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HIV & PERIODONTIUM
1
Presented by
Dr. Dandu Sivasai Prasad
1st yr post graduate
Mamata dental college
CONTENTS
 Introduction
 History
 Epidemiology AIDS
 CDC definition and classification of AIDS
 Virus structure
 Mode...
Contents…
 Classification of oral lesions associated with HIV
 Periodontal manifestations of HIV
 Periodontal managemen...
4
INTRODUCTION:
HISTORY:
5
1959- Scientists isolated earliest known case of AIDs
1978- Gay men in US, Sweden and Hetrosexuals in Tanzania ...
EPIDEMIOLOGY OF AIDS
• As of 2012, approximately 35.3 million people are living with
HIV globally. Of these, approximately...
EPIDEMIOLOGY OF AIDS…
• The total number of people living with HIV in India is
estimated at 2.4 million.
• 61% male and 39...
VIRUS STRUCTURE
8
P17
P24
MODE OF TRANSMISSION:
• HIV detected in most body fluids including.
• Blood
• Semen
• Vaginal secretions
• Cerebrospinal f...
MODE OF TRANSMISSION…
• Sexual contact
• Blood transfusion
• Needle sharing
• Perinatal transmission
• Intrauterine Postna...
LIFE CYCLE OF HIV
11
CDC SURVEILLANCE CASE
CLASSIFICATION:
• 1982- “presence of oppurtunistic illness or malignancies
secondary to defective im...
AIDS patients have been grouped as follows, according
to the CDC Surveillance Case Classification (1993);
 Category A - A...
WHO classification of HIV-associated clinical disease
CLINICAL STAGE 1 CLINICAL STAGE 2 CLINICAL STAGE 3 CLINICAL STAGE 4
...
Classification and diagnostic criteria for oral lesions in HIV infection. 1993
revised
Group 1: Lesions strongly associate...
Group 2: Lesions less commonly associated with HIV
infection:
 Bacterial infections like
 Mycobacterium avium - in trace...
• Group 3. Lesions seen in HIV infection
 Bacterial infections like
 Actinomyces israelii
 Escherichia coli
 Klebsiell...
Fungal infection other than candidiasis
 -Cryptococcus neoformans
 -Geotrichum candidum
 -Histoplasma capsulatum
 -Muc...
MEDICAL MANAGEMENT
19
ANTI-RETROVIRAL DRUGS
One that blocks binding of HIV to target
cells
One that blocks viral RNA clevage
One that inhibits e...
IDEAL REQUIREMENTS
1. Should be as specific as possible.
2. Should reduce viral production from infected cells.
3. Can be ...
ART…
• Zidovudine (AZT, ZDV)
• Retrovir
• Didanosine
• Videx
• Zalcitabine
• Hivid
• Stavudine
• Zerit
22
Nucleoside - sto...
ART…
• Nevirapine
• Viramine
• Delaviradine
• Rescriptor
• Efavirenz
• Sustiva
23
Non-nucleoside Reverse transcriptase inh...
ART…
• .
• Saquinavir
• Invirase
• fortovase
• Ritonavir
• Norvir
• Indinavir
• Crixivan
• Relfiravir
• Viracept
24
Protea...
“COCKTAIL” OR TRIPLE-THERAPY
• HAART
• Regimens include atleast one protease inhibitor or non-
nucleoside reverse transcri...
• Hemo-Modulator
26
works by filtering a patient's blood through the device which blasts
ultraviolet light onto the blood....
PROBIOTICS FOR HIV
• Lin Tao (2008) and his colleagues screened
hundreds of bacteria taken from the saliva of volunteers.
...
WHAT’S THE ROLE OF DENTIST?????
• 1. Provides routine dental care for HIV-infected individuals.
• 2. Understands the signi...
LESIONS COMMONLY
ASSOCIATED WITH HIV
INFECTION
29
30
Pseudomembranous Candidiasis Erythematous candidiasis
Hyperplastic candidiasis Angular cheilitis
ORAL CANDIDIASIS
MANAGEMENT
• 1. More advanced lesions including hyperplastic candidiasis may require
systemic antifungal drugs.
• 2. Early...
 long-term use of ketoconazole may induce liver damage in
individuals with preexistent liver disease.
 The increased ris...
• TOPICAL DRUGS
• 1.Clotrimazole 10mg tablets: dissolve in mouth 3-5tablets daily for 7-14days
• 2.Nystatin
• a.Oral suspe...
