  • C. tropicalis,
    C. glabrata
    C. krusei
  • Extemporaneous- without special preparation. – sucrose free
    Pastilles- pills made of thick liquid that is solidified - troch – lozenges .
  • Periodontal management of HIV patients

    2. 2. Contents 1. Introduction 2. Origin of aids 3. HIV- AIDS in India 4. Structure of HIV 5. Modes of transmission 6. Natural history of HIV infection 7. Stages of HIV infection 2 8. CDC surveillance case classification 9. Classification of the most common oral manifestations of aids 1. Lesions strongly associated 2. Lesions less commonly associated 3. Lesion less seen in HIV. 10. PERIODONTAL TREATMENT PROTOCOL 11. Treatment complications 12. Post exposure prophylaxis (PEP)
    3. 3. INTRODUCTION AIDS is a lethal viral infection caused by human immunodeficiency virus (HIV) and is characterized by severe depletion of T4 lymphocytes with associated opportunistic infections. Oral and perioral lesions are common in patients infected with human immune deficiency virus (HIV), are often the presenting feature, and may predict deterioration in general health and a poor prognosis. 3
    4. 4. • Most HIV-infected patients have head and neck manifestations at some stage of disease and oral lesions are often early signs. (Schiodt & Pendborg 1989, Winkler & Robertson 1992) • Due to multiple oral conditions and periodontal involvement, periodontists are in a unique position to recognize possible HIV infection in its early stage and to be involved in the oral care of these patients. 4
    5. 5. ORIGIN OF AIDS Studies comparing the genetics of HIV with various African monkey viruses has provided some evidence. HIV-1 & -2 are not closely related to each other as they are to simian immunodeficiency virus (SIV).
    6. 6. 6 HIV 1 •HIV-1 is more common worldwide •HIV-1 is more pathogenic •MTCT is relatively common with HIV-1 HIV 2 •HIV-2 is found in West Africa, Mozambique, and Angola. •HIV-2 is less pathogenic •Duration of HIV-2 infection is shorter •MTCT is relatively rare with HIV-2
    7. 7. History • The first well-documented case of AIDS occurred in an African man in 1959. Samples of his blood yielded genetic material from an early version of HIV. • It probably remained in small isolated villages, causing sporadic cases and mutating into more virulent strains that were readily transmitted from human to human. • AIDS was first recognized in 1981 in USA. 7
    8. 8. • The causative virus was isolated in 1983 from blood lymphocytes and was called Lymphadenopathy Associated Virus (LAV). • 1984 - Human T-cell Lymphotropic Virus –III (HTLV-III). • The International Committee on virus nomenclature in 1986, decided on the generic name Human Immunodeficiency Virus (HIV). 8
    9. 9. HIV- AIDS in INDIA • India’s first cases of HIV were diagnosed in Chennai in 1986. • It is estimated that around 2.5 million people(61% male, 39% female, 3.5% children) are currently living with HIV. • High Prevalence States: Tamil Nadu, Maharashtra, Karnataka, Andhra Pradesh, Manipur and Nagaland 9
    12. 12. STAGES OF HIV INFECTION 1. ACUTE HIV SYNDROME First stage seroconversion Virus rapidly spreads to organs, especially the lymphoid tissues HIV virus not very aggressive in causing diseases or severe symptoms 2. ASYMPTOMATIC STATE Infection is latent , No signs of HIV, immune system controls virus production Virus starts to grow and multiply in the lymph nodes 12
    13. 13. 3. SYMPTOMATIC DISEASE/AIDS Viremia (spread of virus in the blood) Physical signs of HIV infection Loss of immune system, mainly due to infection of CD4 T- Lymphocytes 4. END STAGE DISEASE Immune system collapses Virus continues to slowly destroy the Immune System for up to 10 years Usually an opportunistic infection is the cause of death 13
    14. 14. 14
    15. 15. CDC SURVEILLANCE CASE CLASSIFICATION Category A : includes patients with acute symptoms or asymptomatic diseases, along with individuals with persistent generalised lymphadenopathy, with or without malaise , fatigue , or low grade fever. Category B : patients have symptomatic conditions such as :  Oropharyngeal or vulvo-vaginal candidiasis  Herpes zoster  Oral hairy leukoplakia  Idiopathic thrombocytopenia  Constitutional symptoms of fever, diarrhoea and weight loss
