Aids and periodontium

1. PRESENTED BY: DR. NEELAM MISHRA
MENTOR: DR. PRAKASH TALREJA
GUIDE: DR. PRAJAKTA RAO
HOD: DR. VARSHA RATHOD
SEMINAR 04

2. INDEX
• INTRODUCTION
• EPIDEMOLOGY
• ETIOLOGIC AGENTS
• CLASSIFICATION AND STAGING
• ROUTES OF TRANSMISSION
• PATHOGENESIS
• ORAL AND PERIODONTAL MANIFESTATIONS
• CONCLUSION

3. INTRODUCTION
• The lentivirus human immunodeficiency virus (HIV) causes AIDS by interacting
with a large number of different cells in the body and escaping the host immune
response against it.
• Lentiviruses constitute a separate genus of the Retroviridae family, which
includes a large number of different viruses infecting a diverse group of animal
species.
• Acquired immunodeficiency syndrome (AIDS) is characterized by profound
impairment of the immune system.

4. • HIV has a strong affinity for cells of the immune system, most specifically those
that carry the CD4 cell surface receptor molecule.
• Thus, helper T lymphocytes (T4 cells) are most profoundly affected,but
monocytes, macrophages, Langerhans cells, and some neuronal and glial brain
cells may also be involved.

5. EPIDEMOLOGY
• The World Health Organization (WHO)
has estimated that as many as 38 million
individuals worldwide are infected with
HIV.
• HIV infection in India was first detected
in 1986 among female sex workers in
Chennai.
• Today, with an estimated 5.134 million
infections, India is home to the second
largest population of people living with
HIV and AIDS.

6. • Transmission from health care
workers to patients has been
documented on three occasions,
with one dentist infecting six
patients either accidentally or
deliberately.
• High prevalence state: T.N.,
Maharashtra, Karnataka, A.P,
Manipur and Nagaland.

7. CLASSIFICATION AND STAGING
• WHO and CDC each have published guidelines regarding the definition of HIV
infection and HIV disease staging.
• WHO staging was developed in 1990 and revised in 2007.
• It is primarily based on the clinical appearance of the disease, and it includes the
following:

8. CLINICAL STAGE 1
Asympomatic
infection or persistent
generalised
lymphadenopathy
CLINICAL STAGE 2
Mild symptoms: mild
unexplainable weight
loss,angular chilitis,
herpes zoster,
recurrent oral
ulcerations,fungal
infections,recurrent
respiratory infections.

9. CLINICAL STAGE 3
Advanced symptoms: Severe
weight loss, chronic
diarrhoea, persistent
intermittent or chronic fever,
pulmonary tuberculosis,
severe bacterial infections,
unexplained anaemia,
persistent oral candidiasis,
oral hairy leukoplakia, acute
necrotizing stomatitis
gingivitis.
CLINICAL STAGE 4
Severe symptoms such as
HIV wasting
syndrome,pneumocystis
pneumonia,chronic herpes
simplex infections,
esophagal
candidiasis,kaposi’s
sarcoma,lymphoma,candi
diasis, invasive cervical
carcinoma,etc.

10. CDC surveillance case classification
Category A
Includes patients with acute
symptoms or asymptomatic
diseases, along with individuals
with persistent generalized
lymphadenopathy, with or without
malaise, fatigue, or lowgrade fever
Category B
patients have symptomatic conditions
such as oropharyngeal or vulvovaginal
candidiasis, herpes zoster, oral hairy
leukoplakia, idiopathic thrombocytopenia,
or constitutional symptoms off ever,
diarrhea, and weight loss.
Category C
patients with outright AIDS, as
manifested by life-threatening
conditions or identified through
CD4+ T lymphocyte levels of less
than 200 cells/mm3.

11. ROUTES OF TRANSMISSION

12. STRUCTRE OF HIV

13. PATHOGENESIS

14. ORAL AND PERIODONTAL MENIFESTATIONS
• Oral lesions are common in HIV-infected patients, although geographic and
environmental variables may exist.
• Oral lesions less strongly associated with HIV infection include:
• Melanotic hyperpigmentation,
• Mycobacterial infections,
• Necrotizing ulcerative stomatitis,
• Miscellaneous oral ulcerations, and viral
• Infections (e.g., herpes simplex virus, herpes zoster). Etc.