34
SYSTEMIC DRUGS
1. Ketoconazole (Nyzoral) 200mg tablets: take 2 tablets immediately,
then 1-2 tablets daily for 5-14days...
ORAL HAIRY LEUKOPLAKIA
• Microscopically, the lesion shows
A hyperparakeratotic surface with
projections that often resemb...
MANAGEMENT:
• 1. Oral hairy leukoplakia generally does not require
treatment.
• 2. Resolution has been reported after ther...
NON-HODGKIN’S LYMPHOMA
• Occurrence is more common in the gingiva.
• Has a characteristic white verrucous surface or necro...
KAPOSI’S SARCOMA
• Kaposi’s sarcoma is a rare, multifocal
vascular.
• Median survival time after onset of KS
is 7 to 31 mo...
MANAGEMENT
• 1. Treatment includes use of antiretroviral agents,
laser excision, radiation therapy or intralesional
inject...
• Destructive periodontitis has also been reported in
conjunction with gingival KS. In such instances, scaling and root
pl...
ATYPICAL ULCERATIONS
• Most reported oral ulcers are to herpes simplex
virus, CMV, EBV, histoplasmosis, herpes zoster
and ...
ORAL HYPERPIGMENTATION:
• Often appear as spots or striations in the
buccal mucosa, soft palate and the gingiva
or tongue....
PERIODONTALCONSIDERATIONS
43
Periodontal considerations…
 Dennisn et al- first report linking periodontal disease and
HIV
 Parra & slots- HIV in GCF
...
LINEAR GINGIVAL ERYTHEMA:
Clinical features:
• A persistent, linear, easily bleeding,
erythematous gingivitis (LGE) has
be...
Causes and pathogenesis
• candidal infection-Robinson
• Velegrakiet et al - Candida dubliniensis
• Winkler et al- CD4+ T c...
LGE treatment…
Treatment:
- Does not respond well to plaque removal
- Conventional therapy plus rinsing with 0.12% chlorhe...
LGE treatment…
• Step 1: Instruct the patient in performance of meticulous
oral hygiene.
• Step 2: Oral prophylaxis.
• Ste...
NECROTIZING GINGIVITIS:
Clinical features:
• HIV-related necrotizing gingivitis is
defined by EC-WHO as destruction of one...
NUG…
• Causes and pathogenesis
• The isolated organisms include Borrelia, gram-positive
cocci, P-hemolytic streptococci an...
Treatment
• Basic treatment may consist of cleaning and
debridement of affected areas with a cotton pellet
soaked in perox...
NUG…
• Does not always respond to conventional treatment with
scaling and improved oral hygiene (winkler jr et al).
• Adju...
NECROTIZING PERIODONTITIS:
• Clinical features:
• According to the description by EC-
WHO necrotizing periodontitis is
per...
NUP…
• NUP is severely painful in onset and immediate therapy is
necessary
• On occasions, however, patients undergo spont...
NUP…
Causes and pathogenesis:
• Higher proportions of C. albicans and C. rectus.
- Debilitating health and progression of ...
Treatment
 Local debridement
 Scaling and Root planing,
 Irrigation with an effective antimicrobial agent.
In severe NU...
NUP…
• Does not always respond to conventional treatment with
scaling and improved oral hygiene (winkler jr et al).
• Prop...
INDICATIONS FOR HIV TESTING OF DENTAL PATIENTS
58
DIAGNOSTIC TESTS:
DIAGNOSTIC
TESTS
ELISA
WESTERN
BLOT (WB)
(PCR)
P24
ANTIGEN
LAB-ON-A-CHIP
59
60
OCCUPATIONAL EXPOSURES AND POSTEXPOSURE
PROPHYLAXIS (PEP):
61
62
GENERAL PRECAUTIONS TO BE
TAKEN
• 1. Surgical gloves should be worn when touching
blood, saliva or mucous membranes.
• 2. ...
GENERAL PRECAUTIONS TO BE TAKEN…
• 6. Surfaces should be decontaminated with sodium hypochlorite.
• 7. Needles should be d...
CONCLUSION:
The pathogenesis periodontal diseases in HIV+ subjects
may be due to the microflora, the effects of HIV and
ot...
REFERENCES
• Textbook of clinical periodontology- Carranza 10th Edition
• Textbook of clinical periodontology- Carranza 9t...
