Download to read offline
More Related Content
Similar to 14.HIV and periodontium.pptx
![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)
14.HIV and periodontium.pptx
- 1. HUMAN IMMUNODEFICIENCY VIRUS (HIV)and the periodontium Dr. D.Navya, MDS
- 2. INTRODUCTION • Virus thatcauses AIDS. • Formerly known as HTLV-III and lymphadenopathy-associated virus. • A retrovirus that primarily infects vital components of the human immune system such as CD4+ T cells, macrophages and dendritic cells. • It also directly and indirectly destroys CD4+ T cells.
- 3. Mode of transmission 1.Un protected sex 2. Sharing of needles 3. Unsafe Blood 4. Improperly sterilized hospital tools 5. Parent to child
- 4. SALIVA AND HIVTRANSMISSION: There is only a very slight evidence that HIV may be transmitted by saliva, for the following reasons. • Only a small amount of HIV infected individuals harbour the virus in whole saliva (e.g. in one study HIV was detected in mixed saliva of 5% of infected individuals and only in one of 15 parotid saliva samples).
- 5. • In anycase HIV virions cannot exist in cell free State in saliva, and estimates are that there is less than one infectious particle of HIV per milliliter of mixed saliva • Saliva contains IgA group antibodies to HIV proteins (p24, gp120, gp160) which may neutralize the infectivity of the virus.
- 6. • Other HIVinhibitory factors in saliva include high molecular weight mucins thought to entrap the virus, proline rich proteins, and a serine protease inhibitor termed salivary leucocyte protease inhibitor (SLPI). • The latter possibly blocks cell surface receptors needed for entry of HIV into the cells. • The virus looses its infectivity when exposed to mixed saliva for 30 minutes
- 7. PATHOGENESIS • Direct CellKilling: • Antigenic Diversity: • Receptor Signalling:
- 8. Direct Cell Killing: •This was the first mechanism suggested, based on the behaviour of certain laboratory isolates of HIV. • Subsequent experiments suggested that there is not sufficient virus present in AIDS patients to account for all the damage seen. • Although killing of CD4+ cells may contribute to the overall pattern of pathogenesis seen in AIDS. e.g. disturbances in cell biochemistry may also affect the regulation of the immune system:
- 9. Antigenic diversity • Thistheory holds that the continual generation of new antigenic variants eventually overcomes the immune system, leading to its collapse. There is no doubt that new antigenic variants of HIV constantly arise during the long course of AIDS • It has not been completely established how this might lead to the collapse of the immune system, but it is envisaged that there might be an effect, with each new variant contributing to the slight but irreversible decline in immune function.
- 10. Receptor signalling • Therehave been several reports that HIV binding to CD4 induces an intracellular signal which may have a detrimental effect on cells. • However, there is a second component to the HIV receptor which is required for cell entry: chemokine receptors such as CXCR4 & CCR5. • Although HIV-mediated signal transduction is not required for fusion & entry, at least some HIV isolates induce a signal when the envelope protein binds to CCR5.