    16. 16. • Category C : patients are those with outright AIDS , as manifested by life- threatening conditions or identified through CD4+ T lymphocyte levels of less than 200 cells /mm3 (< 14% of total lymphocytes) 16
    17. 17. Classification of the Most Common Oral Manifestations of AIDS Pindborg in 1989 • The first classification of the oral manifestations associated with HIV-infection- based on etiological aspects and distinguished between lesions caused by fungi, bacteria, viruses, neo- plastic lesions. 17
    18. 18. EEC-Clearinghouse on oral problems related to HIV-infection and WHO collaborating center on oral manifestations of the human immunodeficiency virus. In 1990, the classification was modified to establish three main groups: 1. Lesions strongly associated with HIV-infection 2. Lesions less commonly associated with HIV-infection, and 3. Lesions seen in HIV-infection 18
    19. 19. Lesions strongly associated with HIV/ AIDS • Oral candidiasis • Oral hairy leukoplakia • Kaposi’s sarcoma • Non-Hodgkin’s lymphoma • Periodontal diseases -  Linear Gingival Erythema  Necrotizing Ulcerative Gingivitis  Necrotizing Ulcerative Periodontitis 19
    20. 20. Lesions less commonly associated • Bacterial infections- • Mycobacterium tuberculosis • Mycobacterium aviumintracellularae • Melanotic hyperpigmentation • Necrotizing ulcerative stomatitis • Salivary gland diseases- xerostomia 20 • Thrombocytopenic purpura • Ulceration (not otherwise specified) • Viral infections – • Herpes simplex virus • Human papilloma virus • Condyloma accuminatum • Multifocal epithelial hyperplasia
    21. 21. Lesions seen in HIV infection Bacterial infections: • Actinomyces israelii • Escherichia coli • Klebsiella pneumonia • Cat-scratch disease Drug reactions, • erythema multiforme, • lichenoid, • Toxic epidermolysis Epitheliod (bacillary)angiomatosis 21 Fungal infection other than candidiasis • Cryptococcus neoformans • Geotrichum candidum • Histoplasma capsulatum • Mucoraceae (mucomycosis zygomycosis) • Aspergilus flavus Neurological disturbances • Facial palsy • Trigeminal neuralgia
    23. 23. ORAL CANDIDIASIS • Most oral candidal infections are associated with candida albicans • Candidiasis is the most common oral lesion in HIV diseases and found in 90% AIDS patients It has 4 clinical presentations : 1. pseudomembraneous candidiasis 2. erythematous candidiasis 3. hyperplastic candiasis 4. angular cheilitis
    24. 24. Pseudomembraneous candidiasis Oral Thrush Multiple superficial, creamy white plaques that can be easily wiped off revealing erythematous base. Yellow white curd-like lesion Common on hard and soft palate, buccal and labial mucosa and dorsal surface of tongue
    25. 25. • Erythematous candidiasis Appears as red patches Seen on tongue or palatal mucosa Associated with depapillation of the tongue
    26. 26. • Hyperplastic candidiasis  Least common form  Lesions appear white and cannot be removed by scrapping.  Seen in buccal mucosa and tongue  More resistant to removal than other types
    27. 27. • Angular cheilitis  Seen on commissures of lips  Appear as erythematous with surface crusting and fissuring
    28. 28. 1. Early oral lesions are usually responsive to topical antifungal therapy. 2. More advanced lesions, including hyperplastic candidiasis may require systemic antifungal drugs. 3. Most oral topical antifungal agents contain large quantities of sucrose, which may be cariogenic after long-term use. MANAGEMENT
    29. 29. Topical drugs • CLOTRIMAZOLE (candid® ) 10mg tablets: dissolve in mouth 3-5tablets daily for 7-14days • NYSTATIN ( mycostatin® , nystec ® ) a) Oral suspension - (100,000 U/ml : Disp 240ml) Rinse with 1tsp qid. b) Oral suspension- (extemporaneous) mix 1/8tsp with 4 oz water c) Tablets(500,000U)- Dissolve 1tablet in mouth 4-5times daily. d) Pastilles (200,000U)- dissolve 1-2 pastilles in mouth,4-5times daily. e) Ointment 15g tube- Apply to affected area 3-4times daily 29
    30. 30. 30 CLOTRIMAZOLE ( candid) ointment 15g tube: apply to affected area qid. MICONAZOLE (oravig)2% ointment 15g tube: qid application. ITRACONAZOLE ( icoz , sporonox) oral suspension 100-200mg once daily for 7-28 days. FLUCONAZOLE oral suspension 200mg of 1st day followed by 100mg once daily for atleast 2weeks. (3mg/kg) AMPHOTERICIN B oral suspension 100mg four times daily for 2 weeks.
