the diseases that is related to the periodontium during AIDS

1. PERIODONTAL MANIFESTATIONS
IN HIV
KIRAN VINCENT

2. CONTENTS
• Introduction
• Classification
• Oral and periodontal manifestation of HIV infection
linear gingivitis
necrotizing ulcerative gingivitis
necrotizing ulcerative periodontitis
necrotizing stomatitis

3. • Most common oral and periodontal manifestation of
HIV infection
1. Oral hairy leukoplakia
2. Oral candidiasis
3. Kaposi’s sarcoma
4. Bacillary angiomatosis
5. Oral hyperpigmentation
6. Atypical ulcers
7. Non – hodgkin’s lmphoma
8. Salivary gald disorders and xerostomia
• Dental treatment complication
• Periodontal treatment protocol

4. INTRODUCTION
• Acquired immunodeficiency syndrome – AIDS
is characterized by profound impairment of
the immune system
• The condition is caused due to a viral
pathogen human immunodeficiency virus –
HIV
• The primary means of transmission include
sexual activity which is un protected and drug
abuse.

5. • HIV has a strong affinity for cells of the
immune system mainly the CD4 cell surface
receptor molecule
• Thus helper T cells are mostly affected but
monocytes, macrophages, Langerhans cells
are also involved
• Viral replication occurs in lymphorecticular
tissue of lymph nodes, spleen, gut- associated
lymphoid cells and macrophages

6. CLASSIFICATION
CDC Surveillance case classification
AIDS patients have been grouped as following
CATEGORY A- includes patients with acute
symptoms or asymptomatic diseases along
with individuals with persistent generalised
lymphadenopathy, with or without malaise,
fatigue or low grade fever

7. • CATEGORY B- patients have symptomatic
conditions such as oropharyngeal or vulvoviginal
candidiasis, herpes zoster, oral hairy leukoplakia,
idiopathic thrombocytopenia or constitutional
symptoms of fever, diarrhoea and weight loss
• CATEGORY C- patients are those with outright
AIDS as manifested by life-threatening conditions
or identified through CD4+T lymphocyte levels of
less than 200cells/mm3

8. • CLASSIFICATION OF PERIODONTAL DSEASES
ASSOCIATED WITH HIV INFECTION
Four distinct disease types are seen
1. HIV – associated gingivitis (HIV- G)
 A distinctive linear inflammation is seen
around the gingival margin with possible
punctate erythema extending throughout the
width of the attached gingiva that may occur
in the presence of excellent oral hygiene

9. 2. HIV- associated periodontitis (HIV- P)
Characterized by rapid loss of attachment,
connective tissue destruction and deep bone
pain
3. HIV – necrotizing gingivitis (HIV – NG)
4. Necrotizing stomatitis (NS)
in this spontaneous sequestration of
interdental bone along with extensive soft
tissue necrosis occurs

10. THE NEW CLASSIFICATION
Dropped the term HIV from individual titles
1. HIV – G has been changed to linear gingivitis
2. HIV necrotizing gingivitis has been changed
to necrotizing ulcerative gingivitis (NUG)
3. HIV- P has been changed to necrotizing
ulcerative periodontitis (NUP)
4. Necrotizing stomatitis

11. ORAL AND PERIODONTAL
MANFESTATIONS OF HIV INFECTION

12. LINEAR GINGIVITIS
Characterised by
• Marginal linear erythema across the attached
gingiva generally involving all teeth
• Punctate lesions appear to coalesce giving the
entire gingiva a bright-red appearance
• Spontaneous bleeding or bleeding on probing
• No ulceration and no loss of attachment is seen
• Does not respond to the removal of plaque by
intense scaling, root planing and plaque control
measures

13. • Candida infection is implicated as a major
etiologic factor and HHV is proposed as
possible triggers or cofactors
• Linear gingivitis lesions may be localised or
generalised in nature
• Erythematous gingivitis may be limited to
marginal tissue, may extend into attached
gingiva in a punctate or a diffuse erythema or
may extend into the alveolar mucosa