- 11. CDC SURVILLANCE CASECLASSIFICATION AIDS PATIENTS HAVE BEEN GROUPED as follows according to the CDC classification 1993 Category A Includes patients with acute symptoms or asymptomatic diseases ,along with individuals with persistent generalized lymphadenopathy ,with or without malaise ,fatigue, or low grade fever
- 12. Category B; patients havesymptomatic conditions such as oropharyngeal or vulvo vaginal candidiasis, herpes zoster ,oral hairy leukoplakia,idiopathic thrombocytopenia or constitutional symptoms of fever , diarrhea, and weight loss
- 13. Category C; patients arethose with outright AIDS ,as manifested or identified through CD4 T lymphocyte levels or <200cells /mm3
- 14. Cell count Disease 400Most patients have no signs of immunosupression 301 to 400 Bacterial skin infection Staphylococcus 201 to 300 Herpes zoster Candidiasis Tinea pedia Oral hairy leukoplakia
- 15. 101 to 200Pneumocystis carnii Histoplasmosis Coccidiomycosis Cryptococcal Toxoplasmosis Herpes simplex Cryptosporidiosis Kaposi sarcoma 0 to 100 Wasting syndrome Cytomegalovirus Lymphoma Mycobacterium avium complex
- 16. STAGE OF ILLNESS Acute retroviral Syndrome Window Period HIV positive asympt omatic phase HIV positive symptomatic phase AIDS Symptoms Fever,skin rash Nil Nil Prolonged fever, recurrent common infections, TB, diarrhoea, Generalized lymphadenopathy AIDS defining illness, Opportunistic infections, wasting syndrome, dementia positive HIV test: ELISA/WB Onset Within 2 -4 weeks of infection From time of getting HIV infected 6-12 weeks after HIV infection About 2-5 years after HIV infection 5-10 years after getting HIV infection Diagnosis PCR Antigen test PCR or P 24 antigen test 3 ELISA or 1 WB & 1 ELISA 2 ELISA and 2 major symptoms 2 ELISA and AIDS defining illness Transmission of disease YES YES YES YES YES
- 17. DIAGNOSIS • It ispossible to diagnose HIV infection by isolating the virus itself from a blood sample or by demonstrating the presence of HIV antigen in the blood. • ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA) • WESTERN BLOT (IMMUNOBLOT) • POLYMERASE CHAIN REACTION (PCR)
- 18. GENERAL MANIFESTATIONS OFAIDS: • Clinical findings in Acute HIV syndrome include, GENERAL: • Fever, • Pharyngitis • lymphadenopathy • Headache / Retroorbital pain • Arthralgias / Myalgias • Lethargy /Malais • Nausea, Vomiting, Diarrhoea. • Anorexia / Weight loss,
- 19. NEUROLOGIC: • Meningitis, • Encephalitis, •Peripheral neuropathy DERMATOLOGIC : • Erythematous maculopapular rash • Mucocutaneous ulceration.
- 20. Severe weight loss Persistent headache High fever White patcheson tongue Heavy night sweats Loss of appetite Memory loss Chronic Diarrhea Fatigue & muscle weakness Swelling Lymph Nodes Symptoms of HIV infection
- 21. ORAL MANIFESTATIONS OFHIV INFECTION: • In 1993, European Commission (EC) clearing house on oral problems related to HIV Infection and WHO collaborating center on Oral Manifestations of Immuno-deficiency virus released following classifications.
- 22. Group 1: lesionsstrongly associated with HIV infection. 1. Candidiasis 2. Hairy Leukoplakia 3. Kaposi’s sarcoma 4. Non- Hodgkin’s lymphoma 5. periodontal diseases -Linear gingival erythema, -Necrotising ulcerative gingivitis, -Necrotising ulcerative periodontitis
- 23. Group 2: Lesionsless commonly associated with HIV infection 1 .Bacterial infections -Mycobacterium avium-intercellulare -Mycobacterium tuberculosis. 2. Melanotic hyperpigmentation 3. Necrotising ulcerative stomatitis
- 24. Group 3: Lesionsseen in Hiv infection 1.Bacterial infections -Actinomyces israelli -Escherichia coli -Klebsiella pneumoniae -Cat-scratch disease 2. Drug reactions (ulcerative, erythema multiformae, lichenoid reaction, toxic epidermolysis) 3. Epitheloid (bacillary) angiomatosis
- 25. Fungal infections otherthan candidiasis -Cryptococcus neoformans -Geotrictum candidum -Histoplasma neoformans -Miscoraceae (zygomycosis) -Aspergillus flavus
- 26. 5. Neurological disturbances -Facialpalsy -Trigeminal neuralgia 6. Recurrent apthous stomatitis(RAS) -Viral infections -CMV -Molluscum Contagiosum.
- 27. Oral candidiasis Etiology: candidaalbicans 4 clinical patterns are seen, 1.Pseudomembranous, 2.Erythema, 3.Hyperplastic 4.Angular cheilitis:
- 28. PSEUDOMEMBRANOUS • Presents aspainless or slightly sensitive • Yellowish-white curd like lesions that can be readily scraped and separated from the surface of the oral mucosa. • -Mostly seen on hard,soft palate, buccal and labial mucosa but can occur anywhere in the oral cavity
- 29.