    31. 31. Systemic drugs • Ketoconazole (hyphoral) 200mg tablets: 2 tablets immediately, then 1-2 tablets daily for 5- 14days. • Fluconazole (Diflucan) 100mg tablets: 2 tablets immediately, then 1 tablet daily for 7-14 days. ( conflu) • Itraconazole (Sporanox) 100mg capsules: 200mg once daily with meals for 4 weeks. 31
    32. 32. ORAL HAIRY LEUKOPLAKIA • Oral hairy leukoplakia most commonly presents as a white ragged, corrugated or irregular lesion with a hair like appearance involving the lateral and dorsolateral tongue. • Lesions may be unilateral or bilateral. • Hairy leukoplakia is caused by infection of the lesion epithelial cells with Epstein-Barr virus (EBV) and is associated with immune deterioration. 32
    33. 33. MANAGEMENT • Oral hairy leukoplakia generally does not require treatment. • Resolution has been reported after therapy with acyclovir, zidovudine, podophyllin and interferon, but usually recurs when treatment is discontinued. • In cosmetically objectionable patients, lesions can be removed with laser or conventional surgery. • The incidence of OHL has been markedly reduced since the advent of multidrug antiviral therapy for HIV infection. 33
    34. 34. KAPOSI’S SARCOMA • Kaposi’s sarcoma is a rare, multifocal vascular neoplasm which is the most common malignant tumor associated with HIV infection. • Herpes virus (HHV-8) • This is an aggressive lesions and involves most frequently the palate 95% and the gingiva 23% • Kaposi’s sarcoma oral lesions may interfere with function, be cosmetically objectionable, and proliferate uncontrollably. 34
    35. 35. • Early lesions are painless, and appear as reddish purple macules of the mucosa. • As lesions progresses it becomes nodular, papular or non-elevated macules, brown or purple in colour. • May ulcerate and become painful with difficulty in eating and speech and may cause cosmetic problems . 35
    36. 36. Management • Treatment of oral KS may include use of • Antiretroviral agents • Laser excision • Radiation therapy • Nichols et al in 1993 described the successful use of intra-lesional injection of vinblastine at a dosage of 0.1 mg/cm sq. 36
    37. 37. • Intra-lesional injections with sodium tetradecyl sulfate (a sclerosing solution) also have been effective. • In case of destructive periodontitis in conjunction with gingival KS, scaling and root planing and other periodontal therapy may be indicated along with intra-lesional or systemic chemotherapy. 37
    38. 38. NON-HODGKIN’S LYMPHOMA • Second most common neoplasm • Lesion are large, painful, ulcerated mass. • Occurrence is more common in the gingiva. • Has characteristic white verrucous surface or necrosis of the gingiva resembling ANUG. 38
    39. 39. MANAGEMENT • Surgical excision • Anti- cancer drugs • Radiation therapy 39
    40. 40. HIV RELATED PERIODONTAL DISEASES • The first report linking periodontal disease and HIV infection was published in 1985 (Dennison et al) • Classification on HIV related periodontal disease of the EC Clearing house on oral problems related to HIV infection 1993. • Linear gingival erythema. • Necrotizing ulcerative gingivitis. • Necrotizing ulcerative periodontitis • Necrotizing ulcerative stomatitis 40
    41. 41. Linear Gingival Erythema • Characterized by a marginal band of intense erythema with more apical focal and/or diffuse areas of erythema that may extend beyond the mucogingival line and is associated with earlier stages of HIV infection and CD4+ suppression. • No ulceration • pocketing or attachment loss and strongly resistant to local treatment The lesion may be- localised generalized • The microflora of LGE may closely mimic that of periodontitis rather than gingivitis (Clark et al, 1991) 41
    42. 42. MANAGEMENT • LGE is often refractory to treatment but lesions may undergo spontaneous remission. • The success of treatment relies on identifying the important causative factors like plaque, tobacco or substance usage, association with candidal infection or presence of a number of periopathogenic bacteria consistent with those seen in conventional periodontitis • Scaling, CHX mouthwash and proper home care. 42