References…
• DCNA 2003, 467-492
• R.G. Nair et al. Coinfections associated with HIV
infection: Workshop 1A. Adv Dent Res ...
68
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Hiv and periodontium

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Hiv and periodontium

  1. 1. HIV & PERIODONTIUM 1 Presented by Dr. Dandu Sivasai Prasad 1st yr post graduate Mamata dental college
  2. 2. CONTENTS  Introduction  History  Epidemiology AIDS  CDC definition and classification of AIDS  Virus structure  Mode of transmission  Life cycle of HIV  Clinical features-WHO classification 2
  3. 3. Contents…  Classification of oral lesions associated with HIV  Periodontal manifestations of HIV  Periodontal management of HIV infected patients  Diagnostic tests  Occupational exposure and Post-Exposure prophylaxis  Sterilization and precautions to be taken  Conclusion  References 3
  4. 4. 4 INTRODUCTION:
  5. 5. HISTORY: 5 1959- Scientists isolated earliest known case of AIDs 1978- Gay men in US, Sweden and Hetrosexuals in Tanzania and Haiti- Showed signs 1981, June 5th- CDC reported confirmed CMV and Candidal infection(LAV) In 1982 july 27th, the term AIDs first used In 1984, Robert Gallo discovered the HIV virus- HTLV-III
  6. 6. EPIDEMIOLOGY OF AIDS • As of 2012, approximately 35.3 million people are living with HIV globally. Of these, approximately 17.2 million are men, 16.8 million are women and 3.4 million are less than 15 years old. There were about 1.8 million deaths from AIDS in 2010, down from 2.2 million in 2005 • Sub saharan africa is the region most affected. In 2010, 68% (22.9 million) of all HIV cases. • 66% of all deaths (1.2 million). 6
  7. 7. EPIDEMIOLOGY OF AIDS… • The total number of people living with HIV in India is estimated at 2.4 million. • 61% male and 39% female. • The four high prevalence states of South India account for 57% of all HIV infections in the country. Andhra Pradesh- 500,000 cases; Maharashtra- 420,000 cases, Karnataka - 250,000 cases and Tamil Nadu-150,000 cases • IDU-12.22% :MSM- 6.82% :FSW at 5.92%. HIV prevalence amongst IDU, MSM and FSW is 14.92%, 10.31% and 9.48% respectively 7
  8. 8. VIRUS STRUCTURE 8 P17 P24
  9. 9. MODE OF TRANSMISSION: • HIV detected in most body fluids including. • Blood • Semen • Vaginal secretions • Cerebrospinal fluid • Breast milk • Urine 9
  10. 10. MODE OF TRANSMISSION… • Sexual contact • Blood transfusion • Needle sharing • Perinatal transmission • Intrauterine Postnatal • Occupational exposure • Organ transplantation • Artificial insemination 10
  11. 11. LIFE CYCLE OF HIV 11
  12. 12. CDC SURVEILLANCE CASE CLASSIFICATION: • 1982- “presence of oppurtunistic illness or malignancies secondary to defective immunity in HIV+ individuals” • 1993-“ inclusion of severe immunodeficiency as definitive for AIDS” 12
  13. 13. AIDS patients have been grouped as follows, according to the CDC Surveillance Case Classification (1993);  Category A - Acute symptoms or asymptomatic diseases,.  Category B - Patients have symptomatic  Category C - Life-threatening conditions. 13
  14. 14. WHO classification of HIV-associated clinical disease CLINICAL STAGE 1 CLINICAL STAGE 2 CLINICAL STAGE 3 CLINICAL STAGE 4 Asymptomatic Unexplained moderate weight loss (<10) Unexplained severe weight loss (> 10%), diarrhoea /persistent fever (longer than one month) Pneumocystis pneumonia Persistent generalized lymphadenopathy Recurrent upper RTI Persistent oral candidiasis Recurrent bacterial pneumonia Herpes zoster Oral hairy leukoplakia Chronic herpes simplex infection Angular cheilitis Pulmonary tuberculosis Oesophageal candidiasis Recurrent oral ulceration Severe bacterial infections Extrapulmonary tuberculosis Papular pruritic