15. MANAGEMENT
 affected site should be scaled and polished
Subgingival irrigation with chlohexidine or
10%povidone-iodine is beneficial
Patient should be instructed to follow proper oral
hygeine procedures
Reevaluate the condition after 2 to 3 weeks of
initial therapy
If the lesions persist possibility of a candidal
infection
Treatment of choice is administration of systemic
antifungal agent fluconazole for 7 to 10 days

16. NECROTIZING ULCERATIVE GINGIVITIS
• Sudden onset, bleeding on tooth brushing
• Pain and characteristic halitosis
• The gingiva appears fiery-red and swollen and
yellow to grayish necrosis is observed on the
tip of the interdental papilla and margins of
the gingiva
• Mostly anterior gingiva is affected and
normally limited to the soft tissue of the
periodontium

18. TREATMENT OR MANAGEMENT
Cleaning and debridement of affected areas
with a cotton pellet soaked in peroxide after
application of a topical anesthetic
Escharotic oral rinses such as hydrogen
peroxide should on be rarely used and are
contraindicated in immunocompromised
individuals
Patient should be seen daily or every other
day for the first week and debridement of
affected areas is repeated at each visit

19. Plaque control methods are gradually
introduced
Patient should avoid tobacco, alcohol and
condiments
Prescribe antimicrobial oral rinse
chloehexidine glucocnate 0.12%
Systemic antibiotics such as metronidazole or
amoxicillin is prescribed for patients with
moderate to severe tissue destruction,
localised lymphadenopathy or systemic
symptoms

20. Metronidazole os the drug of choice in NUG
and its narrow bacterial spectrum minimises
the risk of secondary opportunistic infection
such as candidiasis

21. NECROTIZING ULCERATIVE PERIODONTITIS (NUP)
• A necrotizing, ulcerative, rapidly progressive form
of periodontitis occurs more frequently among HIV
positive individuals
• NUP represent an extension of NUG in which bone
loss and periodontal attachment loss occurs
• NUP is characterized by soft tissue necrosis, rapid
periodontal destruction and interproximal bone
loss
• Lesions may occur anywhere in the dental arches
• Bone is exposed, resulting in necrosis and
subsequent sequestration

22. • Affected gingiva- severe pain, localized soft
tissue necrosis, ulceration and interproximal
cratering
• Not associated with deep pocket formation
• Loss of crestal bone coinciding with soft tissue
destruction
• Rapid horizontal bone loss in the absence of
severe gingival inflammation
• Tooth mobility
• Severe immune suppression with CD4+ cell
count below200cells/mm3

23. • NUP is severely painful at onset
MANAGEMENT
Local debridement
Scaling and root planning
Irrigation with an antimicrobial agent such as
chlorhexidine gluconate or povidone-iodine
In severe NUP if antibiotic therapy is
necessary, metrodinazole 250mg with 2
tablets taken immediately and then 2 tablets 4
times daily for 5 to 7 days- is the drug of
choice

25. NECROTIZING ULCERATIVE STOMATITIS (NUS)
• NUS is severely destructive and acutely painful
• Extensive soft tissue and bony necrosis with
sequestration is seen
• It may occur separately or as an extension of
NUP and is associated with severe suppression
of CD4immune cells and elevated viral load
• It resembles noma and cancrum oris and
represents the most severe form of
periodontal infection seen in association with
HIV

26. MANAGMENT
Antibiotic s- metronidazole
Antimicrobial mouth rinse such as chlorhexidine
gluconate
If osseous necrosis is present, it should be
removed the affected bone to promote wound
healing

28. MOST COMMON ORAL AND
PERIODONTAL MANIFESTATIONS OF HIV
INFECTION
1. Oral hairy leukoplakia
2. Oral candidiasis
3. Kaposi’s sarcoma
4. Bacillary angiomatosis
5. Oral hyperpigmentation
6. Atypical ulcers
7. Non – hodgkin’s lmphoma
8. Salivary gald disorders and xerostomia

29. ORAL HAIRY LEUKOPLAKIA
• Primarily occurs in persons with HIV infection
• Site – lateral borders of the tongue
bilateral distribution and may extend to
the ventrum
Causative organism – human papilloma virus but have
association with EBV
Characteristics:
o The lesion is characterized by an asymptomatic, poorly
demarcated keratotic area ranging in size from a few
millimetres to several centimetres
o Charateristic vertical striations are present, imparting a
corrugated appearence or the surface may be shaggy
and appear hairy when dried