    43. 43. • Step I: Instruct the patient in performance of meticulous oral hygiene • Step II: Scale and polish affected areas, and perform subgingival irrigation with chlorhexidine. • Step III: Prescribe chlorhexidine gluconate mouthrinse for 2 weeks • Step IV: Reevaluate in 2-3 weeks. If lesions persist evaluate for possible candidiasis. Consider empiric administration of a systemic antifungal agent such as fluconazole for 7-10 days • Step V: Re-treat if necessary and place the patient on 2-3 month recall. 43
    44. 44. NECROTIZING ULCERATIVE GINGIVITIS • NUG has been associated with HIV infection. • NUG is characteristic of red and swollen gingiva with yellowish – grey marginal areas of necrosis leading to destruction of inter-dental papillae usually takes a chronic or sub acute course. • Spontaneous hemorrhage and characteristic fetor accompanied by severe pain. • NUG rapidly progresses and becomes NUP. 44
    45. 45. Management • Basis treatment consists of cleaning and debridement of affected areas with a cotton pellet soaked in peroxide after application of topical anesthetic • The patient should be seen daily or every other day for the first week; debridement of affected areas is repeated at each visit and plaque control methods are gradually introduced. • A meticulous plaque control program should be taught and started as soon as the sensitivity of the area allows it. 45
    46. 46. • Patient should refrain from tobacco, alcohol and condiments • An antimicrobial mouthrinse such as chlorhexidine gluconate 0.12% should be prescribed • Systemic antibiotics such as metronidazole or amoxicillin may be prescribed for patients with moderate to severe tissue destruction, localized lymphadenopathy or systemic symptoms or both. The use of prophylactic antifungal medication should be considered if antibiotics are prescribed. • The periodontium should be re-evaluated 1 month after resolution of acute symptoms to assess the results of treatment and determine the need for further therapy. 46
    47. 47. NECROTIZING ULCERATIVE PERIODONTITIS • NUP is necrotizing, ulcerative, rapidly progressive form of periodontitis which occurs in HIV Positive individuals • NUP may represent an extension of NUG in which bone loss and periodontal attachment loss occurs. • NUP is characterized by soft tissue necrosis, rapid periodontal destruction and interproximal bone loss. Lesions may be localized or generalized and may be present after marked CD4+ cell depletion. 47
    48. 48. • Bone is often exposed resulting in necrosis and subsequent sequestration. • On treatment, patients undergo spontaneous resolution of the necrotizing lesions, leaving painless, deep interproximal craters that are difficult to clean and may lead to conventional periodontitis (Glick et al, 2000). • Data implicate a similar microbial component in both NUP and chronic periodontitis (Glick et al 1994, Murray et al 1991). • They found NUP in only 6.3% and concluded that NUP is a predictive marker for severe immune deficiency because patients with NUP were 20.8 times as likely to have CD4+ lymphocyte counts <200/mm3 48
    49. 49. MANAGEMENT • Gradual, gentle, local debridement of affected area. • Scaling and root planing with oral hygiene instruction • In office irrigation with an effective antimicrobial agent such as chlorhexidine gluconate or povidine iodine. • Chlorhexidine gluconate 0.12% - 0. 2% mouth rinse twice daily. • Metronidazole, 500 mg loading dose and 250 mg four times daily until ulcers are healed, alternatively penicillin or tetracycline. • Prophylactic topical or systemic antifungal agent and follow up visit within next 3 days. 49
    50. 50. NECROTISING ULCERATIVE STOMATITIS • NUS maybe severely destructive and acutely painful. • It is characterized by necrosis of significant areas of oral soft tissue and underlying bone. • It may occur separately or as an extension of NUP and is commonly associated with severe depression of CD4+ immune cells and an increased viral load (GRASSI et al 1988) 50
    51. 51. Management • Metronidazole • Antimicrobial mouth rinse • If osseous necrosis is present, its necessary to remove the affected bone to promote wound healing 51
