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Hiv infection /certified fixed orthodontic courses by Indian dental academy

  1. 1. My Friend -Mike INDIAN DENTAL ACADEMY Leader in continuing dental education
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  6. 6. HIV Infection
  7. 7. HIV Infection
  8. 8. Contents • Introduction • Epediomology • Clinical Features • Oral Manifestations • Mode of transmission • Pathogenesis • Anti retroviral drugs • HIV Vaccine
  9. 9. • Anti retroviral drugs and oral diseases • Anti retroviral drugs and oral side effects • Orthodontic Care • Infection control • Post exposure prophylaxis • Preventive Measures to reduce transmission. • Conclusion • References
  10. 10. Introduction • AIDS was first recognized in the United States in the summer of 1981, when the U.S. Centers for Disease Control and Prevention (CDC) reported the unexplained occurrence of Pneumocystis carinii pneumonia in five previously healthy homosexual men in Los Angeles and of Kaposi's sarcoma in 26 previously healthy homosexual men in New York and Los Angeles.
  11. 11. • Within months, the disease became recognized in male and female injection drug users (IDUs) and soon thereafter in recipients of blood transfusions and in hemophiliacs. • As the epidemiologic pattern of the disease unfolded, it became clear that a microbe transmissible by sexual (homosexual and heterosexual) contact and blood or blood products was the most likely etiologic agent of the epidemic.
  12. 12. • In 1983, human immunodeficiency virus (HIV) was isolated from a patient with lymphadenopathy, and by 1984 it was demonstrated clearly to be the causative agent of AIDS. • In 1985, a sensitive enzyme-linked immunosorbent assay (ELISA) was developed, which led to an appreciation of the scope and evolution of the HIV epidemic at first in the United States and other developed nations and ultimately among developing nations throughout the world
  13. 13. Epidemiology Global estimates for adults and children by the end of 2004 • 40 million people are living with HIV infection • 4.9 million people have new HIV infection • 3 million people have lost their lives • 90% live in developing countries • India – 2nd to South Africa
  14. 14. 40 million Adults and children estimated to be living with HIV/AIDS December 2004 Western Europe 570 000 North Africa & Middle East 550 000 Sub-Saharan Africa 29.4 million Eastern Europe & Central Asia 1.2 million South & South-East Asia 6 million Australia & New Zealand 15 000 North America 980 000 Caribbean 440 000 Latin America 1.5 million East Asia & Pacific 1.2 million
  15. 15. In India • First case recognized– in Chennai in 1986 • 5 million Men are affected • 1.9 Million – Women • 5,50,000 – Children • M:F – 1.7 : 1 • 37% - are under age of 30
  16. 16. Clinical Features of HIV Infection Four stages- 1. Primary infection 2. Asymptomatic infection 3. Mildly Symptomatic disease 4. Acquired immunodeficiency syndrome
  17. 17. Primary infection • Symptomatic in 70-80% cases • Occurs 2-6 weeks after exposure • Plasma HIV-RNA levels > 1 million copies/ml • CD4 count – 300-400 cells/cumm • Symptomatic recovery occurs after 1-2 weeks
  18. 18. Clinical Features include- • Fever with rash, • Pharyngitis with cervical lymphadenopathy • Headache • Myalgia/arthralgia Asymptomatic infection • Infected individual remains well with no evidence of disease except the presence of generalized lymphadenopathy • Lasts for 7-10
  19. 19. Mildly Symptomatic disease • Indicates some impairment of cellular immune system. Clinical features- • Oral hairy leukoplakia • Oropharyngeal candidiasis • Chronic Weight loss • Diarrhea • Herpes zoster infection • Fever and night
  20. 20. Acquired immunodeficiency syndrome Characterized by development of specified opportunistic infections and neoplasms Clinical features- • Dementia • Cryptococcal meningitis • Cerebral toxoplasmosis • Cerebral lymphoma • CMV Retinitis
  21. 21. • Oesophageal candidiasis • Pulmonary TB • Diarrhoea • Kaposi Sarcoma • Non-Hodgkin Lymphoma
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  23. 23. Oral Manifestation- Adults
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  25. 25. Oral Manifestation- Pediatric Patient
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  28. 28. Group 1-Oral Lesions Strongly Associated with AIDS (AIDS Defining Oral Diseases)
  29. 29. Candidosis Prevelance- 55 to 69 % Clinical features- White or yellow plaques that can be wiped off to reveal an erythematous surface that may bleed. Definitive diagnosis-An effective response to antifungal agents. •Smears or cultures for the presence of candida albicans or other species Pseudomembraneous
  30. 30. Erythematous Prevalence- 25- 50% Clinical features- Red patches, most commonly found on the palate and dorsal surface of the tongue. • White spots and plaques may also be seen, although erythema predominates. Defenitive diagnosis- the detection of candida albicans by smear and/or culture, and response to antifungal therapy, may help to establish the diagnosis.