30. o The lesion doesnot rub off

31. MICROSCOPICALLY- lesion shows a
hyperparakeratotic surface with projections
that resemble hair
Beneath the parakeratotic surface acanthosis
and some balloon cells resembling koilocytes
are seen
These cells contain viral particles of the HHV
group; these particles have been interpreted
as EBV

32. MANAGEMENT
Vigorous treatment of OHL is not indicated
Lesions are responsive to HIV drug therapy or
the use of antiviral agents like acyclovir,
valacyclovir, ganciclovir
Lesions can be successfuly removed with laser
or conventional surgery
Topical application of podophyllin, retinoids,
oral acyclovir but these agents can induce
unwanted local or systemic side effects
OHL lesion recur when therapy is discontinued

33. ORAL CANDIDIASIS
• Candidiasis is an opportunistic fungal infection
• Candida proliferates on the surface of the oral
mucosa
• This is mainly seen during diminished host
response and in patients receiving
immunosuppressive therapy
• Most oral candidal infections are associated
with Candida albicans

34. Have four clinical presentation:
1. Pseudomembraneous candidiasis
-thrush
-presents as painless or slightly sensitive,
yellow white curdlike lesions
-lesions can be scraped off
-most common on hard and soft palate
and the labial or buccal mucosa but can
anywhere in the oral cavity

36. 2. Erythematous candidiasis
appear as red patches on the buccal or
palatal mucosa, or it may be associated with
depapillation of the tongue

37. 3. Hyperplastic candidiasis
-least common form
- may be seen in the buccal mucosa and tongue
-it is more resistant to removal than the other
types

39. 4. Angular cheilitis
-the commissures of the lips appear
erythematous with surface crusting and fissuring

40. DIAGNOSIS
 Diagnosis is made by clinical evaluation,
culture analysis or microscopic examination of
a tissue sample or a smear of material scraped
from the lesion, which shows hyphae and
yeast forms of the organisms
MANAGEMENT
Although candidiasis in HIV- infected patients
may respond to antifungal therapy, it is often
refractory or recurrent.

41.  Candidal organisms became resistant to long-
term fluconazole therapy, and cross-resistent
to other azoles like ketoconazole, itraconazole,
miconazole or clotrimazol and amphotericin B
may develop
 Administration of HAART in HIV infections has
resulted in a significant decrease in incidence
of oropharyngeal candidiasis and has reduced
the rate of fluconazole resistance
 Early oral lesions of HIV-related candidiasis are
responsive to topical antifungal therapy
 More advanced lesions, including hyperplasyic
candidiasis require systemic antifungal drugs

42. Common antifungal therapeutic agents for oral
candidiasis
TOPICAL DRUGS
1. Clotrimazole- 10mg tablets. Dissolve in
mouth 3-5 tablets daily for 7-14 days
2. Nystatin as oral suspension, tablets, vaginal
tablets, ointment
3. Clotimazole ointment, 15g tube- apply to the
affected area qid
4. Miconazole 2%ointment, 15g tube- apply to
affected area qid

43. 5. itaconazole, fluconazole and amphotericin B
as oral suspensions
SYSTMIC DRUGS
1. Ketoconazole, 200mg tablets
2. Fluconazole, 100mg tablets
3. Itraconazole, 100mg capsules

44. KAPOSI’S SARCOMA
• The most common oral malignancy asociated
with AIDS
• An angioproliferative tumor which is rare,
multifocal, vascular neoplasm
• Site – skin of lower extremities of older men
-homosexuals, heterosexuals
transmission
• Causative organism – HHV eight
• Localised and slow growing lesion
• In early stages the oral lesions are painless,
reddish-purple macules on the mucosa

45. • As they progress, the lesions become nodular
• Lesions manifest as nodules, papules or non
elevated macules that are usually brown, blue
or purple
Intra oral kaposi’s sarcoma

46. kaposi.’s sarcoma associated with Herpes
virus
Occular kaposi’s sarcoms

47. • The kaposi’s sarcoma that occurs in HIV- infected
patients presents different clinical features
• In these individuals Kaposis’s sarcoma is a much
more aggressive lesion and the majority lesion of
the oral mucosa, particularly the palate and
gingiva
• The oral cavity may b the first or only site of the
lesion
• KS has been reported in patients with lupus
erthyematosus who are receiving
immunosuppressant therapy as well as in renal
transplant patients and other individuals
receiving corticosteroid or cyclosporine therapy