15. Oral Candidiasis
• Candida, a fungus found in
normal oral flora, proliferates on
the surface of the oral mucosa
under certain conditions.
• Candidiasis is the most common
oral lesion in HIV diseases and
has been found in approximately
90% of AIDS patients.

16. • Clinical Features:
• Pseudomembranous candidiasis (“thrush”) presents as painless or slightly
sensitive, yellow-white curdlike 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 can occur anywhere in the oral cavity.

17. • Diagnosis:
• Clinical evaluation,
• Culture analysis,
• Microscopic examination of a
tissue sample or smear of
material scraped from the
lesion, which shows hyphae
and yeast forms of the
organisms.

18. • When oral candidiasis appears in
patients with no apparent
predisposing causes, the clinician
should be alerted to the
possibility of HIV infection.
• Many patients at risk for HIV
infection who present with oral
candidiasis also have esophageal
candidiasis, a diagnostic sign of
AIDS.

19. • Treatment:
• Antifungal Therapeutic Agents:
• Topical Drugs:
1. Clotrimazole (Mycelex), 10-mg tablets: Dissolve in mouth, 3-5 tablets daily for
7-14 days.
2.Nystatin (Mycostatin, Nilstat).
3.Clotrimazole ointment, 15-g tube: Apply to affected area qid.
4.Miconazole 2% ointment, 15-g tube: Apply to affected area qid.
5. Itraconazole oral suspension (Sporanox), 100-200 mg once daily for 7-28
days.
6. Fluconazole oral suspension (Diflucan), 200 mg first day followed by 100 mg
once daily for at least 2 weeks.

20. • Systemic Drugs:
1. Ketoconazole (Nizoral), 200-mg tablets: Take 2 tablets immediately, then
1 or 2 tablets daily with food for 5-14 days.
2. Fluconazole (Diflucan), 100-mg tablets: Take 2 tablets immediately, then 1
tablet daily for 7-14 days.
3. Itraconazole (Sporanox), 100-mg capsules: Take 200 mg once daily with
meals for 4 weeks (AIDS and neutropenic patients).

21. Oral Hairy Leukoplakia
• Oral hairy leukoplakia (OHL)
primarily occurs in persons with HIV
infection.
• Found on the lateral borders of the
tongue, OHL frequently has a
bilateral distribution and may
extend to the ventrum.
• Clinical Features:
• Characterized by an asymptomatic,
poorly demarcated keratotic area
ranging in size from a few
millimeters to several centimeters.

22. • Often, characteristic vertical
striations are present,
imparting a corrugated
appearance, or the surface
may be shaggy and
appear“hairy” when dried.
• The lesion does not rub off
and may resemble other
keratotic oral lesions.
• Microscopically, the OHL
lesion shows a
hyperparakeratotic surface
with projections that often
resemble hairs.

23. • Treatment:
• lesions are often responsive to HIV drug therapy or the use of antiviral agents
such as acyclovir or valacyclovir.

24. Kaposi's Sarcoma and Other Malignancies
• Oral malignancies occur more
frequently in severely
immunocompromised individuals
than in the general population.
• An HIV-positive individual with
non-Hodgkin's lymphoma (NHL)
or Kaposi's sarcoma (KS) is
categorized as having AIDS.

25. • Although KS is a malignant
tumor, in its classic form it is a
localized and slowly growing
lesion.
• The KS that occurs in HIV-
infected patients presents
different clinical features.
• In these individuals, KS is a
much more aggressive lesion,
and the majority develop
lesions of the oral mucosa,
particularly the palate and
gingiva.
• The oral cavity may often be
the first or only site of the
lesion.

26. • Clinical Features:
• Lesions manifest as :
• Nodules, papules, or
nonelevated macules.
• Usually brown, blue, or
purple in color, although
occasionally the lesions may
display normal
pigmentation.
• Diagnosis is based on
histologic findings.

27. • Treatment:
• Vinblastine injections remain the most effective treatment in managing localized
lesions.
• Destructive periodontitis has also been reported in conjunction with gingival KS.
In such patients, scaling and root planning and other periodontal therapy may be
indicated in addition to intralesional or systemic chemotherapy.

28. Bacillary (Epithelioid) Angiomatosis
• Infectious vascular
proliferative disease with
clinical and histologic features
similar to those of KS.
• Clinical Feature:
• Gingival BA manifests as red,
purple, or blue edematous
soft tissue lesions that may
cause destruction of
periodontal ligament and
bone.