  31. 31. Angular Chelitis Prevelence- 13-26% Clinical features • Inflammation/irritation • Cracking and fissuring • Pain upon opening the mouth • Reduced vertical dimension Definitive diagnosis: • An effective response to antifungal agents. • smears or cultures for the presence of candida albicans are essential for diagnosis.
  32. 32. Hairy Leukoplakia- Epstein Barr Virus
  33. 33. Prevelence-25-38% Clinical features -Bilateral whitish/grey lesions on lateral margins of the tongue. • Non scrapable, and typically may have vertical corrugations. • May extend to the dorsal and ventral surface. • Defenitive diagnosos- Biopsy with demonstration of Epstein Barr virus, • Lack of response to antifungals.
  34. 34. Kaposi’s Sarcoma
  35. 35. Prevelence 20-50% Clinical features- Caused by HHV 8 • One or more erythematous, slightly bluish or violaceous macules or swellings,with or without ulceration. • Most common on the palate or gingiva and the dorsum of the tongue • Defenitive diagnosis-Biopsy.
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  37. 37. Non-Hodgkin’s Lymphoma Clinical features -Firm, rubbery, pink, reddish or purple swelling, with or without ulceration. • Predilection for the gingival palatal mucosa. Defenitive diagnosis- Biopsy • Appropriate immunocytochemical or molecular biological investigations
  38. 38. Periodontal Diseases Linear Gingival Erythema Prevelence - 47% Clinical features-Distinct fiery red band along the margin of the gingiva, disproportionate to the amount of plaque seen. • No pockets, ulceration or attachment loss. Defenitive diagnosis- None, • But does not respond well to oral hygiene measures. • Microbiology not yet established.
  39. 39. • Necrotizing Gingivitis Necrotizing Periodontitis
  40. 40. Clinical features- Soft tissue loss as a result of ulceration or necrosis. • Destruction may cross the mucogingival junction. • Exposure, destruction, or sequestration of bone • teeth may loosen, and pain may be experienced. Definitive criteria: • None.
  41. 41.
  42. 42. Group 2-Oral Lesions Associated with AIDS (AIDS Associated Oral Diseases)
  43. 43. Herpes Simplex Virus
  44. 44. • Prevelence 1.7 to 27% Clinical features- Vesicles that coalesce into bullae and break • Some report a tingling sensation • Occur on fixed and keratinized tissue • Painful • May have systemic manifestations
  45. 45. Human Papilloma Virus Prevelence 9 to 18 % Clinical features- Condyloma acuminatum begin as a smooth- surface papule • Rough fingerlike projections • Occur mainly on keratinized mucosa • Tend to reccur • May interfere with eating and swallowing and may bleed • Not painful • Transmissible
  46. 46. HERPES ZOSTER INFECTION Prevelence 17% • Indicator of severe HIV infection, but seems to be unlikely. • Preceded by vesicles – rupture – ulceration . • Ulcers – multiple shallow, small with erythematous base, distributed unilaterally along a division of 5th cranial nerve. • Pain, tenderness. Definitive criteria: • Histologic staining for multinucleated giant cells with intranuclear inclusions • Direct immunofluorescence • cytology smears taken from the lesions
  47. 47. Salivary Gland Enlargement • Prevalence - 3-10% • Arises as a consequence of reactive/ inflammatory conditions, infections and neoplasm • Most frequently is due to diffuse infiltration of CD8 lymphocytes.