48. TREATMENT
Antiretroviral agents
Laser excision
Cryotherapy
Radiation therapy
Intralesion injection with vinblastine,
interferon-gamma, sclerosing agents
Intralesional injectons of vinblastine at a dose
of 0.1%mg/cm2 using a 0.2mg/ml solution of
vinblastine sulfate in saline

49. In responsive patients, treatment was
reported at 2 week intervals until resolution or
stabilization of the lesion

50. BACILLARY ANGIOMATOSIS
• An infectious vascular proliferative disease
with clinical and histological features similar to
kaposi’s sarcoma
• Transmitted by cat scratch and caused by
rickettsia- like organism
• Gingival bacillary angiomatosis manifest as
red, purple or blue edematous soft tissue
lesions that cause destruction to PDL and
bone
• The condition is more prevalent in HIV
positive individuals with low CD4 levels

52. DIAGNOSIS
 Biopsy which reveals an epithelioid
proliferation of angiogenic cells accompanied
by an acute inflammatory cell infilterate
MANAGEMENT
Broad-spectrum antibiotics such as
erythromycin doxycyline
Gingival lesions are managed using the
antibiotic in conjunction with consevative
periodontal therapy and excision of the lesion

53. ORAL HYPERPIGMENTATION
• Increased incidence is seen in HIV patients
• Oral pigmented areas appear as spots or
striations on the buccal mucosa, palate, gingiva
or tongue
• Some case may relate to prolonged use of drugs
like zidovudine, ketoconazole, or clofazimine
• May also be a result of adenocorticoid
insufficiency induced in a HIV positive individual
by prolonged use of ketoconazoleor by
Pneumocystis jiroveci infection
• Zidovudine is also associated with excessive
pigmentation of the skin and nails

54. ATYPICAL ULCERS
• Also known as nonspecific oral ulceration
• Atypical ulcers in HIV infected individuals have
simple etiologies that include neoplasms such
as lymphoma, kaposis’s sarcoma, squamous
cell carcinom
• HIV associated neutropenia may also feature
oral ulcerations
• Neutopenia has been successfully treated
using recombinant human granulocyte colony-
stimulating factor with resultant resolution of
oral ulcers

55. • Severe prolonged oral ulcers are managed
using prednisone or thalidomide
• Recurrence is likely if either drug is
discontinued
• HIV infected patients have high incidence of
recurrent herpetic lesions and apthous
stomatitis
• The CDC HIV classification system indicates
the mucocutaneous herpes lasting longer than
1 month is diagnostic of AIDS in HIV infcted
individuals

56. • Apthae andapthae-like are common through
out the course of immunosuppression
• In healthy patients herpetic and apthous
lesions are self limiting and easy to diagnose
by their characteristic clinical features, that is,
herpes on the keratinizing mucosa, apthae on
the nonkeratinizing surface
• In HIV infected patients the clinical
presentation and course of these lesions alters
• Herpes may involve all mucosal surfaces and
extent to the skin and may persist for month

57. • Atypical large, persistent, non specific and
painful ulcers are common in
immunocompromised individuals
• If healing is delayed these lesions are
secondarily infected
• oral ulceration are described in association
with enterobacterial organisms such as
Klebiella pnuemoniae, Enterobacter cloacae
and Escherichia coli
• Neutropenia may also be induced by drugs
like zidovudine, trimethoprim-
sulfamethoxazole and ganciclovir

58. • Atypical ulcers are severe and persistent in
individuals with low CD4 cell counts and the
presence of oral CNV-induced ulcers may be
indicative of systemic CMV infecion
• Herpes labialis in HIV-infected individual
responds to topical antiviral therapy
eg;acyclovir, penciclovir
• Recurrent apthous stomatitis also reported in
HIV infected individualsmand occur as a
component of the intial acute illness of HIV
seroconversion
• Major apthae are seen in oropharynx,
oesophagus or other areas of GIT