eruptions Acute necrotizing ulcerative stomatitis, gingivitis/periodontitis Kaposi sarcoma /Lymphoma/Invasive cervical carcinoma Fungal nail infection Unexplained anaemia (<8 g/dl ), neutropenia (< 0.5 x 109/l) and chronic thrombocytopenia (< 50) Cytomegalovirus infection Central nervous system toxoplasmosis HIV encephalopathy Extra pulmonary cryptococcosis including meningitis Disseminated non-tuberculous mycobacteria infection Chronic cryptosporidiosis Chronic isosporiasis Disseminated mycosis Atypical disseminated leishmaniasis Symptomatic HIV-associated nephropathy or HIV-associated cardiomyopathy
  15. 15. Classification and diagnostic criteria for oral lesions in HIV infection. 1993 revised Group 1: Lesions strongly associated with HIV infection  Candidiasis Erythematous Pseudomembranous  Hairy leukoplakia  Kaposi’s sarcoma  Non-Hodgkin’s lymphoma Periodontal disease  Linear gingival erythema  Necrotizing (ulcerative) gingivitis  Necrotizing (ulcerative) periodontitis 15
  16. 16. Group 2: Lesions less commonly associated with HIV infection:  Bacterial infections like  Mycobacterium avium - in tracellulare  Mycobacterium tuberculosis  Melanotic hyperpigmentation  Necrotizing (ulcerative) stomatitis  Salivary gland disease  Thrombocytopenic purpura  Ulceration not otherwise specified  Viral infections  Dry mouth due to decreased salivary flow rate  Unilateral or bilateral swelling of major salivary glands 16
  17. 17. • Group 3. Lesions seen in HIV infection  Bacterial infections like  Actinomyces israelii  Escherichia coli  Klebsiella pneumoniae  Cat-scratch disease  Drug reactions (ulcerative, erythema multiforme,  lichenoid, toxic epidermolysis)  Epithelioid (bacillary) angiomatosis 17
  18. 18. Fungal infection other than candidiasis  -Cryptococcus neoformans  -Geotrichum candidum  -Histoplasma capsulatum  -Mucoraceae (mucormycosis / zygomycosis)  -Aspergillus flavus Nervous system disturbances  -Facial palsy  -Trigeminal neuralgia  Recurrent aphthous stomatitis Viral infections  Cytomegalovirus  Molluscum contagiosum 18
  19. 19. MEDICAL MANAGEMENT 19
  20. 20. ANTI-RETROVIRAL DRUGS One that blocks binding of HIV to target cells One that blocks viral RNA clevage One that inhibits enzyme reverse transcriptase 20
  21. 21. IDEAL REQUIREMENTS 1. Should be as specific as possible. 2. Should reduce viral production from infected cells. 3. Can be administered orally. 4. Should cross blood- brain barrier easily. 5. Should not develop resistance. 6. Shouldn’t be toxic. 21
  22. 22. ART… • Zidovudine (AZT, ZDV) • Retrovir • Didanosine • Videx • Zalcitabine • Hivid • Stavudine • Zerit 22 Nucleoside - stop HIV from replicating within cells by inhibiting the reverse transcriptase protein.
  23. 23. ART… • Nevirapine • Viramine • Delaviradine • Rescriptor • Efavirenz • Sustiva 23 Non-nucleoside Reverse transcriptase inhibitors- stop HIV replicating within cells by interfering with HIV's reverse transcriptase protein which it needs to make new copies of itself
  24. 24. ART… • . • Saquinavir • Invirase • fortovase • Ritonavir • Norvir • Indinavir • Crixivan • Relfiravir • Viracept 24 Protease inhibitors- binds to the protease molecules and interfere with its cleaving function and are more effective viral inhibitors:
  25. 25. “COCKTAIL” OR TRIPLE-THERAPY • HAART • Regimens include atleast one protease inhibitor or non- nucleoside reverse transcriptse inhibitor in addition to one or more nucleoside reverse transcriptase inhibitors • SIDE EFFECTS 25
  26. 26. • Hemo-Modulator 26 works by filtering a patient's blood through the device which blasts ultraviolet light onto the blood. The ultraviolet light effectively kills the virus and jump starts the patient's immune system.
