1. Oral manifestations are among the earliest signs of HIV infection. Conditions like oral candidiasis, oral hairy leukoplakia, and Kaposi's sarcoma are strongly associated with HIV. 2. Other less common conditions include necrotizing gingivitis/periodontitis, infections by Mycobacterium tuberculosis or M. avium-intracellulare, and salivary gland diseases. 3. The progression of oral lesions correlates with declining CD4 counts and worsening immune suppression in patients with HIV/AIDS.

1. ORAL MANIFESTATIONS OF HIV
Presented by
Anusha.v
MDS

2. Contents :
• Introduction
• Historical review
• Virus structure & lifecycle
• Routes of transmission
• Oral manifestations

3. INTRODUCTION
• HIV INFECTION serious disorder affecting
immune system
• Body’s normal defenses against infection break
down
• Host is vulnerable to life-threatening infections/
conditions including malignances.

4. AIDS most advanced stage of HIV infection
• THE PROGRESSION OF HIV TO AIDS IS DEFINED BY CD4
COUNT < 200/Cu.mm OR ABOUT 14% OF CD4- T
HELPER CELLS
4

5. • AIDS is defined as a condition indicative of a defect in
cell mediated immunity occurring in a person with no
known cause for immunodeficiency other than the
presence of HIV.
• Acquired - not inherited
• Immune - attacks the immune system
• Deficiency - by destroying certain WBC
• Syndrome- a group of symptoms / illnesses that occur
as a result of the HIV Infection.

6. • Before 1956 – patients from Central Africa – reported with
strange pneumonia - Gay fever ( GRID)
• Extra ordinary out break of Pneumocystis Carinii pneumonia
and Kaposi’s Sarcoma in previously fit young men -
Los Angeles and NewYork
• In 1981, the HIV epidemic has spread beyond gay males,
Haitians, and hemophiliacs, and affected many people
worldwide.
• 1982 – condition began to be referred as AIDS
HISTORICAL REVIEW

7. • 1st report of AIDS – by US CDC – in morbidity mortality
weekly report
• In 1986, the initial cases of AIDS was found in chennai–
by Dr. Sunithi solomon

8. CDC – 1993 - AIDS Definition
“The occurrence of one or more group of life-
threatening opportunistic infections,
malignancies, neurologic diseases and other
specific illness in patients with HIV infection or
with CD4 counts less than 200/cu mm”

9. STRUCTURE OF HIV

10. ROUTES OF TRANSMISSION

11. PATHOGENESISHIV in blood
stream
Entrapped in
lymphnodes
Presence of virus
evokes antigenic
stimulation
Activates CD4
T cells,
macrophage
TNF ALPHA, IL-6
INCREASED NO OF CD4

13. Oral manifestations
• Represent earliest manifestations
• First meeting regarding oral problems – 1986 –
European Economic Community in Copenhagen
• 1989 - j. pindborg revised
• 1989 - WHO collaborative center and EC Clearing
house
• Revised classification by EC Clearing house - 1992

14. Sept 1992 revised classification of oral lesions associated with
adult HIV INFECTION
• GROUP 1 : LESIONS STRONGLY ASSOCIATED WITH HIV
INFECTION
• CANDIDIASIS : pseudomembranous , erythematous
• Oral hairy leukoplakia
• Non – hodgkins lymphoma
• Kaposi’s sarcoma
• Periodontal disease –
• linear gingival erythema
• Necrotising ulcerative gingivitis
• Necrotising ulcerative periodontitis

15. • Group 2 : lesions less commonly associated with HIV
infection
• BACTERIAL: M. AVIUM INTERCELLULARE
M. TB
• MELANOTIC HYPERPIGMENTATION
• NECROTISING ULCERATIVE STOMATITIS
• SALIVARY GLAND DISEASE – DRY MOUTH
UNI/BILATERAL SWELLING OF MAJOR SALIVARY
GLANDS
• THROMBOCYTOPENIC PURPURA
• ULCERATION OTHERWISE NOT SPECIFIED

16. • VIRAL :
• HSV INFECTION
• HPV INDUCED WARTS
• CONDYLOMA ACCUMINATUM
• FOCAL EPITHELIAL HYPERPLASIA
• VERRUCA VULGARIS
• VARICELLA ZOSTER VIRUS INFECTION