29. • Treatment:
• Treated using broad-spectrum antibiotics such as erythromycin or doxycycline.
• Gingival lesions may be managed using the antibiotic in conjunction with
conservative periodontal therapy and possibly excision of the lesion.

30. Oral Hyperpigmentation
• An increased incidence of
oral hyperpigmentation has
been described in HIV-
infected individuals.
• Clinical Features:
• Oral pigmented areas often
appear as spots or
striations on the buccal
mucosa,palate, gingiva, or
tongue.

31. • On occasion, oral pigmentation may be the result of adrenocorticoid insufficiency
induced in an HIV-positive individual by prolonged use of ketoconazole.
• Zidovudine is also associated with excessive pigmentation of the skin and nails,
although similar hyperpigmentation has been reported in some individuals who
have never taken zidovudine.

32. Atypical Ulcers
• HIV-infected patients have a
higher incidence of
recurrent herpetic lesions
and aphthous stomatitis.
• Atypical large, persisitent,
non-specific, painful ulcers.
• Caused by:
• HSV
• VZV
• EBV
• CMV

33. • Treatment:
• Herpes labialis in HIV infected individuals may be responsive to topical antiviral
therapy.
• Recurrent aphthous stomatitis (RAS) can be treated by topical or intralesional
corticosteroids, chlorhexidine or other antimicrobial mouth rinses, oral
tetracycline rinses, or topical amlexanox.

34. GINGIVAL AND PERIODONTAL DISEASES
• Periodontal diseases are more common among HIV-infected users of
injection drugs, but this may relate to poor oral hygiene and lack of dental
care rather than decreased CD4 cell counts.
• However, some unusual types of periodontal diseases do seem to occur with
greater frequency in HIV-positive individuals.

35. Linear Gingival Erythema
• Persistent, linear, easily bleeding,
erythematous gingivitis.
• May be localized or generalized in nature.
(1) May be limited to marginal tissue,
(2) May extend into attached gingiva in
a punctate or a diffuse erythema,
(3) May extend into the alveolar
mucosa.

36. • Treatment:
• Affected sites should be scaled and polished.
• Chlorhexidine or 10% povidone-iodine.
• Meticulous oral hygiene procedures.
• Empiric administration of a systemic antifungal agent such as fluconazole for 7 to
10 days.
• Patient should be placed on a 2-to 3-month recall maintenance interval and re-
treated as necessary.

37. Necrotizing Ulcerative Gingivitis
• Characteristic of red swollen
gingiva with yellowish grey
marginal areas of necrosis
leading to destruction of
interdental papillae.
• Spontaneous haemorrhage and
characteristic fetor accompanied
by severe pain.
• It rapidly progresses and become
NUP.

38. • Treatment:
• Cleaning and debridement of affected areas with a cotton pellet soaked in
peroxide after application of a topical anesthetic.
• Patient should be seen daily or every other day for the first week; debridement of
affected areas is repeated at each visit, and plaque control methods are gradually
introduced.
• Systemic antibiotics such as metronidazole or amoxicillin may be prescribed for
patients with moderate to severe tissue destruction, localized lymphadenopathy
or systemic symptoms, or both.
• The periodontium should be reevaluated 1 month after resolution of acute
symptoms to assess the results of treatment and determine if further therapy will
be necessary.

39. Necrotizing Ulcerative Periodontitis
Extension of NUG in which bone loss
and periodontal attachment loss occur.
• Soft tissue necrosis, rapid periodontal
destruction, and interproximal bone
loss.
• May occur anywhere in the dental
arches, usually localized to a few
teeth, although generalized NUP is
sometimes present after marked CD4+
cell depletion.
• Bone is often exposed, resulting in
necrosis and subsequent
sequestration NUP is severely painful
at onset, and immediate treatment is
necessary.

40. • However, patients undergo spontaneous resolution of the necrotizing lesions,
leaving painless, deep interproximal craters that are difficult to clean and that
may lead to conventional periodontitis.
• Treatment:
• Local debridement, scaling and root planing, in-office irrigation with an effective
antimicrobial agent such as chlorhexidine gluconate or povidone-iodine
(Betadine), and establishment of meticulous oral hygiene, including home use of
antimicrobial rinses or irrigation.
• Severe NUP, antibiotic therapy may be necessary.
• If an antibiotic is necessary, metronidazole (250 mg, with two tablets taken
immediately and then one tablet four times daily for 5-7 days) is the drug of
choice.

