Downloaded 357 times
Uploaded byDr Sachin Rathod
Aids and The Periodontium By Dr Sachin Rathod
This document discusses human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS). It covers the definition, classification, structure, pathogenesis and transmission of HIV. It also describes the oral manifestations of HIV/AIDS, including oral candidiasis, oral hairy leukoplakia, Kaposi's sarcoma and periodontal diseases. The management of oral diseases in HIV/AIDS patients is discussed, along with diagnosis and treatment of HIV/AIDS. Infection control procedures for treating AIDS patients in dental offices are also summarized.
More Related Content
Similar to Aids and The Periodontium By Dr Sachin Rathod
![Oral manifestations of AIDS - ACQUIRED IMMUNO DEFICIENCY SYNDROME [ HIV ].pptx](https://cdn.slidesharecdn.com/ss_thumbnails/oralmanifestationsofaids2-240622135504-d533f1c7-thumbnail.jpg?width=640&height=640&fit=bounds)
![Oral manifestations of Acqired Immuno Deficiency Syndrome [ AIDS ]](https://cdn.slidesharecdn.com/ss_thumbnails/oralmanifestationsofaids2-240622131031-9a5e01dc-thumbnail.jpg?width=640&height=640&fit=bounds)
Aids and The Periodontium By Dr Sachin Rathod
- 1.
- 3. • Definition • Epidemiology •Virus • Structure • Pathogenesis • Transmission & Prevention • Classification & Grading • Manifestations • General • Oral • Periodontal • Management of oral diseases • Diagnosis • Treatment of AIDS • The AIDS patient & the dental office
- 4. • Bangui (1985)definition • Exclusion criteria • Pronounced malnutrition • Cancer • Immunosuppressive treatment • Inclusion criteria • Important signs • weight loss > 10% body weight 4
- 5. • Very frequentsigns • continuous attack / repeated bouts of fever 3 • Diarrhoea > 1 month 3 • Other signs • relapsing Herpes 4 • oropharyngeal candidiasis 4 • Nuerological signs 2 • Generalised Kaposi s sarcoma 12 • The diagnosis of AIDS established when the score is equal or more than 12 • 1994 modification…
- 7. Group: Group VI(ssRNA-RT) Family: Retroviridae Genus: Lentivirus Species: Human immunodeficiency virus 1 Species: Human immunodeficiency virus 2
- 8. • Previous names…. • 120 nm in diameter , roughly spherical in shape • two copies of positive single-stranded RNA that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein p24 • matrix composed of the viral protein p17 surrounds the capsid • viral envelope which is composed of two layers of fatty molecules phospholipids
- 9. • High geneticvariability • Fast replication • High mutation rate • Recombinogenic property • Three groups – M, N & O – differ in ENV genes • M most common
- 10. • Heterosexual /Homosexual intercourse • Exposure to infected body fluids/ tissues • Intrauterine or perinatal
- 11. • Some peopleshow resistance to getting infected by HIV 1 or if infected in developing full blown AIDS…??? • Genetic mutation slows / stops progression • CCR5 affects the major coreceptor CKR5 which affects the entry of the virus into the cell • Vaccine for HIV ???
