This document discusses oral manifestations associated with HIV/AIDS. It begins with statistics on the global HIV epidemic. It then describes the pathogenesis of HIV, including how the virus binds to and infects host cells. Several oral conditions are described that are more common in HIV-positive individuals, such as oral candidiasis, oral hairy leukoplakia, Kaposi's sarcoma, and non-Hodgkin's lymphoma. Periodontal manifestations like necrotizing periodontal diseases are also discussed. The document concludes with treatments for oral lesions and how the introduction of antiretroviral therapy has reduced the frequency of oral conditions related to HIV/AIDS.

1. GOOD MORNING

2. AIDS AND PERIODONTIUM

3. CONTENTS
• INTRODUCTION
• STATISTICS
• PATHOGENESIS
• ORAL MANIFESTATIONS
• PERIODONTAL MANIFESTATIONS
• TREATMENT PROTOCOL
• CONCLUSION

4. • ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) IS
CHARACTERIZED BY PROFOUND IMPAIRMENT OF THE
IMMUNE SYSTEM.
THE CONDITION WAS FIRST REPORTED IN 1981, AND A
VIRAL PATHOGEN, THE HUMAN IMMUNODEFICIENCY
VIRUS (HIV), WAS IDENTIFIED IN 1984. THECONDITION
WAS ORIGINALLY THOUGHT TO BE RESTRICTED TO
MALE HOMOSEXUALS.
INTRODUCTION

5. • Subsequently, it was also identified in male and
female heterosexuals and bisexuals who
participated in unprotectedsexual activities or who
abused injected drugs.
Currently, sexual activity and drug abuse remain
the primary means of transmission.

6. • India has the third largest Hiv epidemic in the world
• 37.7 million people globally were living with HIV in
2020.
• 1.5 million people became newly infected with HIV in
2020.
• 680000 people died from AIDS related illness 2020.
• 79.3 million people have become infected with HIV
since the start of epidemic.
• 36.3 million people have died from AIDS related
illness since the start of the epidemic .
STATISTICS

7. CDC CLASSIFICATION
Category A:
• Patient with acute symptoms are assymptomatic
with persistent generalized lymphadenopathy with or
without malaise,fatigue or low grade fever.CD4 cells
greater than or equal to 500cells/mm3
Category B:
• Symptomatic conditions like oropharyngeal or
vulvovaginal candidiasis, Herpes zoster,oral hairy
leukoplakias,idiopathic thrombocytopenia or
constitutional symptoms of fever,diarrhea,and weight
loss.cd4 cells greater than 200-499cells /mm3

8. Category c
Patients with life threatening conditions
CD4+ T lymphocytes less than 200cells
/mm3.

9. PATHOGENESIS
• Binding and fusion : Hiv begins its
life cycle when it binds to a CD4
receptor and one of two co
receptors on the surface of CD4+
T-lymphocyte
• The virus then fuses with the host
cell.
• After fusion,the virus releases
RNA,its genetic material,into the
host cell.

10. • REVERSE TRANSCRIPTION : An HIV enzyme called
reverse transcriptase converts the single stranded HIV
RNA to double stranded HIV DNA
• INTEGRATION : The newly formed HIv DNA enters the
host cell's nucleus , where an HIV enzyme integrase
"hides" the HIV DNA within the host cell's own DNA
• The virus may remain inactive for several
years,producing few or no new copies of HIV.

11. • TRANSCRIPTION :When the host cell receives a
signal to become active, the previous uses a host
enzyme called RNA polymerase to create copies of
the HIV genomic material , as well as shorter
strands of RNA (mRNA).
• The mRNA is used as a blueprint to make long
chains of HIV proteins.

12. ORAL MANIFESTATIONS
*Oral candidiasis
*Oral hairy leukoplakia
*Kaposi sarcoma
*Non Hodgkin lymphoma
*Bacillary Angiomatosis
*Oral hyperpigmentation
*Atypical ulcers
*Recurrent Aphthous
stomatitis
*Salivary gland disorders
and xerostomia
PERIODONTAL
MANIFESTATIONS
• Linear gingival erythema
• Necrotizing ulcerative
gingivitis
• Necrotizing ulcerative
periodontitis
• Necrotizing ulcerative
stomatitis
• Chronic periodontitis

13. • oral lesions are common in Hiv-infected
patients,although geographic and environmental
variables may exist.
• Previous reports have indicated that most patients
with AIDS have head and neck lesions,whereas
oral lesions are common among HIV positive
individuals who do not yet have AIDS.
• Several reports have identified a strong correlation
between HIV infection and oral candidiasis, oral
hairy leukoplakia, atypical periodontal diseases,
oral kaposi sarcoma,and oral non hodgkin
Oral lesions

14. • Oral lesions less strongly associated with HIV infection include
melanotic hyperpigmentation,mycobacterial infections,
necrotizing ulcerative stomatitis (NUS),miscellaneous oral
ulceration,and viral infections (herpes simplex virus(HSV),herpes
zoster,and condyloma acuminatum).
• Lesions that are seen in HIV infected individuals with
undetermined frequency include less common viral infections
(e.g., CMV, molluscum contagiosum), recurrent apthous
stomatitis, and bacillary angiomatosis.
• The advent of HAART has resuited in a greatly diminished
frequency of oral lesion associated with HIV infection and AIDS.

