pptx on Aids & periodontium

1. AIDS AND
PERIODONTIUM

2. CONTENTS
Introduction
History and nomenclature
Transmission of HIV
Factors increasing the risk of HIV
Classifying periodontal diseases in aids patients
Pathogenesis
Periodontal pathologies in hiv infected patients
Diagnosis and management of HIV associated lesion
Haart therapy
Conclusion

3. INTRODUCTION
AIDS is the most severe manifestation of a clinical spectrum of illness resulting from
infection with the immunodeficiency virus and characterized by a defect in cell
mediated immunity that results in susceptibility to Opportunistic Infections And
Neoplasms.
Globally, at least 20 million people are infected with the virus and at least 3 million
have died.
The exact origin of HIV-1 is unknown, although one early theory stated that it could
have come from Green monkeys in central Africa.
AIDS is the major complication of HIV-1 infection.

4. History and Nomenclature
Officially recognized for the first time in - June 1981 , at the CDC (Centre for
Disease Control) USA, in previously healthy homosexual men dying with
Pneumocystis Carinii Pneumonia and Candidiasis.
The virus causing AIDS was independently identified by a
team of French scientists led by Dr. Luc Montagnier who named it as LAV
(lymphadenopathy associated virus) and
by a team of Americans led by Dr.Robert C. Galow who named it as HTLV-III
(Human T-lymphocytotrophic virus-III), both in 1983.
The International committee on nomenclature of viruses named it “The HIV” in
1986. To date, 2 types of HIV have been identified, HIV-1 and HIV-2.

5. 1992 - CDC reports the first and only, dentist to patient HIV transmission -
Patient -Kimberley Bergalis
Dentist -Dr. David Acer.
1993 - CDC redefines AIDS by including immune suppression and additional
opportunistic infections.
1995-96 -Introduction of HAART (Highly Active Anti Retroviral Therapy).
1997 - CDC reports the first case of probably HIV transmission through deep kissing
in presence of periodontal disease.

6. Modes of transmission
HIV – present in high quantity - blood,semen, cerebrospinal fluid, and other body
fluid; breast milk & saliva
Exposure – dependent on –
integrity of exposed site.
type and volume of body fluid
viral load
Transmission risk - over 90% - for blood or blood product
- 15-40% - for the vertical route
- 0.5-1 % - for injection drug use
- 0.2% -0.5% - for genital mucus
membrane
- 0.1% - for non genital mucus membrane
Major route of transmission ( > 75 % )- Heterosexual

7. Factors increasing the risk of HIV

8. CLASSIFYING PERIODONTAL DISEASES IN AIDS PATIENTS
Severe forms of periodontal diseases known to be associated with immune system
defects. Different HIV-related periodontal disease classifications have been presented.

9. According to the CDC Surveillance Case Classification (1993) AIDS patients have been grouped as follows:
Laboratory categories:
Category 1: ≥ 500 CD4 lymphocytes/mm3
Category 2: 200 to 499 CD4 lymphocytes/mm3
Category 3: < 200 CD4 lymphocytes/mm3
HIV associated periodontal diseases are categorized as follow:
1. HIV-associated gingivitis (HIV-G)
2. HIV- associated periodontitis (HIV-P)
3. NUG
4. Necrotizing stomatitis (NS)
In a later classification it was considered important to drop the term HIV, because any of those conditions
could also be found in non-HIV-infected subjects. The HIV associated periodontal lesions accepted by the EC
Clearing house 1993 includes:
1. Linear gingival erythema (LGE), a non-plaque induced gingivitis exhibiting a distinct erythematous band of
the marginal gingiva, which either diffuses or punctuates erythema of the attached gingiva.

10. 2. Necrotizing periodontal diseases, which are subclassified as necrotizing ulcerative
gingivitis (NUG), necrotizing ulcerative periodontitis (NUP), and necrotizing stomatitis
(NS).
NUG involves destruction of one or more interdental papillae and is limited to the
marginal gingiva. NUP extends beyond the papillae and marginal gingiva, causing loss
of periodontal attachment, possibly exposing bone.
When the necrosis extends beyond the periodontium into the mucosa and osseous
tissue, it results in NS. These three conditions appear to be different stages of the
same disease. The only distinction appears to be their severity.

