Oral manifestations of aids

Oral manifestations of AIDS

1. ORAL MANIFESTATIONS OF AIDS 11/07/2020 - Dr.ASWINI SEKAR MDS

2. CONTENTS INTRODUCTION HISTORY OF HIV EPIDEMIOLOGY ETIOLOGICAL AGENT STRUCTURE OF HIV ROUTES OF TRANSMISSION PATHOGENESIS PHASES IN TRANSMISSION CLINICAL MANIFESTATIONS OF AIDS ORAL MANIFESTATIONS CLASSIFICATION VARIOUS LESIONS-CLINICAL APPEARANCE,TREATMENT CONCLUSION PUBLIC HEALTH SIGNIFICANCE REFERENCES

3. INTRODUCTION H-Human I- ImmunoDeficiency V-Virus H -It infects only human beings and also transmitted between humans not from animals. I -The immune system becomes deficient. V -Virus is a small, simplest thing which is in inactive form outside the body and becomes active when it goes inside human body.

4. A -Acquired I - Immuno D -Deficiency S -Syndrome 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/ µl” CDC – 1993

5. HIV vs AIDS HIV is the virus that causes AIDS Not everyone who is infected with HIV has AIDS Everyone with AIDS is infected with HIV AIDS is result of the progression of HIV Infection

6. HISTORY OF HIV HIV originated in Kinshasa, in the Democratic Republic of Congo(AFRICA) around 1920 chimpanzees ( Simian Immuno Deficiency Virus) to humans ( Mutated similar to HIV). originally transmitted to humans through the contamination of blood during hunting

7. 1979 Center for Disease Control and Prevention(CDC) reported unexplained Pneumonia in 5 and Kaposi’s sarcoma in 26 previously healthy, homosexual men in US. The disease was named as GRID (Gay related immune deficiency) 1981-1982 Increased association with IV drug use, recipients of blood transfusions, hemophiliacs

8. 1983 Virus isolated . Then it was 1 st named as LAV(Lymphadenopathy associated virus) 1984 Virus was named as HTLV-III (Human T-cell Lymphotrophic Virus) 1985 Virus was named as ARV (AIDS related Virus) 1986 -Virus was named as HIV by the International committee on the taxonomy of viruses

9. First HIV reported case in India: Chennai, 1986.(6 female sex workers) Dr. Suniti Solomon has been credited with identifying that HIV. Indias National AIDS committee was established.

10. 1992-National AIDS control programme; National AIDS Control Organization (NACO) was constituted to implement the programme.

11. EPIDEMIOLOGY

12. HIV-TYPES The human immunodeficiency virus (HIV) is grouped to the genus Lentivirus within the family of  Retroviridae , subfamily Orthoretrovirinae HIV HIV - 1 HIV - 2 Most prevalent, common worldwide Subtypes- A to I and O Subtype A & D – found in sub Sahara Africa Subtype B – found in US & Canada Subtype C – found in South Africa & India Subtype E – found in south east Asia Subtype G&H-found in Russia & Central Africa Subtype I – found in Cyprus Found in West Africa, Mozambique, and Angola, India. Less easily transmitted. Less pathogenic Longer Window period of infectivity. Transmitted through the same routes Associated with similar opportunistic infections

13. STRUCTURE OF HIV

14. 3 important genes in the virus gag(group antigens) pol(polymerase) env(envelope) These genes and viral components acts as a markers for lab diagnosis of HIV.

15. ROUTES OF TRANSMISSION Sexual transmission Transmission via blood and blood products Perinatal transmission Occupational transmission Transmission by other body fluids

16. PATHOGENESIS OF HIV

17. PATHOGENESIS OF HIV…

18. PATHOGENESIS OF HIV…

19. PATHOGENESIS OF HIV…

20. PATHOGENESIS OF HIV…

21. PATHOGENESIS OF HIV…

22. PATHOGENESIS OF HIV…

23. PATHOGENESIS OF HIV…(SUMMARY)

24. PHASES IN HIV INFECTION ACUTE HIV SYNDROME(3-12 WEEKS) MIDDLE CHRONIC PHASE(10-12 YEARS) FINAL CRISIS PHASE

25. Stage 1 –ACUTE HIV SYNDROME(3-12 weeks) • Viremia Flu like illness-sore throat, fever, myalgia, skin rash Formation of HIV antibodies(seroconversion) Sudden marked reduction in CD4+ Tcells followed by return to normal level Resolve spontaneously in 2-3 weeks.