    52. 52. ORAL HYPERPIGMENTATION • An increased incidence of oral hyperpigmentation has been described in HIV-infected individuals. • Pigmented areas often appear as spots or striations in the buccal mucosa, soft palate and the gingiva or tongue. • The pigmentation may relate to prolonged use of drugs such as zidovudine, ketoconazole or clofazimine. • Zidovudine is also associated with excessive pigmentation of the skin and nails. 52
    53. 53. Oral pigmentation may be caused by, • Adrenocorticoid insufficiency caused by prolonged use of ketoconazole • Pneumocystitis carinii infection • Cytomegalovirus infection 53
    54. 54. ATYPICAL ULCERS • HIV-infected patients have a higher incidence of recurrent herpetic lesion and aphthous stomatitis • Atypical large , persistent , non specific, painful ulcers • Caused by- • herpes simplex virus (HSV) • varicella-zoster virus (VZV) • epstein-barr virus (EBV) • cytomegalovirus (CMV) 54
    55. 55. Herpes labialis • Seen as vesicles on lip and adjacent facial skin which break down to produce shallow ulcers. • HIV infected individuals responsive to topical antiviral therapy • Acyclovir , pencyclovir , doconasol • Reduces healing time of lesion Recurrent aphthous stomatitis • Sites : oropharynx, oesophagus, or other areas of GIT. • Treatment:- Topical or intralesional corticosteroids, chlorhexidine, antimicrobial mouth rinses, oral tetracycline rinses 55
    56. 56. 56
    57. 57. • Topical corticosteroid therapy (fluocinonide gel applied three to six times daily) is safe and efficacious for treatment of recurrent aphthous ulcer or other mucosal lesions in immunocompromised individuals. • Prophylactic antifungal medications should be prescribed • Large aphthae in HIV+ve individuals may be treated with systemic corticosteriods - prednisone 40 to 60 mg daily 57
    58. 58. Xerostomia • Xerostomia may be associated with HIV disease and may be a complication of prescribed medication that may be xerostomic. • The disease is characterized by diffuse enlargement of the major salivary glands and/ or xerostomia. CMV has been demonstrated in the salivary gland of xerostomic patients (Greenspan et al. 1992). • Identification of the dry mouth and reduced saliva production can also lead to further investigation and diagnosis and requires management in order to control the conditions associated with a dry mouth including increased risk of candidiasis and caries risk. In addition, management of xerostomia will improve oral comfort, may affect the quality of speech, and affect the use of any prosthesis. 58
    59. 59. Treatment • Salivary stimulants – sugar free gums • Systemic sialogouges pilocarpin 5 mg - 3 times daily • Flouride rinses- decay 59
    60. 60. BACILLARY (EPITHELIOD) ANGIOMATOSIS (BA) • BA is an infectious vascular proliferative disease with clinical and histologic features very similar to those of kaposi’s sarcoma. • Caused by Rickettsia like organism - Bartonellaciae henselia, quintana, or others. • Gingival manifestations are red purple or blue edematous soft tissue lesions that cause destruction of the periodontal ligament and bone. • Histological picture Epitheloid proliferation of angiogenic cells Acute inflammatory cell infiltrate. 60
    61. 61. TREATMENT • Broad-spectrum antibiotics such as erythromycin or doxycycline in conjunction with conservative periodontal therapy and possibly excision of the lesion. 61
    63. 63. HEALTH STATUS 1. Should be determined from the health history, physical evaluation and consultation with the patient’s physician. 2. Treatment decisions will vary depending on the patient’s state of health 3. Information should be obtained regarding- • CD4+ T4 lymphocyte level • current viral load • difference from previous counts and load • H/o of drug abuse, multiple infections • present medications 63
    64. 64. Viral load 64 Severity of illness is determined by amount of virus in the body (increasing viral load) and the degree of immune suppression (decreasing CD4+ counts) Higher the viral load, the sooner immune suppression occurs
    65. 65. INFECTION CONTROL MEASURES 1. Control measures should be based on American Dental Association (ADA) and the Center for Disease Control and Prevention (CDC) or the Organization for Safety and Asepsis Procedure (OSAP). 2. A number of pathogenic microorganisms may be transmitted in the dental setting and these include: • Airborne pathogens - tuberculosis • Blood borne pathogens -HIV, HBV, HCV • Waterborne pathogens Legionella and Pseudomonas species • Mucosal/ skin borne pathogens VZV or HSV 65