17. • GROUP 3 : LESIONS SEEN IN HIV INFECTION
BACTERIAL INFECTIONS :
• ACTINOMYCES ISRAELLI
• E. COLI, KLEBSIELLA PNEUMONIA
• CAT SCRATCH DISEASE
• EPITHELOID ( BACILLARY) ANGIOMATOSIS
DRUG REACTIONS :
• ULCERATIVE ,
• ERYTHEMA MULTIFORME,
• LICHENOID,
• TOXIC EPIDERMOLYSIS

18. FUNGAL ( OTHER THAN CANDIDIASIS)
• CYPTOCOCCUS NEOFORMANS
• GEOTRICHUM CANDIDUM
• HISTOPLASMA CAPSULATUM
• MUCORACEA
• ASPERGILLUS FLAVUS
NEUROLOGICAL :
• FACIAL PALSY
• TRIGEMINAL NEURALGIA

19. RECURRENT APHTHOUS STOMATITIS
VIRAL INFECTIONS
• CYTOMEGALO VIRUS
• MOLLUSCUM CONTAGIOSUM
“ Classification & Diagnostic Criteria For Oral Lesions In
H.I.V. Infections. EC – Clearing House On Oral Problems
Related To H.I.V. Infection & W.H.O. Collaborative
Centre On Oral Manifestations Of Immunodeficiency
Virus J Oral Pathol Med 1993; 22: 289-91”

20. CLASSIFICATION OF OROFACIAL LESIONS
ASSOCIATED WITH HIV IN PEDIATRIC PATIENTS
GROUP 1 – LESIONS COMMONLY ASSOCIATED WITH
HIV IN PEDIATRIC PATIENTS
• Candidiasis
• HSV Infection
• Linear gingival erythema
• Recurrent aphthous ulcers
major /minor /herpetiform

21. • GROUP 2 – LESIONS LESS COMMONLY ASSOCIATED
WITH HIV IN PEDIATRIC PTS
• BACTERIAL INFECTIONS OF ORAL TISSUES
• PERIODONTAL – NUG , NUP
• NUS
• SEBORRHEIC DERMATITIS
• VIRAL INFECTIONS – CMV , HPV , MOLLUSCUM
CONTAGIOSUM , VARICELLA ZOSTER , HERPES ZOSTER
, VARICELLA , XEROSTOMIA

22. • GROUP 3 – LESIONS STRONGLY ASSOCIATED WITH
HIV ( RARE IN CHILDREN)
• NEOPLASM , KS , NON HODGKIN’S LYMPHOMA
OHL , TB RELATED ULCERS
• Ramos – Gomez Fj , Flait Zc , Catapanop , Et.Al
Classification , Diagnostic Criteria & Treatment
Recommendations For Oro Facial Manifestations In
Hiv Infected Pediatric Patients. Collaborative Work
Group On Oral Manifestations Of Pediatric Hiv
Infection. J Clin Pediatric Dent 1999;23:85-96

23. GROUP 1
1.ORO PHARYNGEAL CANDIDIASIS ( OPC)
• One of initial manifestation of HIV
• 90% of untreated
• 60% - atleast 1 episode per yr with frequent recurrences
• Chiefly caused by yeast – c.albicans
• Other : c. glabrata, c.dubliniensis
• C. tropicalis, c.parapsilosis, c.kruseii
• C.novergensis

24. • Pseudomembranous : commonest form
• characterized by Creamy yellow curd
like plaques that can be easily removed
with wiping with a cotton gauze
or tongue depressor,
often leaving a red, raw base.
Erythematous Form (atrophic) is characterized by reddish
macular lesion .
• loss of papillations when involving the tongue dorsum.

25. • Angular cheilitis affects the labial
commissures & results in
cracking, ulceration &
pseudomembrane formation.
• Hyperplastic: appear white and hyperplastic
• white areas are due to hyperkeratosis
• Non scrapable
• Confused with hairy leukoplakia.

26. • Diagnostic modalities: based on clinical appearance and
response to empirical antifungal therapy.
• Microscopic Examination : swab - budding yeast cells,
pseudohyphae, or filaments
• KOH & PAS - improve Visualization of Fungal elements in
cytologic specimens.
• Culture on Sabouraud dextrose agar medium for 24 to 48
hours

27. 2. Oral hairy leukoplakia
• 2nd most common hiv associated mucosal lesion
• Caused by EBV virus
• latently infects 90% of the population worldwide
without causing disease.
• OHL occurs in pts with CD4+ T cell counts < 400
• Used as a marker of disease activity
• affects men more than women