26. Stage 2 –Asymptomatic/middle chronic phase(10-12 years) Lasts for an average of ten years • This stage is free from symptoms Cliniclly –stage of latency

27. Stage 3 – final crisis phase • The immune system deteriorates • Emergence of opportunistic infections and cancers May last 7-10 years and leads to death.

28. CDC Classification of HIV(1993) Category A: > 500 cells/µl; asymptomatic,lymphadenopathy Category 2: 200-499 cells/ µl( dysententry , candidiasis, hairy leukoplakia, ca cervix) Category 3: < 200 cells/ µl(various opportunistic infections)

29. CLINICAL MANIFESTATIONS OF AIDS Wasting syndrome Persistant generalized lymphadenopathy GIT disorders Pulmonary manifestations Oral lesions Hematological CNS lesions Gynacological lesions Renal Hepatobiliary lesions Cardiovascular manifestations Opthalmic lesions Musculoskeletal lesions Endocrine lesions

30. Symptoms of HIV - “classic 6” Fatigue Lymphadenopathy Weight loss Fever Night sweats Diarrhea

31. ORAL MANIFESTATIONS OF AIDS

32. CLASSIFICATION There are two main classification systems of oral lesions associated with HIV infection based on the etiology according to the degree of their association with HIV infection

33. Based on the etiology Bacterial viral, or fungal infections or as neoplastic lesions or other conditions

34. EC Clearinghouse on Oral Problems Related to HIV Infection and WHO Collaborating Centre on Oral Manifestations of the Human Immunodeficiency Virus— classifies orofacial lesions into three groups according to the degree of their association with HIV infection Lesions strongly associated with HIV Lesions less commonly associated with HIV Lesions seen in HIV

35. 1.LESIONS STRONGLY ASSOCIATED WITH HIV Candidiasis – Erythematous – Pseudomembranous Hairy leukoplakia Kaposi’s sarcoma Non-Hodgkin’s lymphoma Periodontal disease – Linear gingival erythema – Necrotizing (ulcerative) gingivitis – Necrotizing (ulcerative) periodontitis

36. 2. Lesions less commonly associated with HIV infection Bacterial infections – Mycobacterium avium- intracellulare – Mycobacterium tuberculosis Viral infections Herpes simplex virus Human papillomavirus-condyloma acuminatum . Focal epithelial hyperplasia Verucca vulgaris-varicella zoster, Herpes zoster Melanotic hyperpigmentation • Necrotizing (ulcerative) stomatitis Salivary gland disease Thrombocytopenic purpura Ulceration

37. 3. Lesions seen in HIV infection Bacterial infections -Actinomyces isreli , -Escherichia coli. -klebsiella pneumoniae –Viral infections Cytomegalo virus,Molluscum contagiosum Fungal-cryptococcus neoformans, Geotrichum candidum , Histoplasma capsulatum, Mucoraceae , Aspergillus flavus Cat scratch disease drug reactions Neurological disturbances-facial palsy, trigeminal neuralgia

38. ORAL MANIFESTATIONS OF HIV IN CHILDREN

39. ORAL CANDIDIASIS Most common 72% in children and 94% in adults with HIV Etiologic factor of oral candidiasis is the fungus candida albicans, although other species of candida may be involved C. Glabrata C. Tropicalis C. krusei and C. dublinieusis The presence of candidiasis developed AIDS died within a 24-month period. Jeffrey W. Casiglia , Sook-Bin Woo. Oral Manifestations Of HIV Infection. Clinics In Dermatology 2000; 18:541–551 Pseudomembraneous candidiasis Erythematous candidiasis Hyperplastic candidiasis Angular Cheilitis

40. ORAL CANDIDIASIS.. Pseudomembranous candidiasis in an HIV CLINICAL APPEARANCE : creamy white curd-like plaques on the buccal mucosa, tongue and other oral mucosal surfaces (palate, lips etc.) that can be wiped away, leaving a red or bleeding underlying surface. DIAGNOSIS: In most clinical conditions, the presumptive diagnosis of oral candidiasis is made based on the typical clinical appearance. The diagnosis can be confirmed by obtaining a direct smear and performing either a Potassium Hydroxide (KOH) wet mount or a Gram’s stain.