- 31.
- 32. Diagnosis: • Diagnosed byits clinical appearance • PAS staining for candidal hyphae • Culturing organism on sabouraud’s agar • When oral candidiasis appears in patients with no apparent predisposing causes, the clinician should be alerted to the possibility of HIV infection.
- 33. Treatment: Topical drugs • Clotrimazole10 mg tablets 3 to 5 tab for 7 to14 days • Nystatin oral suspension 1,00,000u/ml administer 240ml rinse with 1tsp(5ml) • Clotrimozole ointment 15 gm tube apply to affected area • Itraconazole oral suspension 100 to 200 mg once daily for 7 to 28 days Systemic drugs: • ketaconazole, 200mg tabs take 2 tabs immediately, then 1 or 2 tabs daily with food for 5 to 14 days.
- 34. Etiology: Epstein BarrVirus (EBV) Clinical Features: • It appears bilaterally on lateral borders of the tongue as painless,faint white vertical streaks. (or) • Thickend & furrowed areas with shaggy keratotic surface with vertical striations imparting corrugated appearance. • Microscopically-lesion shows a hyperparakeratotic surface with projections that often resembles hairs. HAIRY LEUKOPLAKIA:
- 36. Histological features: • Epithelialhyperplasia with acanthosis & hyperkeratosis • Varying numbers of lightly stained,swollen,balloon cells in upper prickle cell layer are seen. • Dense aggregates of nuclear chromatin material marginated along the nuclear membrane known as nuclear beading is seen.
- 37. Treatment: • Use ofantiviral agents such as acyclovir or valacyclovir are often responsive. • Lesions can be successfully removed with laser of conventional surgery. • HAART has resulted in a greatly diminished incidence of OHL.
- 38. • It isa multifocal neoplasm of vascular endothelial origin. Etiology: Human Herpes virus-8 is involved. Clinical features: • Commonly palate, gingival, tongue & oropharynx are affected. • Red to purple macular nodular or raised & ulcerated lesions appear. • Colour darkens as the lesion ages. Kaposi sarcoma
- 42. Treatment: • The adventof HAART has resulted in a marked reduction in the incidence of kaposi sarcoma • Treatment can also be through antiretroviral agents • Laser excision, radiation therapy, and intralesional injection with vinblastine.
- 43. Non hodgkins lymphoma Etiology:Epstein-Barr virus. Clinical features: • Lesions present as a large, painful ulcerated mass on the palate or gingival tissues. Treatment: • Combination of chemotherapy & radiation
- 45. Periodontal diseases Etiology: In HIV-positivepatients, the predisposing factors include • Age, smoking, viral load Microorganisms such as • Fusobacterium nucleatum • Prevotella intermedia • Actinobacillus actinomycetemcomitens.
- 46. Clinical features: Periodontal lesionsinclude 1. Linear gingival erythema (LGE) – It is a non- plaque induced gingivitis which is erythematous. 2. Necrotising Ulcerative Periodontitis. 3. Necrotising Stomatis. 4.Chronic periodontitis.
- 47. Linear gingival erythema •It is a distinct fiery red band along the margin of gingiva • The amount of erythema is disproportionately intense for the amount of plaque • There is no ulceration present and according to EC – WHO criteria there is no evidence of pocketing or attachment loss • Charecerstic feature of this lesion is it doesnot respond well to improved oral hygiene
- 49. TREATMENT • Prominent featureis it does not respond to the plaque control. • Conventional therapy plus rinsing with 0.12% chlorhexidine gluconate twice daily has shown significant improvement after treatment in HIV uninfected patients • However HIV associated free gingival erythema did not respond to removal of plaque by intense scaling and root planing and improved plaque control alone or supplimented with povidine – iodine
- 50. Necrotizing ulcerative periodontitis •Necrosis and ulceration of the coronal portion of interdental papillae and gingiva margin. • Painful bright red marginal gingiva that bleeds easily. • Deep interdental osseous craters typical periodontal lesions of NUP. • Advanced lesions lead to severe bone loss, tooth mobility and ultimately tooth loss. • The periodontal attachment and bone loss is extremly rapid.
