Oral Health and HIV Disease

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Presentation transcript:

Oral Health and HIV Disease Consequently, Screening for dental disease and oral lesions is an essential component of a patient evaluation and would hopefully occur at the first or second visit. I’m Dr. Stewart – and during the next few minutes, I’d like to share with you some of the common oral signs and symptoms one might see during that oral screening evaluation. an HIV infected patient might present with. Carol M. Stewart DDS, MS

Program Objectives Appreciate importance of oral health as integral to total patient care Appreciate the significance of oral manifestations in era of HAART Review common oral manifestations

Goals of Oral Health Program Treat pain, eliminate sources of infection, and identify/diagnose pathology Facilitate maintenance of adequate nutrition by stabilizing and preserving oral tissues and restoring chewing function Educate patient regarding health maintenance – oral hygiene, nutrition, xerostomia management, and medication compliance Contribute to self-esteem and quality of life

Oral Health In a healthy mouth, the gingiva (gum tissue) is generally pink/coral in color No bleeding is noted Teeth are free from dental caries (tooth decay) In this photo, no restorations or “fillings” are observed

Poor Oral Health Gingiva is diffusely erythematous (red) with areas of marked inflammation Teeth have deposits of plaque and calculus (tartar) near the tooth/ gingiva interface Defective dental restorations are noted

Significance of Oral Lesions Often first clinical sign of HIV disease Signify disease progression Marker for HAART failure Impact medication compliance Impact nutrition CDC CDC

Oral Lesions and HAART Appear to be Decreasing: Candidiasis Oral Hairy Leukoplakia Kaposi’s Sarcoma Necrotizing Periodontitis Appear to be Increasing: HPV assoc. Condyloma acuminata Xerostomia Dental decay

Traditional Outline of Oral Conditions Malignant neoplasms Kaposi’s sarcoma (KS) Non-Hodgkins Lymphoma Squamous cell carcinoma Stomatitis/ Ulcers Aphthous (major/minor) Stomatitis NOS Salivary Gland Disease Xerostomia Fungal Candidia albicans (Candidiasis) “Thrush” Histoplasmosa capsulatum (Histoplasmosis) Cryptococcus neoformans Viral Oral hairy leukoplakia (Epstein-Barr virus) Herpes simplex virus (HSV) Herpes Zoster “Shingles” ( Varicella-zoster virus) Human Papilloma Virus (HPV) Cytomegalovirus (CMV) Periodontal disease Linear gingival erythema (LGE) Necrotizing ulcerative periodontitis (NUP)

Fungal Diseases Candidiasis Histoplasmosis Cryptococcus

Oral Candidiasis, Candida albicans fungal infection associated with: antibiotic treatment corticosteroid treatment (inhaled and systemic) diabetes, xerostomia, smoking removable dental appliances defects in cell-mediated immunity observed in 60-80% of individuals with HIV (pre-HAART)

Oral Candidiasis- symptoms Oral burning Dysphagia Dysgeusia Loss of appetite

Erythematous Candidiasis red, flat patches on any Hard palate oral mucosal surface Dorsal tongue

Diagnostic Tools for “yeast” Cytologic smear KOH Prep 3. Culture To confirm diagnosis, a culture, KOH prep, or cytologic smear may be obtained. For a smear, use a cytobrush or tongue blade to scrape the surface of the lesion, spread on a glass slide,fix and request a PAS stain from the lab. Positive smears will demonstrate the red hyphae among the epithelial cells. Cheek cells showing fungal hyphae

Pseudomembranous Candidiasis (“thrush”) creamy white or yellowish curd-like plaques on any oral mucosal surface usually on red mucosa, easily wiped off - may bleed soft palate inside of cheek CDC CDC

Pseudomembranous Candidiasis Hard Palate Gingiva Note the physiologic pigmentation (dark brown areas) on the palate and gingiva

Hyperplastic Candidiasis larger areas of white or discolored or coalesced plaques cannot be wiped off sign of severe immune suppression

Angular cheilitis fissures and redness radiating from either or both corners of the mouth usually concurrent with intraoral candidiasis bottom -post-treatment healing

Oral Candidiasis - Treatment Topical - nystatin clotrimazole (Mycelex) amphoteracin B oral suspension (Fungizone) Systemic - fluconazole 100 mg tabs (Diflucan) ( Two tabs day one, then 1 per day for two weeks.) Public Health Service is advising to be careful with Diflucan – not use it as drug of first choice…. Due to resistant strains emerging. IF do, intraconazole will work. Vaginal tabs do not have sugar

Candidiasis Treatment - for Partials and/or Dentures Treat oral removable appliances **Get a NEW toothbrush Remind patient to obtain a new toothbrush to avoid “re-infection”

Histoplasmosis Affects any oral site - gingiva most common, also tongue, buccal mucosa and palate Usually has ill-defined margins and may be accompanied by submandibular lymphadenopathy Clinical - chronic ulcer, Silver stain (GMS) erythema, and swelling shows histoplasmosis organisms

Viral Conditions Oral Hairy Leukoplakia (OHL) Herpes Simplex (HSV) Varicella-zoster (VZV) Human Papilloma Virus (HPV) Cytomegalovirus (CMV)

Oral Hairy Leukoplakia (OHL) white lesion, usually present on lateral borders of tongue, vertically corrugated hyperkeratotic patches CDC