15. ORAL CANDIDIASIS
• Candidiasis is the most common oral
lesion associated with HIV disease,and
it has been found in approximately
90%of patients with AIDS.
• Pseudomembranous Candidiasis
(thrush) presents as painless or
slightly sensitive, yellow-white,curd
like lesions that can be readily scraped
and separated from the surface of the
oral mucosa.This type is most common
on the hard and soft palate and the
buccal or labial mucosa,but it can

16. ERYTHEMATOUS
CANDIDIASIS
• It may be present as a
component of the
psedomembranous type,
appearing as red patches on the
buccal or palatalmucosa, or it
may be associated with
depapillation of the tongue.
• If the gingiva is affected, it may
be misdiagnosed as
desquamative gingivitis.

17. HYPERPLASTIC
CANDIDIASIS
• It is the least common
form,and it may be seen in
the buccal mucosa and the
tongue.
• It is more resistant to
removal than the other
types.

18. CANDIDA RELATED
ANGULAR CHEILITIS
• In candida related angular
cheilitis, the commissures
of the lips appear
erythematous ,with surface
crusting and fissuring.

19. ORAL HAIRY
LEUKOPLAKIA
• It primarily occurs in persons
with Hiv infection.It is found on
the lateral borders of the
tongue,it frequently has a
bilateral distribution, and it
may extend to the ventrum.
• OHL is caused by the Epstein
Barr virus.The lesion is
characterized by
asymptomatic,poorly
demarcated,keratotic area that
ranges in size from a few
millimeters to several

20. • Often,vertical striations are present,and these
impart a corrugated appearance .,surface
may also be shaggy and appear hairy when
dried.The lesion does not rub off,and it may
resemble other kerototic oral lesions.

21. KAPOSI'S SARCOMA
• Oral malignancies occur more
frequently in severely
immunocompromised
individuals than in the general
population.
• An HIV positive individuals with
Non Hodgkins lymphoma or
kaposi's sarcoma is
characterized as AIDS.

22. • It is the most common oral malignancy associated with
AIDS.This angioproliferative tumor is a rare,
multifocal, vascular neoplasm;it was originally
described in 1872 as occurring in the skin of lower
extremities of older men of Mediterranean origin.
• The causative agent has been identified as human
herpes virus-8.

23. • Lymphedema of the neck and face has been reported in
association with oral lesions.
• During the early stages,the oral lesions are painless,reddish-
purple Macules of the mucosa.
• Lesions may manifest as nodules,papules,or non-related
Maccules that are usually brown,blue, or purple, although
occasionally the lesions may display normal pigmentation.
• The lesion may become painful if they become ulcerated or
traumatized by opposing teeth as they enlarge.

24. • Gingival ks lesions may be exacerabated on
periodontal lesions or necrotizing periodontal
diseases may be superimposed on existing gingival
KS.
• On occasion, the expansion of gingival lesions may
result in bone resorption,and increased tooth mobility
and loss has been reported.
• The treatment of oral ks includes antiretroviral
agents,laser excision,cryotherapy, radiation therapy
and intralesional injections with vinblastibe
interferons-gamma,sclerosis agents,or other
chemotherapeutic drugs.

25. NON HODGKINS LYMPHOMA
• Lymphoma represents a
heterogeneous malignancy that is
characterized by the proliferation
of lymphoma cells.
• It is broadly classified as Hodgkins
disease or NHL.
• NHL in individuals with HIV
infection is an AIDS defining
condition,and elevated cumulated
viremia may be a strong predictor
of AIDS related lymphoma.

26. • It's treated by chemotherapy, and HAART does not
appear to significantly reduce the incidence or
prognosis of the malignancies,although HIV associated
NHL may be less common.
• Oral lesions usually appear as erythematous, painless
enlargements that may become ulcerated as a result of
traumatic injury.

27. • In some cases,bone involvement occurs.
• Lesions commonly affect the gingival,palatal,and alveolar
mucosa,and they may mimic dental infections.