11. PATHOGENESIS
Periodontitis is a multifactorial disease where environmental, genetic and systemic
conditions play a role together with altered host response and this interplay may be
even more significant than the microbial challenge.
Risk factors for periodontitis in HIV-positive patients are age, smoking, viral load,
micro-organisms (viz. Fusobacterium nucleatum, Prevotella intermedia,
Aggregatibacter actinomycetemcomitans) andenzymes (viz. GCF neutrophil elastase
and beta glucuronidase).
immunosuppression is a risk factor for gingival inflammation. The attachment loss of
HIVpositive patients can also be caused by lifestyle factors such as smoking habits and
poor oral hygiene rather than HIV infection alone.
There are indications that periodontitis progresses more rapidly in HIV-positive
patients than in HIV-negative patients. Still, there is generally no difference in
periodontopathogens of HIVpositive or HIV-negative patients.
Alterations in local host response could explain the accelerating rate of chronic
periodontitis in HIV-positive patients. Both local and systemic host inflammatory and
humoral immune responses in HIV infection may play a role in the progression of
periodontal disease

13. PERIODONTAL PATHOLOGIES IN HIV INFECTED PATIENTS
Linear gingival erythema (LGE):
defined as a gingival manifestation of immunosuppressed patients which is
characterized by a distinct linear erythema limited to the free gingival margin.
The lack of response of linear gingival erythema to conventional periodontal
therapy, including plaque control, scaling and root planing is a key diagnostic feature
of linear gingival erythema.
Another key feature of LGE is its association with Candida infection (Candida
dubliniensis). Linear gingival erythema presents as a red band along the gingival
margin and may or may not be accompanied by occasional bleeding and discomfort.
It is seen most frequently in association with anterior teeth. The microbiologic
findings are consistent with that of conventional periodontitis rather than gingivitis. It
is a potential clinical marker of HIV infection.

14. Treatment of Linear gingival
erythema (LGE):
• Meticulous oral hygiene
(severe oral hygiene
instructions)
• Scaling, sub-gingival
irrigation with
chlorhexidine.
Chlorhexidine digluconate
0.12% mouth wash.
• If persists, evaluate for
candidiasis and retreat if
necessary

15. Necrotizing ulcerative gingivitis (NUG): It is characterized by ulcerated, necrotic
papillae and gingival margins are covered by pseudo-membrane which is associated
with intense pain and spontaneous gingival bleeding. It frequently may or may not be
associated with depressed CD4+ T cell count.
Necrotizing ulcerative periodontitis (NUP):
It is a marker of severe immune suppression. The condition is characterized by
severe pain, loosening of teeth, bleeding, fetid odor, ulcerated gingival papilla, and
rapid loss of bone and soft tissue.
Patients often refer to the pain as deep jaw pain.
Other features include oral malodor, lymphadenopathy, fever and malaise.
The microbial flora is similar to that of chronic periodontitis, it has same pathogen
but at a higher level. There is evidence of increased prevalence of Candida. NUP is a
predictive marker for CD4+ lymphocyte count less than 200/mm

17. Treatment of
Necrotizing ulcerative
gingivitis (NUG):
• Debridement of
necrotic lesion and light
scaling
• Scaling and root
planing • Chlorhexidine
digluconate 0.12%
mouth wash.
• Meticulous oral
hygiene.
• Antibiotic:
Metronidazole 400 mg
b.i.d for 5-7 days
Treatment of
Necrotizing ulcerative
periodontitis (NUP):
• Scaling, root planing
and subgingival
irrigation.
• Removal of necrotic
soft tissues utilizing a
0.12% chlorhexidine
digluconate or 10%
povidone-iodine lavage
• Antibiotic:
Metronidazole 400 mg
b.i.d for a week
• Prophylactic systemic
antifungal agent.
• Frequent follow-up
visits.