- 52. Necrotizing ulcerative gingivitis •NUG is characterized by sudden onset of symptoms • Lesions are punched out, crater like depressions at the crest of interdental papillae, extending to the marginal gingiva and rarely to the attached gingiva and oral mucosa. • The surface of gingival craters is covered by a gray, pseudomembranous slough demarcated from the remainder of gingival mucosa by a pronounced linear erythema.
- 54. TREATMENT • Basic treatmentmay consists of cleaning and debridement of affected areas with a cotton pellet soaked in peroxide after application of a topical anaesthetic. • An antimicrobial oral rinse such as chlorhexidine gluconate 0.12% given. • Systemic antibiotics such as metronidazole or amoxicillin given for patients with moderate to severe tissue destruction.
- 55. HERPES SIMPLEX VIRUS INFECTION: Clinically seen as vesicles on lip and adjacent facial skin which rapidly break down to produce shallow ulcers. Lesions on gingival, referred as Acute Herpetic Gingivostomatitis are seen. Lesions can be treated using acyclovir.
- 57. Aphthous ulcers • InHIV-infected patients, these ulcers are large and more extensive usually measure more than 2cm in diameter with regular borders. • It is characterised by development of painful, recurring solitary or multiple ulcerations of oral mucosa. • The apthous ulcer begins as a single or multiple superficial erosions covered by a grey membrane . • It has a well circumscribed margin surrounded by an erythematous halo.
- 59. Chronic periodontitis • Ithas been defined as an infectious disease resulting in inflammation of the supporting tissues of the teeth, progressive attachment and bone loss. Clinical findings • supragingival and subgingival accumulation • gingival inflammation • pocket formation • loss of periodontal attachment • loss of alveolar bone • occasional suppuration. • Gingival recession and early attachment loss are more common in HIV groups.
- 60. Treatment • Treatment decisionsshould be based on the overall Health Status of the patient Degree of potential involvement With proper home care and appropriate periodontal treatment and maintainance, HIV positive individuals can anticipate reasonably good periodontal health throughout the course of their disease.
- 61. Treatment • The Foodand Drug Administration (FDA) has approved a number of drugs for treating HIV infection. • The first group of drugs used to treat HIV infection, called nucleoside reverse transcriptase (RT) inhibitors, interrupts an early stage of the virus making copies of itself.
- 62. IF MOTHER ISHIV POSITIVE MOTHER • First 14 to 34 weeks Azathioprine has to be taken • Later HAART is prescribed INFANT • Baby should take an antiretroviral drug called ZIDOVIDINE syrup for 6 weeks after birth. • After 6 weeks TRIMETHOPRIM OR SULPHAMETHEZOLE (SEPTRA) for 6 weeks.
- 63. HIV VACCINES There arethree types of vaccines: Preventive: to protect against those people who are not already HIV positive Therapeutic: to stimulate the immune system in HIV positive individuals and prevent progression to AIDS. Prenatal: to prevent spread to the fetus in a pregnant woman.
- 64. Highly Active AntiretrovialTherapy (HAART) Fusion Inhibitor Nucleoside Analogs/ Nuceloside Reverse Transcriptase Inhibitors Non Nucleotide Reverse Transcriptase Inhibitors Protease Inhibitors
- 65.
- 66. The class ofdrugs, called nucleoside analogs, include • Zidovidine – 500mg / day in 2 to 4 divided doses • Didanosine – 200 mg twice daily • stavudine - 400mg twice daily • Lamivudine – 150 mg once daily for HIV
- 67. • The drugscalled protease inhibitors, interrupt the virus from making copies of itself at a later step in its life cycle. They include • Ritonavir – 600 mg twice daily • Indinavir – 800 mg thrice daily • Nelfinavir – 750 mg thrice daily
- 68.