  48. 48. Psychological Impact
  49. 49. Mode of Transmission Sexual transmission- HIV infection is predominantly a sexually transmitted disease world wide. • In US 42% new infections are among homosexuals and 33% are among heterosexuals. • Male to female transmission is 8 times more efficient than female to male.
  50. 50. • Blood and blood products- 90 to 100% individuals who receive HIV contaminated whole blood transfusion, packed red blood cells, platelets, leukocytes, and plasma, • In contrast, hyperimmune gamma globulin, hepatitis B immune globulin, plasma derived hepatitis B vaccine and Rh immune globulin are not associated with transmission of HIV infection. The procedure involved in processing these products either inactivates or remove the virus.
  51. 51. Occupational Transmission of HIV • There is a small, but definite, occupational risk of HIV transmission to health care workers and laboratory personnel and others, particularly when sharp objects are used. • An estimated 600,000 to 800,000 health care workers are stuck with needles or other sharp medical instruments in the United States each year. • Large, multi-institutional studies have indicated that the risk of HIV transmission following skin puncture from a needle or a sharp object that was contaminated with blood from a person with documented HIV infection is –0.3% and after a mucous membrane exposure it is 0.09%.
  52. 52. HIV transmission after non-intact skin exposure has been documented, but the average risk for transmission by this route has not been precisely determined; however, it is estimated to be less than the risk for mucous membrane exposure. An increased risk for HIV infection following percutaneous exposures to HIV-infected blood is associated with 1. Exposures involving a relatively large quantity of blood, as in the case of a device visibly contaminated with the patient's blood, 2. A procedure that involves a needle placed directly in a vein or artery, or a deep
  53. 53. Factors that might be associated with mucocutaneous transmission of HIV include 1. Exposure to an unusually large volume of blood, 2. Prolonged contact, and 3. Blood from patients with advanced-stage disease, probably owing to the higher titer of HIV in the blood 4. Presence of more virulent strains of virus.
  54. 54. Maternal – Fetal/Natal Transmission • The relative proportions of mother-to-child transmissions were 1. 23 to 30% before birth, 2. 50 to 65% during birth, and 3. 12 to 20% via breast-feeding. Risk of transmission increases with the increase in the number of plasma HIV RNA count.
  55. 55. Transmission by other body fluids • Although HIV can be isolated typically in low titers from saliva of a small proportion of infected individuals, there is no convincing evidence that saliva can transmit HIV infection, either through kissing or through other exposures, such is occupationally to health care workers. • Saliva contains endogenous antiviral factors 1. HIV -specific immunaglobulins of IgA, IgG, and IgM isotypes 2. Large glycoproteins such as mucins and thrambospondin 1 which sequester HIV into aggregates far clearance by the hast
  56. 56. 3. A number of soluble salivary factors inhibit HIV to various degrees in vitro, probably by targeting host cell receptors rather than the virus itself. Perhaps the best studied of these, secretary leukocyte protease inhibitor (SLPI), blocks HIV infection in several cell culture systems, and it is found in saliva at levels that approximate those required far inhibition of HIV in vitro. 4. Sub-mandibular saliva reduces HIV infectivity by stripping gp120 from the surface of the virus and that saliva-mediated disruption and lyses of HIV infected cells occurs because of the hypotonicity of oral secretions.
  57. 57. • Transmission of HIV by human bite can occur but is a rare event. • Although virus can be identified, if not isolated, from virtually any any fluid, there is no evidence that HIV transmission can occur as a result of exposure to tears, sweat, and urine.