28. BACILLARY ANGIOMATOSIS
• Bacillary (epithelioid) angiomatosis (BA) is an
infectious vascular proliferative disease with
clinical and histologic features similar to
those of KS. BA is caused by facultative
intracellular Gram-negative mobile bacilli of
the genus Bartonella and the order
Rickettsia (eg, Bartonella henselae,
Bartonella quintana).
• Cats are the primary host of B. henselae,
and the infection is usually transmitted to

29. • Man is the primary reservoir for B. quintana, and
it is usually transmitted by human lice.
• BA can occur in immunocompetent persons, but
it is most commonly associated with AIDS.
• Skin lesions are similar to those associated with
KS or cat-scratch disease. Gingival BA manifests
as red, purple, or blue edematous soft-tissue
lesions that may cause the destruction of
periodontal ligament and bone.

30. • BA is usually treated with the use of
broadspectrum antibiotics such as
erythromycin or doxycycline.
• Gingival lesions may be managed by using
the antibiotic in conjunction with
conservative periodontal therapy and
possibly the excision of the lesion.

31. • An increased incidence of oral hyperpigmentation
has been described in HIV-infected individuals.
• Oral pigmented areas often appear as spots or
striations on the buccal mucosa, the palate, the
gingiva, or the tongue. At present, most reports
describing the oral features of HIV/AIDS or post
HAART HIV/AIDS come from areas of the world in
which racial pigmentation may be common.
• In these areas, oral evaluation may often be
accomplished by nondental health care workers.
• Consequently, it is not possible to accurately assess
the degree of HIV-related oral hyperpigmentation
before or after ART.
ORAL HYPERPIGMENTATION

32. • In some cases, the pigmentation may relate to the
prolonged use of drugs such as zidovudine,
ketoconazole, or clofazimine.
• Zidovudine is also associated with the excessive
pigmentation of the skin and nails, although similar
hyperpigmentation has been reported in some
individuals who have never taken zidovudine.
• On occasion, oral pigmentation may be the result of
adrenocorticoid insufficiency that has been induced in
an HIV-positive individual via the prolonged use of
ketoconazole or by Pneumocystis jiroveci, CMV, or other
viral infections.

33. • Atypical ulcers (nonspecific oral
ulcerations) in HIV-infected
individuals may have multiple
etiologies that include neoplasms
such as lymphoma, KS, and
squamous cell carcinoma.
• HIV-associated neutropenia may
also feature oral ulcerations.
• Neutropenia has been successfully
treated with the use of
recombinant human granulocyte
colony-stimulating factor, with the
resultant resolution of oral ulcers.
ATYPICAL ULCERS

34. • Severe and prolonged oral
ulcers have been successfully
managed with the use of
prednisolone or thalidomide,
a drug that inhibits tissue
necrosis factor-a. Recurrence
is likely, however, if either
drug is discontinued.

35. SALIVARY GLAND DISORDERS AND
XEROSTOMIA
• Salivary gland hypofunction and
xerostomia may be most common
among HIV-infected men during both
the early and advanced stages of HIV
infection and immunosuppression.
• Salivary function does not appear to be
affected by HAART, despite the fact that
some individual antiretroviral medications
are reported to induce xerostomia.

36. . However, it is clear that xerostomia is a relatively
common condition among HIV-infected individuals
and that up to 10% of these patients may be affected.
Xerostomia appears to become more severe as
immunosuppression worsens, and increased candidal
carriage is associated with reduced salivary flow rate.

37. LINEAR GINGIVAL ERYTHEMA
• A persistent, linear, easily bleeding,
erythematous gingivitis has been described
in some HIV-positive patients.
• The intensity of the erythema is
disproportionate to the amount of plaque
present.
• There is no ulceration, pocketing, or
attachment loss, and the condition does not
respond predictably to conventional
periodontal therapy Lesions that are
clinically identical to linear gingival erythema
were observed before the advent of HIV in
association with severely
immunocompromised individuals or in those
with NUG.

38. • Linear gingival erythema (LGE) may or may not serve as a precursor to
rapidly progressive NUP .
• The microflora of LGE may closely mimic that of periodontitis rather than
gingivitis.
• However, Candida infection has been implicated as a major etiologic
factor, and human herpesviruses have been proposed as possible triggers
or cofactors.
• Linear gingivitis lesions may be localized or generalized in nature.
• The erythematous gingivitis may be limited to marginal tissue, extend
into attached gingiva in a punctate or diffuse erythema, or extend into the
alveolar mucosa.
• The affected sites should be scaled and polished.
• Subgingival irrigation with chlorhexidine or 10% povidone iodine may be
beneficial. The patient should be carefully instructed regarding the
performance of meticulous oral hygiene

39. NECROTIZING ULCERATIVE
GINGIVITIS
• The affected gingiva may be extremely
painful, and caution must be taken to avoid
un due patient discomfort.
• Basic treatment may consist of the cleaning
and debridement of affected areas with a
cotton pellet soaked in peroxide after the
application of a topical anesthetic.
• Escharotic oral rinses such as hydrogen
peroxide should only rarely be used for any
patient, and they are especially
contraindicated in immunocompromised
individuals.