41. Necrotizing Ulcerative Stomatitis
• Severely destructive and acutely
painful.
• Chracterised by necrosis of significant
areas of oral soft tissue and underlying
bone.
• May occur separately or an extension
of NUP and is commonly associated
with severe depression of CD4+ cells
and increased viral load. (GRASSI et al
1988).

42. • Treatment:
• Metronidazole
• Antimicrobial mouth rinse.
• If osseous necrosis is present it is necessary to remove affected bone to promote
wound healing.

43. Chronic Periodontitis
• The majority of HIV-positive individuals
experience gingivitis and chronic
periodontitis in a manner similar to the
general population.
• With proper home care and appropriate
periodontal treatment and maintenance,
HIV-positive individuals can anticipate
reasonably good periodontal health.
• Treatment decisions should be based on
the overall health status of the patient,
the degree of periodontal involvement,
and the motivation and ability of the
patient to perform effective oral hygiene
(oughout the course of their disease.

44. PERIODONTAL TREATMENT PROTOCOL
• Health Status
• Infection control measures
• Goals of therapy
• Supportive periodontal therapy

45. Health Status
1. Should be determined from the history, physical evaluation and consultation
with the patients physician.
2. Treatment decisions will vary depending on the patient’s state of health.
3. Information should be obtained regarding :
• CD4+ T4 lymphocyte level,
• Current viral load,
• Difference from previous counts and load,
• H/o of drugs abuse, multiple infections,
• Present medications.

46. • VIRAL LOAD:
• Severity of illness is determined by
amount of virus in the body
(increasing viral load) and the body,
and degree of immune supression
(decreasing CD4+ counts).
• Higher the viral load, sooner
immune supression occurs.

47. Infection control measures
• Control measures should be based on ADA and the centre of disease control and
prevention (CDC) or the Organisation for safety and Asepsis procedure (OSAP).
• A number of pathogenic microorganism may be transmitted in dental settings
and this includes:
• Airborne Pathogens: T.B.
• Blood Borne Pathogens: H.V., H.B.V., H.C.V.
• Water borne Pathogens: Pseudomonas species.
• Mucosal/skin borne Pathogens: VZV or HSV.

48. Goals of therapy
• The primary goals of dental therapy should be the restoration and maintenance
of oral health, comfort, and function.
• Treatment should be directed toward control of HIV-associated mucosal diseases
such as chronic candidiasis and recurrent oral ulcerations.
• Effective oral hygiene maintenance.
• Conservative, nonsurgical periodontal therapy should be treatment option for
virtually all HIV+ patients.
• NUP and NUS can be severely destructive to periodontal structures and should be
treated appropriately.

49. Supportive periodontal therapy
• It is imperative that the patient maintain meticulous personal oral hygiene.
• Recall visits should be conducted at short intervals (2-3 months) .
• Systemic antibiotic therapy should be administered with caution.
• Blood and other medical laboratory tests may be required to monitor the
patient's overall health status, and close consultation and coordination with the
patient's physician are necessary.

50. Psychologic Factors
• HIV infection of neuronal cells may affect brain function and lead to outright
dementia.
• Coping with a life-threatening disease may elicit depression, anxiety, and anger in
such patients, and this anger may be directed toward the dentist and the staff.
• Treatment should be provided in a calm, relaxed atmosphere, and stress to the
patient should be minimised.

51. CONCLUSION
• Early diagnosis and treatment of HIV infection can have a profound
effect on the patient's life expectancy and quality of life, and the
dentist should be prepared to assist the patient in obtaining testing.
• Any patient with oral lesions suggestive of HIV infection should be
informed of the findings.

52. REFERENCES
• Carranza, 10th edition, Clinical Periodontology, Page no. 1007-1057.
• Harsh Mohan, 7th edition, Textbook of Pathology, Pge no 51-57.
• Gaurav Sharma et al, Oral manifestations of HIV/AIDS in Asia: Systematic review and future
research guidelines, Jul 2015, J clin exp dent, e419–e427.
• Atessa Pakfetrat et al, Oral Manifestations of Human Immunodeficiency Virus-Infected Patients,
2015 Jan; 27(78): 43–54.
• Ranganathan K, et al . Oral lesions and conditions associated with human immunodeficiency virus
infection in 300 south Indian patients. Oral Dis. 2000;6:152–7.

53. Thank you