  58. 58. Classification Of Retroviruses
  59. 59. Morphology of HIV Virus
  60. 60. Role of CD4 Cells in Immunity
  61. 61. Co-receptor For HIV Virus And Cell Membrane Fusion • HIV virus infect CD4 T lymphocyte which has a co- receptor – CCR5 • And Macrophage/Monocyte which have co-receptor – CXCR4
  62. 62. Life cycle of the virus
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  64. 64. Life Cycle of the HIV Virus and Mechanism of Anti retroviral Therapy
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  66. 66. Investigations Antibody Based • Sreening Test- ELISA 99.5% sensivity. • Confirmatory Test- Western Blot; high specificity. Virus based tests • Viral culture • Polymerized chain reaction(RNA, DNA PCR) • P24 antigen detection
  67. 67. Salivary tests
  68. 68. Serologic Test For HIV Diagnosis
  69. 69. Western Blot Test
  70. 70. Medical Management of HIV infection Aims • Reduce the viral load (<50 copies/ml) • Improve the CD4 count (above200cells/cumm) • Improve the quality of life without unacceptable drug related side effects • Reduce transmission
  71. 71. Nucleoside reverse transcriptase inhibitors (N R T I s ) Zidovudine, Stavudine Lamivudine, Didanosine Abacavir Emitricitabine Zalcitabine. Non-nucleoside reverse transcriptase inhibitors (NN R T I s) Delavirdine , Nevirapine, Efavirenz. Protease inhibitors (P I s) Indinavir, Ritonavir, Saquinavir, Tipranavir, Nelfinavir, Lopinavir, Atazanavir, Fosamprenavir,, Amprenavir,. Antiretroviral drugs
  72. 72. NRTI’s
  73. 73.
  74. 74. NNRTI’s
  75. 75.
  76. 76. Protease’s Inhibitor
  77. 77.
  78. 78. • Treatment with a combination of drugs is termed Highly Active Antiretroviral Therapy (HAART). • Z DV, Abacavir, and Tenofovir • Lopinavir / ritonavir and Efavirenz
  79. 79. • A number of clinical trials ranging from several small phase I trials and fewer intermediate-sized phase II trials to determine safety and immunogenicity have taken place and are under way. • The single completed phase III trial of a recombinant gpl20 protein failed to show protection despite evidence of HIV -specific antibodies and CD4 + T cells in phase II. These results suggest the potential importance of CD8+ T cell immunity in host defense against HIV -1. HIV Vaccines
  80. 80.
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  82. 82. • The furthest advanced among the current phase II trials in-volves a combination approach using a live canarypox vector expressing one or multiple HIV epitopes given together with gpl20 or using the gpl20 as a boost. • This approach has resulted in neutralizing anti-bodies in virtually all recipients and HIV - specific cytolytic T cells in -30% of individuals at any given time during the course of the trial.
  83. 83. HART and Oral Diseases • Since the introduction of specific anti-HIV- therapies there have been striking changes in the frequency and character of the oral complications of HIV disease. • Anti-retroviral drugs significantly lessen HIV viral load, increase CD4+ T-cell count and lessen the frequency and severity of opportunistic diseases. It would thus be expected that HAART will reduce most HIV related oral diseases
  84. 84. • 30% decrease in the frequency of HIV-related oral manifestations was described in Spanish patients receiving HAART. • HAART decreased the prevalence of Oral hairy leukoplakia (25.8 down to 11.4%) and necrotizing periodontal disease (4.8 down to 1.7%), whilst increased salivary gland disease (1.8–5%)
  85. 85. HAART And Oral Side Effects • A range of oral diseases can arise as a consequence of HAART. These adverse orofacial side effects are usually not very troublesome • The oral side effects of some NRTIs are related to the bone marrow suppression, and they can manifest as neutropenic mouth ulcers. Erythema multiforme and toxic epidermal necrolysis have also been described, as well as lichenoid reactions, particularly related to zidovudine. This drug can also give rise to mucocutaneous hyperpigmentation by an, as yet, unknown mechanism
  86. 86. Melanotic Hyperpigmentation
  87. 87. • Adverse effects seem to be less common with NNRTIs; however, erythema multiforme has been described in association with NNRTIs, particularly Nevirapine • Protease inhibitor-related oral side effects include taste abnormalities, affecting about 10–20% of patients, and oral and perioral paraesthesia. Ritonavir in particular can give rise to circumoral paraesthesia in over 25% of patients
  88. 88. HAART And Vertical Transmission • Treatment with Zidovudine alone of an HIV infected pregnent women from the beginning of 2nd trimester through the delivery and of the infant for 6 weeks following birth can reduce the risk from 22% to < 5% • Rate of vertical transmission can be < 1% with combined retroviral therapy.
  89. 89.
  90. 90. Orthodontic Treatment • Overall, the provision of orthodontic treatment for HIV – infected individuals in asymptotic stage is same to that of non- infectious patients. 1) Treatment Planning- should be based on the condition of the patient eg Mental condition of the patient Financial condition 2) Antibiotic prophylaxis Neutropenia
  91. 91. 3) Before inititing the procedure- antibacterial mouthrinses - in patients with the history of increased bleeding tendencies placement of separators and bands should be avoided.