- 12. • WHO classification(1990) modified September 2005 • Stage I: HIV disease is asymptomatic and not categorized as AIDS • Stage II: includes minor mucocutaneous manifestations and recurrent upper resp tract infections • Stage III: includes unexplained chronic diarrhoea for longer than a month, severe bacterial infections and pulmonary tuberculosis • Stage IV: includes toxoplasmosis of the brain candidiasis of the esophagus, trachea bronchi or lungs and Kaposi’s sarcoma; these diseases are indicators of AIDS
- 13. • CDC (1993) •Category A – acute symptoms / asymptomatic conditions individuals with PGL without malaise , fever (low grade), fatigue • Category B – Symptomatic conditions oropharyngeal candidiasis, Herpes Zoster oral hairy leukoplakia, ITP Constitutional symptoms fever ,weight loss ,diarrhoea
- 14. • Category C– full blown AIDS CD4 count < 200/mm3 Candidiasis-trachea, bronchi, lungs Cervical cancer –invasive Toxoplasmosis brain Kaposis Sarcoma
- 15. Category Classification CD4level 1 Asymptomatic >/ 500/ mm3 2 AIDS related complex 200-499 cell/ mm3 3 AIDS < 200/ mm3
- 16. • General • Acute– fever, myalgia, arthralgia , pharyngitis diarrhoea, thrush, persistent generalized lymphadenopathy • ARC – Candidiasis mucosal, constitutional symptoms, Herpes Zoster, ITP, oral hairy leukoplakia, peripheral neuropathy • AIDS defining conditions- • Candidiasis ( pulmonary , esophageal) cervical cancer, coccidiomycosis, CMV infection, Kaposi Sarcoma
- 17. • Challecombe SJ,Greenspan J, Williams DM J Oral Path 1993; 22: 289-291
- 20. • Erythematous Candidiasis– • presumptive – red areas on the palate / dorsum • No definitive criteria-detection of candida organisms • Psuedomembranous Candidiasis- • White /yellow spots plaques, any part of the oral cavity • Response to anti fungal • Hairy Luekoplakia- • Bilateral whitish grey lesions (lateral margins), non scrapable • Demonstration of EBV
- 21. • Kaposi’s Sarcoma •Erythematous ,bluish , violaceous macules swellings • Biopsy • Non Hodgkins Lymphoma • firm, elastic reddish purplish • Biopsy
- 22. • Oral hairyluekoplakia- lat borders of tongue ,extends to ventral surface asymptomatic, keratotic areas vertical striae, corrugated appearance non scrapable, candidial superinfection strong indicator psuedo hairy luekoplakia in HIV –ve pts H/P…
- 23. • Diff diagnosis-lichen planus frictional keratosis geographic tongue cancer , dysplasia • Treatment – antiviral therapy but recurs after stoppage laser or conventional surgery , ART
- 24. • 90% patients •Psuedomembranous, • Erythematous and • Hyperplastic • Esophageal candidiasis – diagnostic sign • Diagnosis – smears • Recurrence rate high….
- 27. • Vascular proliferativedisorder • Rickettsiae like organisms , • Gingival – red, purplish edematous soft tissue destruction of pdl & bone • lesion seen , CD4 levels dip • Biopsy – epitheloid proliferation of angiogenic cells acute inflammatory cell infiltrate organism stains with Warthen starry silver stain
- 28. • Treatment –broad spectrum antibiotics conservative periodontal therapy excision of lesion
- 29. • Multifocal ,vascularneoplasm • HHV-8 –decreased immunocompetence activates the latent virus • Palate & Gingiva most common sites • Painless red macules, progress to nodular lesions • H/P…. • Diff diagnosis- hemangioma, varicosity bacillary angiomatosis , pyogenic granuloma
- 30. • Treatment –intralesional; injections of vinblastine 0.1 mg/cm2 or 0.2mg/ml saline • ART, interferon , • If destruction of periodontium ,conventional periodontal therapy
- 32. • Linear gingivalerythema • HIV ass gingivitis • Persistent linear, easily bleeding, erythematous gingiva • Disproportionate to amount of plaque, increased chances ofsmokers • No ulcerations , no pockets • No response to plaque control • Localised / generalised • Candida spp…. Candida dubliniensis • Periodontal pathogens seen in periodontitis (Gornisky’91) • CD4 count…. Barr C ’92
- 33. • no inflammatoryinfiltrate and increased blood vessels • Diff diagnosis – lichen planus pemphigoid plasma cell gingivitis • Treatment - Step 1: Instruct the patient in performance of meticulous oral hygiene. Step 2: Scale and polish affected areas, and perform subgingival irrigation with chlorhexidine.