41. ORAL CANDIDIASIS.. Erythematous candidiasis in an HIV Red lesion commonly located on the palate, dorsum of the tongue (as areas of depapillation ) and buccal mucosa. The lesions tend to be symptomatic with patients complaining of burning mouth and change of taste, most frequently while eating salty or spicy foods or drinking acidic beverages

42. ORAL CANDIDIASIS.. Presents as fissures or linear ulcers at the corners (commissures) of the mouth and often associated with small white plaques, could be unilateral or bilateral. It can occur with or without the presence of erythematous candidiasis or pseudomembranous candidiasis. Angular cheilitis can also exist for an extensive period of time if left untreated. Angular cheilitis

43. ORAL CANDIDIASIS.. This type of candidiasis is unusual in persons with HIV infection. The lesions appear white and hyperplastic. The white areas are due to hyperkeratosis and, unlike the plaques of pseudomembranous candidiasis, cannot be removed by scraping. These lesions may be confused with hairy leukoplakia. Diagnosis of hyperplastic candidiasis is made from the histologic appearance of hyperkeratosis and the presence of hyphae. Periodic acid-Schiff (PAS) stain is often used to demonstrate hyphae. Hyperplastic candidiasis in an HIV

44. ORAL CANDIDIASIS.. Treatment. Treatment with topical and systemic antifungal agents is recommended

45. ORAL HAIRY LEUKOPLAKIA OHL was seen and investigated in 1981 by Greenspan et al., who published the initial report of its existence among homosexual men in San Francisco. Etiology is not clear, OHL seems to be caused by Epstein- barr virus infection The reported prevalence of OHL in adults is about 20%-25%, whereas in children it is 2%-3%

46. ORAL HAIRY LEUKOPLAKIA vertical corrugations with a hairlike appearance. The lesions usually start on the lateral margins of the tongue and sometimes inside the cheeks and lower lip. They may be unilateral or bilateral, and they are asymptomatic. OHL is often associated with oral candidiasis. Although originally postulated to be pathognomonic for HIV infection, this lesion has subsequently been reported in other immune deficiency states as well as in immunocompetent individuals e.g. among organ or bone marrow recipients and those receiving long-term steroid therapy

47. ORAL HAIRY LEUKOPLAKIA

48. KAPOSI’S SARCOMA This is the most common malignancy encountered in HIV/AIDS patients (Iain et al., 2000). Kaposi's sarcoma-associated herpes virus (KSHV)/ Human Herpes Virus-8 (HHV-8) is the causative agent of the endothelial cell-derived tumour Kaposi's sarcoma ( Sturzl et al., 2009). The lesions are commonly seen in homosexual men than heterosexuals. Twenty two percent of the lesions are present intraorally, with 45% of patients presenting with skin and 33% in other organs.

49. KAPOSI’S SARCOMA The lesions are characterized by reddish, bluish or purple, single or multiple macules or nodules. These are seen on the palate or gingivae and may ulcerate, gingival involvement may lead to underlying bone destruction and tooth mobility. Biopsy is essential for a definitive diagnosis. It is considered pathognomonic of HIV infections.

50. KAPOSI’S SARCOMA.. Localised treatment  can also be used, primarily to enhance physical appearance. A drug called vinblastine can be injected directly into the lesions. Radiotherapy is an alternative technique. These techniques cannot affect the development of lesions in untreated areas or be used to treat large areas.

51. Non- Hodgkin’s Lymphoma (NHL) This is an uncommon feature of HIV disease. It is however, the second most common malignancy in this condition . The etiopathogenesis of NHL remains obscure, but there has been much interest in the role of the epstein barr virus, with 50% of AIDS related tumours demonstrating EBV genomes and also aetiologic role of human herpes virus-8 (HHV-8) (Boshoff et al., 1997)

52. Non- Hodgkin’s Lymphoma (NHL) Characteristically, oral tumours involve the fauces and gingivae but atypically may involve other sites such as the tongue. It often clinically presents as a rapidly enlarging mass with associated bony destruction. Survival rates are low and biopsy is essential for definitive diagnosis. Therapy depends on the stage of the disease: Radiation for regional disease and systemic chemotherapy for extra nodal disease. Prognosis is poor, with most patients dying within the first year after diagnosis.