28. Clinical features :
• Site : lateral borders of tongue,
dorsum
• Rarely FOM, buccal mucosa
• Bilaterally as painless, faint white vertical streaks/
thickened & furrowed areas with shaggy keratotic
surface ( hyper keratotic hair like projections)
• Vertical striations imparts a corrugated appearance.
• Non scrapable lesion
• Asymptomatic

29. • PROVISIONAL DIAGNOSIS : clinical characteristics
• PRESUMPTIVE DIAGNOSIS : HISTOPATHOLOGY
• hyperkeratosis & acanthosis leading to corrugations,
Koilocytosis, Nuclear beading, chromatin
margination
• DEFINITIVE DIAGNOSIS : VIRAL DEMONSTRATION
• Fluorescent In Situ Hybridisation
• IHC, PCR, EM

30. 3. KAPOSI SARCOMA
• Angiogenic disorder in which multi centric neoplastic
proliferation of vascular, spindle cell components
occurs in response to circulating growth factors.
• Wahman et.al. cofactor model : inf, host, env
• Chang et.al., moore et.al. – HHV 8, KSHV
• Four types : Classic,
• African type
• Transplant associated, AIDS related

31. AIDS RELATED
• seen in 55% homosexual pts
• Represents 1st sign of progression of AIDS
• Many cutaneous lesions are seen
• Oral lesions can occur on any mucosal surface
• Mainly on hard palate, maxillary gingiva,
• Also – tongue, uvula, tonsils, pharynx
• Associated with cervical lymphadenopathy
• Salivary gland enlargement

32. Multiple Flat,
blue/red/purpl
e patches
Coalesce to
form plaques
Surface papules
/ nodules
develop
Lesion becomes
exophytic,
ulcerate and
bleed
Asymptomatic initially
• May cause discomfort during speech, eating
• on palate, alv . Ridge : resorption - tooth loss
• compromise airways
Diagnosis : biopsy
Patch stage
Plaque stage
Nodular stage

33. NON HODGKINS LYMPHOMA
• Second most common neoplasm associated with
AIDS
• HIV pts are 60 times at risk
• Lesions tend to present as large, painful, ulcerated
mass on palate, gingival tissues.
• Biopsy – for definitive diagnosis

34. 4.A. Linear gingival erythema
• As distinctive fiery red band of marginal gingival tissue
without ulceration or attachment loss, prone to
bleeding
• Some times extend beyond the MGJ.
• The lesion redness is disproportional to the amount of
plaque and persists after removal of plaque
• HP : reveals little inflammation
• Clinical redness represents vascular reponse with no
lymphocytic infiltration.

36. 5.B. Necrotising ulcerative gingivitis
• Fusospirochaetal infection
• Involves primarily free gingiva , crest of gingiva, id
papilla
• Rarely soft palate, tonsil
• Occurs at any age, middle age – common
• Stress, immunosuppression, malnutrition, trauma,
smoking

37. • Painful , hyperemic gingiva & sharply punched out
crater like erosions of id papilla of sudden onset
• Ulcerated remanants bleed when touched
• Covered by greyish pseudomembrane
• Ulcers tend to spread to all margins
• Pt c/o inability to eat, fetid odour
• Excessive salivation, metallic taste
• Systemic manifestations

39. 5.C.Necrotising ulcerative periodontitis
• characterized by recession and increased attachment
loss with shallow probing depths, bleeding, tissue
sloughing, loss of id papillae, fetid odor, and moderate
pain.
• Periods of activity (tissue necrosis and loss) may be
followed by
• periods of quiescence (healing with no signs of
inflammation, but evidence of permanent residual
tissue loss)

41. • Typical : P. gingivalis, P. intermedia, T.denticola,
Actinobacillus actinomycetemcomitans
• Atypical bacteria seen in NUP ( HIV PTS) : Bulleidia
Extructa, Dialister, fusobacterium, selenomonas,
peptostreptococcus, veillonella
• Condition may be exacerbated by Candida, herpes like
viruses & by an HIV disease–related increased
inflammatory cytokine response
• Fusobacterium necrophorum plays a major role in
progression of NUP to noma.

42. • Diagnostic modalities : clinical appearance
Measurements of recession, periodontal probing
depths, attachment levels, and mobility
• Imaging : of areas of NUP involvement may show loss
of crestal cortication associated with rapid alveolar
bone loss.