  92. 92. Infection control 1)Barrier techniques – Gloving, Hand washing, wearing masks, protective eye wears, Gowns, Disposable caps etc. 2)Sterilization - Cleaning of instrumentsusing ultrasonic cleaner - Heat sterilization – Autoclave, Dry heat 3)Disinfection – Ethyl alcohol, isopropyl alcohol Phenols Sodium Hypochloride Gluteraldehyde
  93. 93. Post Exposure Prophylaxis • First aid should be given immediately after the injury. • Punture wounds & other cutaneous injuries – rinsed thoroughly with water or saline and then washed with soap and water • Mucosal exposures involving mouth should be flushed vigorously with water • Eyes – irrigated with water , saline or sterile eye irrigants
  94. 94. • Combination therapy is now recommended for occupational post-exposure prophylaxis (PEP) • Recommended PEP is Zidovudine , Lamivudine and Indinavir for 28 days. • Post exposure follow up HIV testing- 6 weeks, 3 months, and 6 months
  95. 95. Preventive measures for HIV transmission • Comprehensive sex education programmes in schools • Public awareness campaigns for HIV • Easily accessible/discreet testing centres • Safe sex practices • Effective treatment of HIV-infected persons
  96. 96. • Routine screening of donated blood, • Education/training (universal precautions, needle stick avoidance) • Counselling about planning/risks of pregnancy if HIV-seropositive • Measures to reduce vertical transmission • Post exposure prophylaxis
  97. 97. Conclusion • All the dental care providers should remain alert to the oral conditions that may represent a manifestation of HIV infection • The dental profession has an essential role to play in identifying the oral manifestations of HIV disease and AIDS, and in management of oral conditions that are associated with immunodeficiency.
  98. 98. Reference 1. Kasper- Harrision’s Principles of internal Medicine 16th ed McGraw Hill Publication. 1059-1139. 2. Greenberg- Burket’s Oral Medicine, Diagnosis & Treatment . 10th ed Elsever Publication 538-556. 3. Neville- Oral and Maxillofacial pathology – 2nd ed, W.B. Saunder’s Company. 235-249
  99. 99. 4. S Rajendra- Shafer’s textbook of oral pathology- 5th Ed Elsevier Publication 488-497. 5. Mosca NG .HIV-positive patients: dental management considerations. Dent Clin North Am. 2006 Oct;50(4):635-57 6. Hodgson TA- Oral lesions of HIV disease and HAART in industrialized countries. Adv Dent Res. 2006 Apr 1;19(1):57-62. 7. Patton-HIV disease.Dent Clin North Am. 2003 Jul;47(3):467-92.
  100. 100. 8. Barr CE- Practical considerations in the treatment of the HIV-infected patient. Dent Clin North Am. 1994 Jul;38(3):403-23. 9. Frezzini C- Current trends of HIV disease of the mouth. J Oral Pathol Med. 2005 Oct;34(9):513- 31. 10. Hodgson TA Oral lesions of HIV disease and HAART in industrialized countries. Adv Dent Res. 2006 Apr 1;19(1):57-62. 11. Petersen PE -Policy for prevention of oral manifestations in HIV/AIDS: the approach of the WHO Global Oral Health Program. Adv Dent Res. 2006 Apr 1;19(1):17-20
  101. 101. 12. Owotade FJ - Clinical experience with parotid gland enlargement in HIV infection: a report of five cases in Nigeria. J Contemp Dent Pract. 2005 Feb 15;6(1):136-45. 13. Ceballos-Salobreña AThe effect of antiretroviral therapy on the prevalence of HIV-associated oral candidiasis in a Spanish cohort. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Mar;97(3):345-50. 14. Patton LL -Prevalence and classification of HIV-associated oral lesions. Oral Dis. 2002;8 Suppl 2:98-109.
  102. 102. 15. Valiathan Ashima, KL Pai, Sunil Sachdeva & Snehalata Oberoi: Aids in Dentistry. Journal of International College of Dentist1997; 41: 15- 20.
  103. 103. Thank you For more details please visit