    66. 66. GOALS OF THERAPY • Primary goals should be restoration and maintenance of oral health, comfort and function. • Treatment should be directed toward control of HIV-associated mucosal diseases such as chronic candidiasis and recurrent oral ulcerations • Effective oral hygiene maintenance • Conservative, nonsurgical periodontal therapy should be a treatment option for virtually all HIV + patients • NUP & NUS can be severely destructive to periodontal structures and should be treated appropriately. 66
    67. 67. SUPPORTIVE PERIODONTAL THERAPY • Patient should be encouraged to maintain meticulous personal oral hygiene. • Recall visits should be conducted at short intervals (2 to 3 months) • Systemic antibiotic therapy should be administered with caution • Blood and other medical laboratory tests may be required to monitor the patients overall health status and consultation and co-ordination with the patient’s physician are necessary 67
    68. 68. PSYCHOLOGIC FACTORS • HIV infection of neuronal cells may affect brain function and lead to outright dementia. • Coping with a life-threatening disease may elicit depression, anxiety and anger in such patients and this anger may be directed toward the dentist and the staff (Asher et al 1993). • Treatment should be provided a calm, relaxed atmosphere, and stress to the patient must be minimized. • Early diagnosis and treatment of HIV infection can have a profound effect on the patient’s life expectancy & quality of life • In case of suspected cases, testing for HIV antibody should be advised after patient counseling and information. 68
    69. 69. DENTAL TREATMENT COMPLICATIONS 1. Adverse Drug Effects • Foscarnet, Interferon - Oral ulcerations • Didanosine - Erythema Multiforme • Zidovudine & Ganciclovir - Leucopenia • Dithiocarb - Xerostomia & Altered taste sensation • HIV-positive patients more susceptible to drug-induced Mucositis & Lichenoid drug reactions 69
    70. 70. 2. HAART drugs • Insulin resistance, gynecomastia, blood dyscrasias, nausea, development of kidney stones, oral warts • Individuals with Hepatitis C + HIV co- infection are susceptible to liver cirrhosis Lipodystrophy • Redistribution of body fat • Gaunt facial features yet display excessive abdominal fat or even a fat pad on the rear of the shoulders (buffalo hump) Severe systemic hyperlipidemia Oral or perioral adverse effects oral lichenoid reactions, xerostomia, altered taste sensation, perioral parasthesia, and exfoliative cheilitis 70
    71. 71. TO ERR IS HUMAN 71
    72. 72. Post exposure prophylaxis (PEP) • The term post-exposure prophylaxis mean the medical response given to prevent the transmission of blood-borne pathogens following a potential exposure to HIV. • PEP should be provided following exposure of non-intact skin (through percutaneous sharps injury or skin abrasion) or mucous membranes (through sexual exposure or splashes to the eyes, nose or oral cavity) to a potentially infected body fluid from a source that is HIV-positive or has unknown HIV status. • 72
    73. 73. • When exposure occurs, Provide immediate care to the exposure site. • Wash needlestick injuries and cuts with soap and water. • Flush mucous membranes with a sterile solution of water or saline. If sterile solutions are not available, use clean potable water. • No data have demonstrated that using antiseptics or squeezing a wound reduces the risk of transmission of a bloodborne pathogen. 73
    74. 74. Evaluating eligibility for HIV post-exposure prophylaxis involves assessing the following: • The timing of the potential exposure • The person’s HIV status • The nature and risk of the exposure and • The HIV status of the source of the potential exposure 74
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    80. 80. Conclusion • HIV associated oro-facial lesions have been considered- • Early clinical picture thus act as Clinical indicators of HIV in otherwise healthy individual • Also oral lesions are predictors of disease progression. 80
    81. 81. THANK YOU 81