  27. 27. PROBIOTICS FOR HIV • Lin Tao (2008) and his colleagues screened hundreds of bacteria taken from the saliva of volunteers. Results showed that some lactobacillus strains had produced proteins capable of binding a sugar found on HIV envelope, called mannose. • One strain secreted abundant mannose-binding protein particles into its surroundings, neutralizing HIV by binding to its sugar coating. 27
  28. 28. WHAT’S THE ROLE OF DENTIST????? • 1. Provides routine dental care for HIV-infected individuals. • 2. Understands the significance of oral lesions associated with HIV disease, and performs evaluations, diagnostics, and institutes treatment • 3. Collaborates with other health care workers and social support systems involved in the overall care of HIV-infected patients. 28
  29. 29. LESIONS COMMONLY ASSOCIATED WITH HIV INFECTION 29
  30. 30. 30 Pseudomembranous Candidiasis Erythematous candidiasis Hyperplastic candidiasis Angular cheilitis ORAL CANDIDIASIS
  31. 31. MANAGEMENT • 1. More advanced lesions including hyperplastic candidiasis may require systemic antifungal drugs. • 2. Early oral lesions of HIV-related candidiasis are usually responsive to topical antifungal therapy. • 3. Most oral topical antifungal agents contain large quantities of sucrose, which may be cariogenic after long-term use. • 4. Sucrose-free nystatin, itraconazole and amphotericin-B are available. • 5. Fluconazole oral suspension, chlorhexidine and cetyl pyridinium chloride oral rinses may also be effective against oral candidal infection. • 6. Systemic antifungal agents such as ketoconazole, fluconazole, itraconazole and amphotericin-B are effective in treatment of oral candidiasis. 31
  32. 32.  long-term use of ketoconazole may induce liver damage in individuals with preexistent liver disease.  The increased risk of chronic hepatitis B or hepatitis C infection in immunosuppressed individuals may put some patients at risk for ketoconazole induced liver damage.  If ketoconazole is prescribed, patients should receive liver function tests at baseline and at least monthly during therapy.  The drug is contraindicated if the patient's aspartate transaminase (AST) level is greater than 2.5 times normal.  Its absorption also may be hampered by the gastropathy experienced by many HIV-infected individuals 32
  33. 33. • TOPICAL DRUGS • 1.Clotrimazole 10mg tablets: dissolve in mouth 3-5tablets daily for 7-14days • 2.Nystatin • 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) disolve 1-2 pastilles in mouth,4-5times daily. • e.Ointment 15g tube: Apply to affected area 3-4times daily. • 3. Clotrimazole ointment 15g tube: apply to affected area qid. • 4. Miconazole 2% ointment 15g tube: qid application. • 5. Itraconazole oral suspension 100-200mg once daily for 7-28 days. • 6. Fluconazole oral suspension 200mg of 1st day followed by 100mg once daily for atleast 2weeks. • 7. Amphotericin B oral suspension 100mg four times daily for 2 weeks.
  34. 34. 34 SYSTEMIC DRUGS 1. Ketoconazole (Nyzoral) 200mg tablets: take 2 tablets immediately, then 1-2 tablets daily for 5-14days. 2. Fluconazole (Diflucan) 100mg tablets: take 2 tablets immediately, then 1 tablet daily for 7-14 days. 3. Itraconazole (Sporanox) 100mg capsules: 200mg once daily with meals for 4 weeks.
  35. 35. ORAL HAIRY LEUKOPLAKIA • Microscopically, the lesion shows A hyperparakeratotic surface with projections that often resemble hairs. • Beneath parakeratotic surface are acanthosis and some characteristic balloon cells resembling koilocytes. • Epithelial displasia is not a feature and in most OHL lesions little or no inflammatory infiltrate in underlying C.T is seen 35
  36. 36. MANAGEMENT: • 1. Oral hairy leukoplakia generally does not require treatment. • 2. Resolution has been reported after therapy with acyclovir, zidovudine, podophyllin and interferon, but usually recurs when treatment is discontinued. • 3. Laser or Conventional surgery. • 4. The incidence of OHL has been markedly reduced since the advent of multidrug antiviral therapy for HIV infection. 36
  37. 37. NON-HODGKIN’S LYMPHOMA • Occurrence is more common in the gingiva. • Has a characteristic white verrucous surface or necrosis of the gingiva resembling ANUG. • TREATMENT • 1. Anti-malignancy drugs • 2. Surgical excision • 3. Radiation therapy 37