18. HIV Associated Periodontitis
HIV-associated periodontitis – resembles ANUG superimposed on a rapidly
progressive periodontitis.
Severe pain, gingival bleeding, extensive soft tissue necrosis, rapid & severe loss
of periodontal attachment , exposure of bone.
Attachment loss of more than 90% - 3-6 months .
Soft tissue cratering & interproximal necrosis & ulceration.
Deep aching bone – “hit the jaw bone”
Presence of blood clots – at the affected soft tissue ( noctural bleeding ).
Along with bone destruction – soft tissue necrosis – results in typically shallow pocket
– severe gingival recession

19. Mainly localized – severe soft tissue necrosis surrounded by areas of normal tissue.
Most frequently seen in molar or incisor region.
Early lesion – similar to ANUG. Lesion of ANUG is restricted to soft tissue of
periodontium.
Moderate HIV-Associated Periodontitis - involves entire attached gingiva with
exposure and partial sequestration of bone to the mucogingival junction.
Severe HIV-associated periodontitis – extensive necrosis of soft tissue & underlying
bone.- frank mobility.
Necrosis of soft tissue progresses at a greater rate than the alveolar bone – denude &
sequester the bone (NOMA)

20. If untreated – progress to necrotizing stomatitis. ( life threatening).
Characterized by an acute, massively destructive ulcerative and necrotizing infection
of gingiva extending into palatal & mucosal tissue – exposure of bone.
Distinguishing feature from ANUG – necrosis beyond mucogingival junction into
palatoparyngeal and mucosal tissues.(D/D – cytomegalovirus infection )
Creation of oro-antral fistula – unusual complication.

23. Diagnosis and management of HIV associated lesion
Antimicrobial therapy - Metronidazole ( 250 mg 4times a day for 5days. ( oral
necrotizing ulcerative lesions ).
Microbiological analysis – fusobacterium nucleatum,porphyromonas
gingivalis,prevotella intemedia.
Antibiotics – causes candidal overgrowth.
Antifungal therapy – Clotrimazole Troches ( 10mg 5 times daily), Nystatin Vaginal
Tablets (1000000 u, 3times daily ), systemic fluconazole.
Chlorohexidine rinse
Linear gingival erythema – chlorohexidine rinse along with topical antifungal agents.

25. HAART (Highly Active Anti Retroviral Therapy)– combines various antiretroviral drugs,
protease inhibitors, and fusion inhibitors.
Treatment with HAART - ↑ in T4 cell level
- ↓ in plasma viral load.
Patients remain potentially infectious.
Initial exposure – develops acute symptoms ( sudden onset of Acute Mononucleosis like
illness) lasting 2- 3 weeks.
Seroconversion – 3- 8 weeks
Mean time from infection – to development of AIDS 15 Years or more.

26. The goal of antiretroviral therapy is to reduce the amount of virus in the body (viral
load) to a level that can no longer be detected with current blood tests.
1. Nucleoside/nucleotide reverse transcriptase inhibitors, also called nucleoside
analogs - such as Tenofovir, Emtricitabine, Lamivudine, And Abacavir.
2. Nonnucleoside reverse transcriptase inhibitors (NNRTIs), such as Efavirenz,
Nevirapine, Or Etravirine.

27. Protease inhibitors (PIs), such as Atazanavir, Saquinavir, Ritonavir, Indinavir, Nelfinavir,
Fosamprenavir, Lopinavir, Darunavir, Or Tipranavir.
5. Fusion and entry inhibitors, such as Enfuvirtide And Maraviroc.
6. Integrase inhibitors, such as Raltegravir
these drugs act at various points in the lifecycle of the virus and are administered with
the aim of reducing the viral load to undetectable levels to allow immune restoration.
HAART significantly increases absolute CD4+ lymphocyte counts, reduces HIV viral load
and improves survival, even in patients with very low absolute CD4+ lymphocyte
counts

28. Conclusion
Periodontal disease in HIV infected individuals present unique challenges in diagnosis,
monitoring treatment and maintainence.
The presence and severity of LGE, NUP,ANUG and other oral lesions may indicate the
presence of HIV infection. The prevalence of these lesions increase with progressive
impairment of the immune system.
These factors should be taken into consideration in the treatment and prevention of
periodontal diseases in HIV patient.