43. GROUP II
A) Mycobacterial infections
• MAC, M.TB
• Approx 1/3rd of AIDS-related deaths worldwide are due to
TB
• increased reactivation of latent TB infections as well as
higher primary rates of TB
• Pulmonary TB is the most common
• Extrapulmonary disease affecting the liver, spleen,or
kidney may occur in patients with CD4 < 100 cells/mm3

44. ORAL MANIFESTATIONS :
• Primary TB : gingiva, tooth extraction sockets, buccal
folds
• Sec. TB : tongue, palate, lips, alveolar mucosa & jaw
bones
• present as ulcers or nodules, vesicles, fissures,,
plaques, granulomas and verrucous proliferations.
• single or multiple, painful or painless

45. • Ulcer – irregular, ragged, undermined edges,
minimal induration , with yellowish granular base
• Tongue : lateral border, ant. Dorsum, base of tongue
• Painful, grayish-yellow, firm well demarcated
• Palate : Small granulomas or ulcerations
• Lips : shallow granulating ulcers
• TB OSTEOMYELITIS
• TB SIALADENITIS

47. B) MELANOTIC HYPERPIGMENTATION
• HIV pts hyperpigmentation of oral mucosa , skin, nails
occurs suddenly
Due to
• Direct result of HIV infection
• Adrenocortical destruction due to several infections
associated with hiv
• Medication intake : ketoconazole, zidovudine

48. C) NECROTISING ULCERATIVE STOMATITIS
• NUG, NUP, NUS – different clinical stages of same disease (
robinson et.al)
• Collectively – necrotising gingivostomatitis
• NUS is an outcome of NUG/P progressing beyond mucogingival
demarcation
• Sometimes arise on mucosa seperately
• NUS involves mainly soft tissues, may extend into underlying
bone causing massive tissue destruction.
• If NUS extends from oral mucosa to involve facial skin, it will
result in noma

49. Hiv
infects lc
cells
Depletion
of lc cells
Decreased
local
immune
response
Increased
susceptibility
to infections
NPD,
NUS
STIMULATES
CYTOTOXIC T-
CELL RESPONSE
PATHOGENESIS

50. D)UNI/BILATERAL SWELLING OF MAJOR SALIVARY GLANDS
• HIV-associated lymphoepithelial lesions which are
known as hiv associated salivary gland lesions ( HIV
SGD)
• Hyperplastic reactive lymphadenopathy,
• Benign lymphoepithelial cysts,
• Malignant : lymphoma, ks
• benign neoplasms
• Bacterial , mycobacterial , and viral infections

51. • Diffuse Infiltrative Lymphocytosis Syndrome (Dils)
• In 3% of hiv pts multiple lymphoepithelial cysts
proliferate in parotid gland
• Painful enlargement of gland
• Lesion involves entire parotid parenchyma, so presents
as localised mass
• Not moveable, Tender on palpation
• Tense , due fluid accumulation in multiple cysts
• Reduced salivary gland function : xerostomia, sicca
symptoms

52. • In HIV +ve, CT scan showing multiple hypodense areas
is suggestive of DILS .
Histopathology :
• Characterized by persistent infiltration of CD8 cells that
have the ability to destroy HIV-infected cells
• lymphocytic infiltration involving the salivary glands (~
to Sjogren syndrome)
• Differentiation : DILS also involves lungs, kidney, git
• Sj autoab’s will be absent in pts with DILS

53. • Fine-needle aspirates can be useful in differential
diagnosis of salivary gland masses
• Confirmatory - histopathologic diagnosis
• If ct shows a defined mass, then superficial
parotidectomy
• If no defined mass is seen in ct then incisional biopsy
• Immunohistochemical analysis from a biopsy are
essential to determine the nature of the salivary gland
enlargement.

54. E) THROMBOCYTOPENIC PURPURA
• HIV related immune thrombocytopenic purpura
• Immune mediated destruction
• Circulating immune complexes are non specifically
deposited on platelet membrane, resulting in
reticuloendothelial clearance.
• Us studies , HIV directly infects megakaryocytes , leading
to impaired production

55. • Thrombotic thrombocytopenic purpura is also
seen in HIV pts.
• Other causes of thrombocytopenia in HIV :
• Infections / neoplastic conditions involving
bone marrow
• Any medication causing myelosuppression

56. F) ULCERATIONS NOT OTHERWISE SPECIFIED
• single or multiple, well-circumscribed, extremely
painful
• often with a pseudomembrane, > 0.5 cm to 2/ 3 cm
• may have a recurrent pattern/ not
• may last for several weeks, healing with scarring.
• Typically found on nonkeratinized epithelial mucosa

57. • In immune-suppressed patients ulcers are deeper
and devoid of the classic erythematous halo at ulcer
margin
• Biopsy should be obtained for lesions lasting > 3
weeks