53. PERIODONTAL DISEASES Earlier reports included unusual and severe forms of periodontal disease in HIV-infected individuals, particularly among homosexual males. These lesions ranged from severe gingivitis to advanced, painful periodontitis characterized by spontaneous bleeding, bone exposure and bone destruction . The exacerbated periodontitis described in HIV infected patients is however not clinically distinguishable from that occurring in non-HIV-infected populations (Robinson et al., 2002). HIV associated gingivitis (HIV-G) NUG NUP

54. LINEAR GINGIVAL ERYTHEMA distinct fiery red band along the margin of gingiva and is limited to the soft tissues. It is usually seen 2-3mm from the free gingival margin in anterior teeth, occasionally extending to the posterior teeth (Reznik , 2006) Plaque that is commonly seen in conventional gingivitis is usually not associated with LGE. Bleeding on gentle probing is seen in majority of cases of LGE.

55. Treatment usually includes scaling and debridement, rinsing twice a day with 0.12% Chlorhexidine gluconate for 2 weeks.  LINEAR GINGIVAL ERYTHEMA..

56. Necrotizing Ulcerative Gingivitis(NUG) Necrotizing Ulcerative Periodontitis(NUP) Necrotizing Ulcerative Gingivitis(NUG)- rapid onset of necrotic and ulcerated papillary and marginal gingiva covered by a yellowish-white or grey coloured slough or “ pseudomembrane ” , blunting of papillae, spontaneous bleeding, pain and fetid breath. Necrotizing Ulcerative Periodontitis(NUP)- sharp and intense pain, bleeding with ulcerated marginal gingiva. Rapid and extensive soft tissue necrosis with progressive periodontal attachment loss that results in bone exposure is seen.

57. Necrotizing Ulcerative Gingivitis(NUG) Necrotizing Ulcerative Periodontitis(NUP) Treatment of NUP includes prescription of antibiotics (metronidazole 500mg, twice daily for 7 to 10 days or clindamycin or amoxicillin) along with pain management and nutritional supplementation or counseling if necessary during the initial visit. Follow up visits include periodontal care like scaling and root planning

58. ORAL ULCERS Around 50% of AIDS patients present with oral ulcerations during the course of their disease. Recurrent aphthous ulcers (RAU) can be classified as Minor aphthous Ulcers ( MiAU ) and Major Aphthous ulcers ( MjAU ) . their frequency in AIDS patients is not any different from that in the general population.

59. ORAL ULCERS.. MiAU : RAU have a prolonged course in AIDS patients as well as being more painful and difficult to treat. These ulcers are shallow in appearance,about 2-5mm in diameter, are generally covered with a whitish pseudomembrane and surrounded by an erythematous lining.

60. ORAL ULCERS.. These larger ulcers develop generally on the lateral border of the tongue, soft palate, floor of the mouth, buccal mucosa and oropharynx (occurring on both keratinized and non-keratinized surfaces). They are crater-like in appearance with elevated borders and covered with a white-yellowish pseudomembrane , measuring over 1cm in diameter

61. SALIVARY GLAND DISEASES Salivary gland diseases such as enlargement of the major salivary glands and xerostomia. The cause of HIV related salivary gland diseases is unclear, for no etiological agents have been identified Enlargement of the salivary glands due to infilteration by CD4 lymphocytes is seen in both adult and paediatric HIV infection ( Schoidt et al., 1989). Oral Mucoceles and ranulas are recently discovered to be oral manifestations of HIV infection

62. Xerostomia This may be associated with the salivary gland enlargement but is also a common consequence of medications used by this population. Cytomegalovirus (CMV) has been demonstrated in the salivary gland of xerostomic patients (Greenspan et al., 1992). Symptomatic relief may be provided by salivary stimulants such as sugarless chewing gums or saliva substitutes. Prevention of dental caries in people with xerostomia is extremely important, and the use of topical fluoride gels and rinses should be encouraged (Greenspan et al., 1996). In addition, management of xerostomia will improve oral comfort, the quality of speech and use of any prostheses ( Narani et al., 2001).

