This document provides information on periodontal management of HIV patients. It discusses the stages of HIV infection and common oral manifestations such as oral candidiasis, oral hairy leukoplakia, Kaposi's sarcoma, and non-Hodgkin's lymphoma. It also covers HIV-related periodontal diseases including linear gingival erythema, necrotizing ulcerative gingivitis, and necrotizing ulcerative periodontitis. Treatment protocols are provided for oral lesions and periodontal diseases seen in HIV patients.

1. PERIODONTAL
MANAGEMENT OF HIV
PATIENTS
1
ACHI JOSHI
SAIMS, INDORE

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. 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. • 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. 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
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. 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. • 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. 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

10. STRUCTURE OF HIV
10
VIRAL ENEVELOP
VIRAL PROTEIN
CAPSID
RNA
RNA virus.

11. MODES OF TRANSMISSION
11

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. 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

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. • 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. 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. 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. 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. 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. 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

22. MOST COMMON ORAL
MANIFESTATIONS OF AIDS
22

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. 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. • Erythematous candidiasis
Appears as red patches
Seen on tongue or palatal mucosa
Associated with depapillation of the tongue

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. • Angular cheilitis
 Seen on commissures of lips
 Appear as erythematous with surface crusting and fissuring

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. 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
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. 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. 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. 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. 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. • 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. 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. • 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. 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. MANAGEMENT
• Surgical excision
• Anti- cancer drugs
• Radiation therapy
39

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. 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. 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. • 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. 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. 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. • 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. 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. • 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. 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. 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. Management
• Metronidazole
• Antimicrobial mouth rinse
• If osseous necrosis is present, its necessary to remove the affected bone to promote wound
healing
51

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. Oral pigmentation may be caused by,
• Adrenocorticoid insufficiency caused by prolonged
use of ketoconazole
• Pneumocystitis carinii infection
• Cytomegalovirus infection
53

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. 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

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. 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. Treatment
• Salivary stimulants – sugar free gums
• Systemic sialogouges pilocarpin 5 mg - 3 times daily
• Flouride rinses- decay
59

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. TREATMENT
• Broad-spectrum antibiotics such as erythromycin or doxycycline in conjunction with
conservative periodontal therapy and possibly excision of the lesion.
61

62. PERIODONTAL TREATMENT PROTOCOL
• HEALTH STATUS
• INFECTION CONTROL MEASURES
• GOALS OF THERAPY
• SUPPORTIVE PERIODONTAL THERAPY
• PSYCHOLOGIC FACTORS
62

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. 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. 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. 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. 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. 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. 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. 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. TO ERR IS HUMAN
71

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. • 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. 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

75. 75

76. 76

77. 77

78. 78

79. 79

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. THANK YOU
81