58. G) VIRAL
1)HSV : In HIV pts presents
• as an erythematous pruritus that develops into
painful vesicles and ulcerates over a brief period,
accompanied by painful regional lymphadenopathy.
• HSV infection may involve all oral mucosa
• Both keratinised & non keratinised
• can be more prolonged and severe than in HIV-ve

59. 2) HUMAN PAPILLOMA VIRUS
• 120 strains , 25 – oral lesions
• Epitheliotrophic, it contains epithelial growth factors
• Induce distinct squamous cell proliferation
• VERRUCA VULGARIS – CUTANEOUS HPV 2, 57
• CONDYLOMA ACCUMINATA – HPV 6 & 11
• FOCAL EPITHELIAL HYPERPLASIA – HPV 13 & 32

60. • VERRUCA VULGARIS ( COMMON WART)
• cutaneous lesion, less common on mucos memb
• Numerous finger like projections
• Resulting in lesion with rough, verrucous, cauliflower
like surface
• Well circumscribed, pendculated/sessile
• Contagious, capable of spreading to other parts

61. • CONDYLOMA ACCUMINATUM ( veneral wart)
• Soft, pink nodules which proliferate & coalesce rapidly
to form diffuse papillomatous clusters of varying size
• Occurs on moist, intertriginous areas
• Seen on tongue, commissures
• Also present on other mucosal surfaces

62. • FOCAL EPITHELIAL HYPERPLASIA
• Most contagious oral papillary lesion
• Well circumscribed numerous soft, flat,sessile, non
papillomatous papules are distributed throughout oral
mucosa
• Site : labial, buccal, lingual mucosa, Gingiva, tonsil
• Differs from other HPV infections : extreme acanthosis,
hyperplasia, but minimal production of surface
projections
• Mucosa is 8-10 times thicker than normal.

63. 3) VARICELLA ZOSTER:
• Acute ubiquitous extremely contagious disease occuring in
children, young adults
• Maculopapular rash, vesicular eruptions which begins on
trunk, spreads centrifugally ( face & extremities)
• Occurs in successive crops.
• Skin lesions rupture , form superficial crusting , heals by
desquamation
• Can occur anywhere on oral mucosa
• Vesicles rupture to form eroded ulcers with red margins.

64. • HERPES ZOSTER
• In HIV latent VZV is reactivated by
Immunocompromised state
• Lymphomas like Hodgkins , T Cell Leukemia
• Prodrome : Deep aching / burning pain
• Dermatomatic/ zosteriform distribution of vesicles
• Unilateral, clustered distribution of vesicles, ulcers
• Thoracic > lumbar> craniofacial areas
• V1 is most commonly involved

65. • Post herpetic neuralgia :
• Pain that persists for 30/120 days after onset of rash.
• Occurs at any age
• More common in elderly pts
• Cli. Features: persistent pain, hyperesthesia,
parasthesia, allodynia for months or yrs after zoster
lesions have healed.

66. Diagnostic modalities :
• History, clinical examination
• h/p : tzanck cells ( multinucleated giant cells)
• Fluorescent antibody staining
• Culture, serology

67. Group : 3
lesions seen in HIV

68. ACTINOMYCOSIS
• Actinomyces – filamentous bacteria
• living as commensal organisms in the human oral
cavity and respiratory and digestive tracts
• Becoming invasive when, through a mucosal lesion,
they gain access to the subcutaneous tissue.
• Infection is always endogenous. Doesnot occur by
person to person contact.

69. • Presents as a chronic, fluctuant mass
• Located at the border of the mandible
• Pain is rare, slight fever
• Initially, the mass may be surrounded by
induration or erythema; later, it may become
tender to palpation, on account of a central
necrosis process
• Becoming progressively larger within weeks or
months

70. • Mass breaks down and abscess, sinuses are formed
• Discharging pus contain typical yellow sulphur
granules
• Skin overlying abscess is purplish,red indurated has
appearance of wood.
• Infection may extend into adjoining soft tissue as well
as bone
• Leads actinomycotic osteomyelitis

72. Epitheloid (bacillary) angiomatosis
• Vascular proliferation that ~ ks
• First described in 1983 in HIV pts
• Occurs when CD4 count < 100/cumm
• Rarely seen in immunocompetent pts
• Mucocutaneous disorder
• Lesions – vascular papules that grow to form nodules
• Diagnosis : hp
• Which demonstrate presence of causative bacteria