63. Herpes virus infections Herpes-zoster may present with a prodrome of dental pain, preceding oral and unilateral vesicles on an erythematous base then appear in clusters, chiefly along the course of the nerve , giving the characteristic clinical picture of single dermatome involvement. The vesicles turn to scabs in 1 week, and healing takes place in 2 to 3 weeks and condition can be life threatening in HIV disease. Herpes zoster of the left maxillary branch and the right occipital branch of the trigeminal nerve • Tabs Acyclovir200-400mg 5x daily for 1 week

64. Herpes virus infections… Herpes is caused by a common virus called herpes simplex virus (HSV). Hsv 1 and 2. HSV 2 is most commonly associated with genital herpes, but both viruses can cause either genital or oral herpes. Oral herpes causes tingling or painful fluid-filled blisters on the edge of the lip (‘cold sores’). These can occasionally develop on the nostrils, on the gums or on the roof of the mouth. The virus passes easily through mucous membranes in the mouth, genital areas and anus, so can be passed on by kissing and other sexual contact.  Applying a topical anaesthetic , such as lidocaine, and bathing the affected area in salty water. Applying an ice pack may help.

65. HIV and Tuberculosis Deadly infectious disease caused by Mycobacterium tuberculosis First isolated in 1882 by a German physician named; Robert Koch; who received the Nobel Prize for this discovery. Among HIV-infected individuals, lifetime risk of developing active TB is 50%, the leading cause of death among people with HIV/AIDS .

66. HIV and Tuberculosis..

67. HIV and Tuberculosis Peripheral blood cultures Molecular diagnostic techniques based on detection of M. tuberculosis specific DNA or ribosomal RNA sequences by polymerase chain reaction (PCR) CT scan and magnetic resonance imaging (MRI)

68. Oral lesions and relationship with CD4 count and viral load Several studies have shown high prevalence of oral lesions in patients with low CD4 count, <200 cells/mm3 (500-1500) and high viral load: >55,000 copies/ml. Without intervention, an average of 60 to 80 cells/mm3 is lost every year; this loss is highly variable and occurs in periods of stability and rapid decline.

69. Oral lesions and response to HAART The prevalence of HIV-related oral lesions reduces significantly with HAART. Studies examining the effect of HAART on the prevalence of individual oral manifestations showed reduction in the prevalence by 30% ( patton et al., 2000; schmidt-westhausen et al., 2000; tappuni et al., 2001).

70. ADVISE HIV SCREENING Oral candidiasis Oral hairy leukoplakia Periodontal lesions Kaposi’s sarcoma Non-Hodgkin lymphoma Secondary tuberculosis oral lesions (granulomatous ulcers) Xerostomia Salivary gland swelling Long-evolving HSV lesions Aphthous lesions refractory to conventional treatment Option 1: Refer patient for HIV screening + Counseling: -Sexually transmitted disease clinics -Primary Care -Hospital -Qualified NGOs Option 2: Rapid HIV test with Oraquick Advance® + Counseling

71. CONCLUSION Dental professionals -might adopt a more active role in the early detection of HIV In this sense the study plans of our dental schools will have to be updated and further engage dentists in public health sector . Such information should be conveyed not only to dental professionals but also to patients who thus may begin to regard their “usual dentist” as a healthcare professional concerned about their general health – not only their dental health.

72. REFERENCES World Health Organization. Guidelines on HIV Self-testing and partner notification supplement to consolidated guidelines on HIV testing services, Villars-sous-Yens, Switzerland; 2016 . Neville,Damm,Allen:Oral and Maxillofacial Pathology;3 rd edition,Elsevier,2009. Rajendran R. and Sivapathasundaram B:Shafer’s Textbook of Oral Pathology;7 th edition,New Delhi,Elsevier,2012. http://hivinsite.ucsf.edu/InSite?page=kb-04-01-14 Jeffrey W. Casiglia , Sook-Bin Woo. Oral Manifestations Of HIV Infection. Clinics In Dermatology 2000; 18(3):541–551.