- 34. Step 3: Prescribechlorhexidine 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.
- 36. • Necrotizing gingivitis. No attachment loss • Rapidly progressing into NUP • Difference b/w necrotizing periodontitis and necrotizing stomatitis • Initial – interdental papilla, moderate- att gingiva, tooth mobility , sequestration of crestal bone, extensive bone loss and necrosis of soft tissue • Fetor oris….
- 37. • Severe pain…. •No deep pockets, deep interdental craters • Bleeding on probing • Borrelia spp, gram positive spp, ß hemolytic streptococci C. albicans oppurtunistic spp also seen • Progression correlates with HIV disease and vice versa • NP strong predictor of prognosis…Glick ‘94
- 38. • Treatment –no improvement with conventional SRP • Adjunctive Metronidazole • Anti mycotic drugs
- 40. • Acute ulceronecroticdisorder, extremely painful • Extends from NUP • Exposes underlying bone • More severe but less common • Similar to NOMA • Life threatening strongly related to immune depletion
- 41. • HIV –strong indicator for developing periodontitis Lamster ‘98 • Lucht E’91 –correlates more to the CD4 count than Plaque index • Intensive oral care programs as soon as diagnosis of AIDS done….
- 43. • Antibody tests •Antigen tests • Virus isolation • Demonstration of viral NA • HIV viral load • CD4 counts • Antiviral susceptibility assays
- 44. • ELISA –biochemical technique • detects the presence of an antibody or an antigen in a sample. It uses two antibodies • One antibody is specific to the antigen. The other reacts to Ag-Ab complexes , and is coupled to an enzyme. chromogenic or fluorogenic substrate.
- 45. • View/quantify theresult using a spectrophotometer or other optical device • Enzyme acts as an amplifier …
- 46. • Analysis –qualitative or quantitative • Other types – sandwich competitive
- 47. • Western BlotAssay- individual proteins of HIV-1 lysate are separated using polyacrylamide gel electrophoresis. ↓ nitrocellulose paper and reacted with patients serum ↓ colored bands are produced
- 48. • Earliest detection–GAG, p24 • All HIV pts- ENV, gp120, gp41 • Positive- p24, p31, gp41, gp120 • All other patterns-indeterminate • Negative – no bands detected , not only viral bands
- 49. • Other criteria– presence of any two foll bands gp41, p24, gp120/gp 160 • Red cross – positive test – more than one –GAG, POL & ENV • TRI DOT- rapid HIV testing flow through device with an inbuilt internal control & two separate antigen dots for HIV -1 & 2
- 50. • HAART –Different classes of drugs target different stages • Reverse trancriptase inhibitors- • Nucleoside analogues • Non nucleoside analogues • Protease inhibitors – • Fusion inhibitors • Integrase inhibitors • Entry inhibitors-
- 51. • Fixed dosecombinations • Synergistic enhancers • Combination therapy- • Who should be treated???
- 52. • Limitations ….Mega HAART / salvage therapy • To reduce resistance • drug resistance –FOTO, WOWO • ADVERSE EFFECTS – Alopecia, diarrhoea, Fanconi syndrome, Hepatitis ,hyperbilirubinemia, hyperpigmentation, mental confusion peripheral neuropathy , Steven Johnsons syndrome
- 53. “ Value conflictsare visible most on the faces of those who suffer…. ”
- 54. • Risk oftransmission – low • Trace amounts of HIV in saliva- • Saliva inhibits infectivity of free virus & to a lesser extent ,virus within cells
- 55. • Principles ofinfection control - • take action to stay healthy • Avoid contact with blood • Limit the spread of blood • Make objects safe for use • Instruments – Critical, semi critical and non critical
- 56. • AIDS-diagnosis, treatmentandprevention • Glickman- IX edition • Periodontal medicine- Genco, Rose & Cohen • J Oral Path Med;93 :29:289-294 • Net references
- 57.