40. • The patient should be seen daily or every other day
for the first week, and the debridement of affected
areas is repeated at each visit.
• 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.
• After initial healing has occurred, the patient should
be able to tolerate scaling and root planing, if needed.

41. • The patient should avoid tobacco, alcohol, and condiments.
• An antimicrobial oral rinse 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.
• Metronidazole may be the antibiotic of choice because it has been
demonstrated to be effective for the treatment of NUG, and its narrow
bactericidal spectrum may minimize the risk of secondary opportunistic
infections such as candidiasis.
• The use of prophylactic antifungal medication should be considered if
antibiotics are prescribed.
• The periodontium should be reevaluated 1 month after the resolution of
acute symptoms to assess the results of treatment and to determine
whether further therapy will be necessary.

42. NECROTIZING ULCERATIVE
PERIODONTITIS
• NUP is characterized by soft-tissue necrosis,
rapid periodontal destruction, and interproximal
bone loss.
• Lesions may occur anywhere in the dental
arches; they are usually localized to a few teeth,
although generalized NUP is sometimes present
after marked CD4+ cell depletion.
• Bone is often exposed, which results in necrosis
and subsequent sequestration.

43. • NUP is severely painful at onset, and immediate
treatment is necessary.
• Occasionally, however, patients under go
spontaneous resolution of the necrotizing lesions,
which leave painless, deep interproximal craters
that are difficult to clean and that may lead to
conventional periodontitis.
• Therapy for NUP includes local debridernent;
scaling and root planing; in-office irrigation with
an effective antimicrobial agent such as
chlorhexidine gluconate or povidone-iodine
(Betadine); and the establishment of meticulous
oral hygiene, including the home use of
antimicrobial rinses or irrigation.

44. • In patients with severe NUP, antibiotic therapy may be
necessary, but it should be used with caution in HIV-
infected patients to avoid an opportunistic and potentially
serious localized candidiasis or even candidal septicemia.
If an antibiotic is necessary, metronidazole (250 mg, with
two tablets taken immediately and then two tablets taken
4 times daily for 5-7 days) is the drug of choice.
• The prophylactic prescription of a topical or systemic
antifungal agent is prudent if an antibiotic is used.

45. NECROTIZING ULCERATIVE
STOMATITIS
• NUS has occasionally been reported in
HIV-positive patients.
• NUS may be severely destructive and
acutely painful, and it may affect
significant areas of oral soft tissue and
underlying bone.
• It may occur separately or as an extension
of NUP, and it is often associated with the
severe suppression of CD4 immune cells
and an elevated viral load.
• The condition appears to be identical to
cancrum oris (noma), a rare necrotizing
destructive process that has been variously
described as stomatitisgangrenosa,
cancrum oris, or noma.

46. • Treatment for NUS may include an antibiotic such
as metronidazole and the use of an antimicrobial
mouth rinse such as chlorhexidine gluconate. If
osseous necrosis is present, it is often necessary
to remove the affected bone to promote wound
healing.

47. CHRONIC PERIODONTITIS
• Chronic periodontitis has been
defined as an infectious disease
resulting in inflammation within
the supporting tissues of the
teeth, progressive attachment
loss,and bone loss.

48. • Clinical features
• Supragingival and subgingival plaque and calculus.
• Gingival swelling,redness,and loss of gingival stippling.
• Altered gingival margins
• Pocket formation
• Bleeding on probing
• Attachment loss
• Bone loss
• Root furcation involvement
• Increased tooth mobility
• Change in tooth position
• Tooth loss.

49. INFECTION CONTROL MEASURES FOR HIV PATIENTS
• If health care workers abide by universal precautions
when dealing with blood and body fluids,the risk of
HIV transmission from infected patients to health care
workers is minimal.
• HIV is inactivated by heating at 60 degrees Celsius for
20 minutes,by disinfectants such as 70% alcohol for 2
minutes,and by high doses of ultraviolet irradiation.

50. • Health care workers should concentrate on preventing
needle stick injuries and injuries to sharp instruments.
• Health care workers should immediately and thouroghly
wash hands and other parts of the body exposed to
blood and body fluids with soap and water.
• They should also wash hands after removing protective
gloves and in between handling of patients.
• They should wear gloves for all direct contact with
blood and body fluids and during cleaning and
decontaminating procedures.

51. • A faceshield or mask,eye glasses,and waterproof
gowns should be worn during all procedures where
splashing of blood may occur.
• They should be treated with single use syringes and
needles and discard of them in puncture proof
containers.
• If single use equipment is not available, all
equipment needs to be autoclaved before reuse.

53. References

54. • Newmann and Caranza 3rd south asian edition
• Shrinkage,Shrivastava L,Sengupta D,Lal s.Hiv
infection control in health care settings. J Indian
Med association. 1994 jan;92{1};33-
6.PMD:8207281.