60. MANAGEMENT
• Treatment of RAS include topical or
intralesional corticoseroid, chlorhexidine, oral
tetracycline rinses
• Oral viral infections of immunocompromised
individuals are treated with acyclovir 200-
800mg administered 5 times daily for atleast
10 days
• Daily maintenance therapy of 200mg 2 to 5
times daily required to prevent recurrence

61. • Resistant viral strains are treated with
valacyclovir or ganciclovir
• For recurrent apthous ulcers topical
corticosteroid therapy fluocinonide gel applied
3 to 6 times daily is effective
• Large apthae in HIV positive individuals may
be resistant to conventional topical therapy
and treated with systemic corticosteroid
administration of prednisone 40 to 60mg daily
or thalidomide

62. NON-HODGKIN’S LYMPHOMA (NHL)
• NHL in individuals with HIV infection is an
AIDS-defining condition and elevated viremia
is a strong predictor of AIDS related
lymphoma
• EBV-associated lesions include Burkitt’s
lymphoma and HIV-associated lymphoma
• NHL is characterized by malignancy of B or T
lymphocytes, and tumors are typed by the
WHO classification system as indolent,
aggressive or highly aggressive
• NHL is treated by chemotherapy

63. • Oral lesions appear as erythematous, painless
enlargements that may become ulcerated
because of traumatic injury
• Bone involvement is rare
• Diagnosis- based on clinical examination,
complete blood count with differential,
imaging studies and lymphnode and tissue
biopsy

64. Non-Hodgkin’s lymphoma of
maxilla
Primary Non-Hodgkin’s lymphoma of the mandible
Extranodal Non-Hodgkin’s lymphoma
of the gingiva

65. SALIVARY GLAND DISORDERS AND XEROSTOMIA
• Saliva contains many HIV inhibitors such as
HIV-1 specific antibodies, lysozyme,
peroxidases, lactoferrin
• Also contain a specific salivary anyi-HIV factor,
secretory leukocyte protease inhibitor
• Dryness of mouth or xerostomia is is most
common in HIV-infected men in both early
and advanced stages of HIV infection and
immunosuppression
• Increased chance of candidal infection in
association with HIV

66. • Parotid enlargement in association with HIV
infection occurs as a result of diffuse
infiltrative lymphocytosis syndrome
characterized by persistent circulating
CD8+lymphocytosis and visceral lymphocytic
infiltration and infiltration
• Other causes are lymphoepithelial lesions,
hyperplastic lymphadenopathy, bacterial and
viral infections, sjogrens syndrome and
lymphoma

67. DENTAL TREATMENT COMPLICATIONS
• Potential for post operative complications like
haemorrhage, infection or delayed wound
healing in individuals with HIV/AIDS
• Careful management of medically
compromised patients
• The poor overall status of an individual with
AIDS may limit periodontal therapy to
conservative minimally invasive procedures
and antibiotic therapy is required

68. PERIODONTAL TREATMENT PROTOCOL
1. HEALTH STATUS
 Patient’s health status should be determined
from the health history, physical
examination, and consultation with the
patient’s physician
 Treatment decisions will vary depending on
the patient’s state of health
 Delayed wound healing and increase risk of
postoperative infection are possible
complication factors in AIDS patients

69. 2. INFECTION CONTROL MEASURES
Infection control with universal precautions
3. Goals of therapy
Primary goal of dental therapy should be
restoration and maintenance of oral health,
comfort and function
Treatment should be directed towards control
of HIV-associated mucosal diseases such as
chronic candidiasis and recurrent oral
ulcerations

70. 4. MAINTENANCE THERAPY
The patient should maintain proper oral
hygiene
Periodontal maintenance recall visits should
be conducted at short intervals of 2 to 3
months
Systemic antibiotics should be administered
with caution

71. 5. PSYCHOLOGIC FACTORS
HIV infection of neuronal cells may affect
brain function and lead to dementia
Maintain medical confidentiality
Coping with a life threatening disease may
elicit depression, anxiety and anger in such
patients

72. CONCLUSION
As a dentist we should advice and counsel
patients on their oral health status and should
encourage HIV- infected patients who are
unaware of their disease status. Early
diagnosis and treatment of HIV infection can
have a profound effect on the patient’s life
expectancy