  38. 38. KAPOSI’S SARCOMA • Kaposi’s sarcoma is a rare, multifocal vascular. • Median survival time after onset of KS is 7 to 31 months • Histologic picture: • Endothelial cell proliferation with formation of atypical vascular channels • Extravascular hemorrhage with hemosiderin deposition • Spindle cell proliferation • Mononuclear inflammatory infiltrate, consisting mainly of plasma cells 38
  39. 39. MANAGEMENT • 1. Treatment includes use of antiretroviral agents, laser excision, radiation therapy or intralesional injection with vinblastine, interferon α, or other chemotherapeutic drugs. • 2. Nicholas et al in 1993 described the successful use of intralesional injection of vinblastine at a dosage of 0.1 mg/cm2 using a 0.2mg/ml solution of vinblastine sulfate in saline. • 3. Intralesional injections with sodium tetradecyl sulfate 39
  40. 40. • Destructive periodontitis has also been reported in conjunction with gingival KS. In such instances, scaling and root planing and other periodontal therapy may be indicated in addition to intralesional or systemic chemotherapy. 40
  41. 41. ATYPICAL ULCERATIONS • Most reported oral ulcers are to herpes simplex virus, CMV, EBV, histoplasmosis, herpes zoster and mainly recurrent apthous ulcers are often associated. • Resistant viral strains are treated with foscarnet, ganciclovir or valacyclovir hydrochloride. • Topical corticosteroid therapy (fluocinonide gel applied three to six times daily) is safe 41
  42. 42. ORAL HYPERPIGMENTATION: • 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. Oral pigmentation may be caused by:  Adrenocorticoid insufficiency caused by prolonged use of ketoconazole  Pneumocystitis carinii infection  Cytomegalovirus infection 42
  43. 43. PERIODONTALCONSIDERATIONS 43
  44. 44. Periodontal considerations…  Dennisn et al- first report linking periodontal disease and HIV  Parra & slots- HIV in GCF  Barr et al- HIV RNA quantification in oral fluids  Shugers et al- serum viral load corelates with the salivary viral load  Mononuclear cells present in GCF harbour HIV-1 DNA that represents as a sourse of HIV in the oral cavity in the presence or absence of bleeding- Maticic et al. 2000 44
  45. 45. LINEAR GINGIVAL ERYTHEMA: Clinical features: • A persistent, linear, easily bleeding, erythematous gingivitis (LGE) has been described in some HIV-positive patients. • May be localised or generalised • No evidence of pocketing or attachment loss. 45
  46. 46. Causes and pathogenesis • candidal infection-Robinson • Velegrakiet et al - Candida dubliniensis • Winkler et al- CD4+ T cell depletion • Barr et al 46
  47. 47. LGE treatment… Treatment: - Does not respond well to plaque removal - Conventional therapy plus rinsing with 0.12% chlorhexidine gluconate twice daily has shown significant improvement after 3 months (Grassi M et al). - Povidone-iodine substantially reduced pain associated with the lesions (winkler et al). 47
  48. 48. LGE treatment… • Step 1: Instruct the patient in performance of meticulous oral hygiene. • Step 2: Oral prophylaxis. • Step 3: Chlorhexidine gluconate mouthrinse. • Step 4: Reevaluate the patient in 2 to 3 weeks. If lesions persist, evaluate for possible candidiasis. Consider empiric administration of a systemic antifungal agent such as fluconazole for 7 to 10 days. • Step 5: Re-treat if necessary. • Step 6: Place the patient on 2- to 3-month recall. 48
  49. 49. NECROTIZING GINGIVITIS: Clinical features: • HIV-related necrotizing gingivitis is defined by EC-WHO as destruction of one or more interdental papillae. • In the acute stage -ulceration, necrosis and sloughing may be seen with ready hemorrhage and characteristic fetor • The anterior gingiva is most commonly affected (Greenspan1993). 49
  50. 50. NUG… • Causes and pathogenesis • The isolated organisms include Borrelia, gram-positive cocci, P-hemolytic streptococci and C. albicans (reichert et al) • Thompson et al • Barr et al 50
  51. 51. Treatment • Basic treatment may consist of cleaning and debridement of affected areas with a cotton pellet soaked in peroxide after application of a topical anesthetic. • Escharotic oral rinses such as hydrogen peroxide should only rarely be used, however, and are especially contraindicated in immuno-compromised individuals. • Patient should be seen daily or every other day for the first week • 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. 51