73. Drug reactions
• Ulcerative
• Erythema multiforme
• Lichenoid reactions
• Toxic epidermolysis

74. 4)Fungal other than candidiasis
• cryptococcus neoformans
• Geotrichum
• Histoplasma
• Mucoracea
• Aspergillus flavus

75. Cryptococcosis:
• Cryptococcus neoformans
• Meningoencephalitis
• Symptoms include headache, nausea, irritability,
and diminished cognitive function
• physical findings include cranial nerve palsies,
hyperreflexia, and papilledema.
• Rarely, intraoral ulcerations may occur in mucosal
tissues with dissemination of cryptococcosis

76. • Histoplasmosis
• Primary infection – self limiting pulmonary infection.
• Heals with fibrosis, calcification
• In HIV PTS progressive disseminated form
• Predilection for RE SYSTEM
• Involves liver, spleen, lymphnodes, bone marrow
• Oral histoplasmosis in HIV occurs alone/ as a part of
disseminated infection.

77. • Oral : nodular / ulcerative/ vegetative lesions
• Ulcerated areas covered by pseudomembrane
• Indurated margins
• Dissemination of histoplasmosis to the oral mucosa
may occur primarily on the gingival, tongue, palate,
and buccal mucosa.
• Gingival lesions will appear as diffuse granulomatous
inflammation with progressive alveolar bone erosion
and loosening of teeth

78. ASPERGILLOSIS
• Aspergillus spore is found in decaying vegetation and
in the immunocompromised host may cause acute
invasive pulmonary aspergillosis.
• Aspergillus species have also been isolated from the
air and environmental surfaces of hospital settings
• Hospitalized immunosuppressed individuals may be at
increased risk.

79. • Invade blood vessels causing thrombosis and infarction
of the perivascular tissues.
• Less commonly Aspergillus invades the sinuses and can
progress through the underlying soft tissue and bone to
cause palatal and oral lesions, typically described as
black or yellow necrotic lesions of the soft tissue

80. Recurrent aphthous stomatitis
• Most commonly reported type of ulcers in HIV +ve
pts
• Etiology remains undetermined
• Ulcers appear clinically as painful, round-to-oval,
yellow or white, & are surrounded by a halo of
erythema.
• HIV-positive patients usually experience increased
frequency and severity of typical minor aphthous
ulcers

82. CYTO MEGALO VIRUS :
• May cause oral ulceration in HIV-positive pts with
• disseminated cytomegalovirus (CMV) disease
• Ulcers may occur anywhere in the oral cavity
• Resemble MAU in size.
• Instead of an erythematous margin, CMV ulcers
appear necrotic with a white halo.
• Deep tissue biopsy with biopsy punch or scalpel is
used to confirm diagnosis
• .

83. • large intracellular inclusion bodies are characteristic of
infection.
• Patients may develop CMV retinitis, esophagitis, colitis,
pneumonitis, and neurological disease

84. Molluscum contagiosum
• Infection of skin caused by pox virus
• Shiny, white, skin coloured dome shaped papules that
often demonstrate a central depressed crater.
• In pts with AIDS numerous lesions may be present
• No tendency to undergo spontaneous resolution
• Hp : large intracytoplasmic inclusions are seen
• Molluscum bodies

86. CONCLUSION
• Dentists play an important role in managing
the oral health of patients with HIV disease
• Knowledge of HIV oral lesion clinical
appearance, lesion symptoms and behavior,
various treatment approaches, and anticipated
response to treatment are important for oral
disease control and oral health maintenance

87. REFERENCES
• Lauren L Patton, Oral Lesions Associated With Human
Immunodeficiency Virus Disease. Dent Clin N Am 57
(2013) 673- 698
• Nicholas G Mosca, Alicia Rose Hathorn , HIV Positive
Patients : Dental Managent Considerations. Dent Clin
N Am 50 (2006) 635-657
• Charles E Barr, Michael Glick , Diagnosis And
Management Of Oral & Cutaneous Lesions In HIV -1
Disease. Dent Clin N Am 10 (1998)25-45

88. • Burkets Oral Medicine , 11th Edition, Bc Decker Inc
Hamilton 2008
• Robert E Marx, Diane Stern Oral And Maxillofacial
Pathology: A Rationale For diagnosis & Treatment.
1st edition, Quintessence.2003
• R Rajendran B Sivapathasundharam Shafer’s
Textbook Of Oral Pathology. 5th Edition, Elsevier,
2008

89. HIV does not make people dangerous
to know, so you can shake their
hands and give them a hug: Heaven
knows they need it !!