  52. 52. NUG… • Does not always respond to conventional treatment with scaling and improved oral hygiene (winkler jr et al). • Adjunctive use of metronidazole & Antimycotic agents in these patients is reported to be extremely effective in reducing acute pain and promoting rapid healing (scully et al) 52
  53. 53. NECROTIZING PERIODONTITIS: • Clinical features: • According to the description by EC- WHO necrotizing periodontitis is periodontitis characterized by soft tissue loss as a result of ulceration or necrosis. Exposure, destruction or sequestration of bone may be seen. • The distinctive feature- loss attachment 53
  54. 54. NUP… • NUP is severely painful in onset and immediate therapy is necessary • On occasions, however, patients undergo spontaneous resolution of the lesions, leaving painless, deep interproximal craters that are difficult to clean and may lead to conventional periodontitis 54
  55. 55. NUP… Causes and pathogenesis: • Higher proportions of C. albicans and C. rectus. - Debilitating health and progression of disease - However, some studies have also indicated that the association between HIV-related immune depletion and periodontal destruction is less strong (Martinez-Canut P, Guarinos J, jp 1996) 55
  56. 56. Treatment  Local debridement  Scaling and Root planing,  Irrigation with an effective antimicrobial agent. In severe NUP, antibiotic therapy may be necessary but should be used with caution in HIV-infected patients to avoid an opportunistic and potentially serious localized candidiasis or even candidal septicemia. 56
  57. 57. NUP… • Does not always respond to conventional treatment with scaling and improved oral hygiene (winkler jr et al). • Prophylactic prescription of a topical or systemic antifungal agent is prudent if an antibiotic is used. • 57
  58. 58. INDICATIONS FOR HIV TESTING OF DENTAL PATIENTS 58
  59. 59. DIAGNOSTIC TESTS: DIAGNOSTIC TESTS ELISA WESTERN BLOT (WB) (PCR) P24 ANTIGEN LAB-ON-A-CHIP 59
  60. 60. 60
  61. 61. OCCUPATIONAL EXPOSURES AND POSTEXPOSURE PROPHYLAXIS (PEP): 61
  62. 62. 62
  63. 63. GENERAL PRECAUTIONS TO BE TAKEN • 1. Surgical gloves should be worn when touching blood, saliva or mucous membranes. • 2. Surgical masks and protective eyewear should be worn. • 3. Disposable or washable gowns should be used. • 4. Instruments should be sterilized by autoclaving. • 5. Debris should be removed by scrubbing with soap and water before sterilization. 63
  64. 64. GENERAL PRECAUTIONS TO BE TAKEN… • 6. Surfaces should be decontaminated with sodium hypochlorite. • 7. Needles should be disposed with safety guard. • 8. Droplets and aerosol production should be avoided where possible by use of rubber dam and high-speed evacuation. • 9. Apparent Fumigation of the operating room is required as a part of disinfection. 64
  65. 65. CONCLUSION: The pathogenesis periodontal diseases in HIV+ subjects may be due to the microflora, the effects of HIV and other viral agents, and/or alterations in the host response. These factors should be taken into consideration in the treatment and prevention of periodontal diseases in the HIV patient. 65
  66. 66. REFERENCES • Textbook of clinical periodontology- Carranza 10th Edition • Textbook of clinical periodontology- Carranza 9th Edition • Textbook of periodontology and implantology- Linde 5th Edition • Textbook of periodontology- Rose & Mealey • Textbook of periodontology- Eley & Manson • Textbook of Microbiology- AnanthNarayana • Textbook of Immunology- Roitt’s • The American Academy of Oral Medicine, Clinician’s guide to HIV- infected patients. 3rd Edition. • Periodontology 2000,vol 60, 2012: 78-97 • Periodontology 2000,Vol 50, 2009: 52–64 • Periodontology 2000,vol 44, 2007: 55-81 66
  67. 67. References… • DCNA 2003, 467-492 • R.G. Nair et al. Coinfections associated with HIV infection: Workshop 1A. Adv Dent Res 2011;23(1): 97- 105 • Scheutz F et al. Is there an association between periodontal condition and HIV infection. JCP 1997, 24: 580-587 • Murray et al. the Microbiology of HIV- Associated periodontal lesions. JCP 1989; 16: 636-642 • Angelika Langford. Gingival and periodontal alterations associated with infection with HIV. Quintessence Int 1994; 25: 375-387 • http://www.ambha.org/new-hiv-aids-treatment- methods.html 67
  68. 68. 68 Thank u…

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