Oral Hairy Leukoplakia (OHL) may appear as hairy or feathery projections does not wipe off associated with Epstein Barr virus asymptomatic (unless co-infected with Candida) This patient came into graduate program – consult re lichen planus. Was not - Bx OHL with positive for Epstein Barr virus. Tested neg for HIV using PCR

Oral Hairy Leukoplakia - Diagnosis Biopsy for definitive diagnosis If positive with EBV DNA, suggest HIV counseling and testing EBA/DNA in-situ hybridization Punch biopsy Biopsy if patient unaware of HIV status White lesions on the lateral border of the tongue could be Lichen planus, frictional keratosis, dysplasia or cancer

Herpes Simplex Virus (HSV) Affects peri-oral areas, lips, palate, gingiva, and intraoral mucosa Multiple small vesicles in a cluster (left) Vesicles may become ulcerated and coalesce to appear as large ulcers (right) Vesicles contain live virus Vesicles eventually crust CDC slide CDC

Herpes Simplex Virus (HSV) In HIV+, reactivation clinically appears similar to primary herpes

Varicella-Zoster Virus (“Shingles”) Result of reactivation of latent Varicella-Zoster virus Painful clusters of vesicles – usually localized to one neurodermatome May develop recurrent HSV Third division of trigeminal nerve affected in photo- (stops at midline of face)

Human Papilloma Virus (HPV) Condyloma Acuminatum - also called “Oral or Venereal Warts” Intraoral or perioral, gingiva, palate, buccal mucosa, covering large areas single or multiple cauliflower-like or flat at site of sexual contact

Human Papilloma Virus (HPV) Maybe sessile, flat, or raised High recurrence rate Lips Inside lips and cheek Cure difficult, Counseling important

Cytomegalovirus (CMV) Human herpes virus (HHV-5) Serologic evidence of infection common CMV retinitis may affect 1/3 of patients with AIDS- may progress to blindness May appear as chronic ulcer anywhere in oral cavity Biopsy to confirm diagnosis

Periodontal Disease Linear Gingival Erythema (LGE) Necrotizing Ulcerative Periodontitis (NUP) Linear gingival erythema is somewhat unique to HIV patients – as it may initially appear similar to periodontal disease in immune competent hosts. The difference is that the pain is more than one would expect – and it does not respond well to conventional therapy

Periodontal Disease Etiology Microbial dental plaque initiates periodontal disease Disease behavior is dependent on host defenses Systemic factors modify all forms of periodontal disease by their effects on normal immune and inflammatory defenses Bacterial infectionPlaque causes attachment loss – Toxic Microbes include Porphyromonas gingivalis and Baceroides forsythus, Actinobacillus actinomycetemcomitans (Aa) comitatns , release toxins There are over 500 organisms identified in perio pockets- but primarily gram negative anaerobic rods, and some Gram positive facultative and anerobic cocci and rods, andcgram negative facultative rods. Chara by loss of clinical attachment due to destruction of periodontal ligament, and loss of adj. supporting bone IN health, host keeps organisms in balance

Linear Gingival Erythema (LGE) profound red band along gingiva where tissue meets the teeth mild pain responds poorly to conventional treatment mild more advanced

Linear Gingival Erythema (LGE) Treatment Dental debridement 0.12% Chlorhexidine gluconate (PerioGard or Peridex) Rinse 2 times per day for 2 weeks Patient must brush 2-3x/day and floss daily

Necrotizing Ulcerative Periodontitis (NUP) marker of severe immune suppression rapid destruction of gingival tissue and supporting bone VERY painful,“deep jaw pain” exacerbated by tobacco & xerostomia

Necrotizing Ulcerative Periodontitis (NUP) -Treatment Dental debridement with 0.12% chlorhexidine gluconate or povidone iodine Antibiotics Metronidazole 250 mg 3 times per day for 7-10 days OR Clindamycin 300 mg 3 times per day for 7-10 days Nutritional supplements Close follow-up until resolved

Neoplasms Kaposi’s Sarcoma Non-Hodgkin’s lymphoma Squamous Cell Carcinoma

Kaposi’s Sarcoma Diagnostic for AIDS in HIV positive individual Most common oral malignant neoplasm associated with AIDS Associated with sexually transmitted virus (HHV-8) Intraoral site is initial presentation in 20- 70% of reported cases Biopsy necessary to confirm diagnosis Associated with Human Herpes Virus 8 Has been found in semen – supporting theory it may be – in part- sexually transmitted

Kaposi’s Sarcoma Appear as macules, patches, nodules or ulcerations, bluish, brownish, or reddish Location: Intra-orally - hard and soft palate and gingiva Found anywhere - GI tract, skin or viscera If diagnosed, communication with physician, dermatologist, oncologist, and dentist is essential

Kaposi’s Sarcoma – palate CDC

Kaposi’s Sarcoma - gingiva Probable Early lesion

Pyogenic granuloma may “mimic” Kaposi’s sarcoma of the gingiva Smooth lobulated growth, pink, red, or purple in color - May be ulcerated 75% occur on gingiva, also on lips, tongue and inside cheek (buccal mucosa) Exuberant tissue response to local irritation (Not a tumor or malignancy)

Non-Hodgkin’s Lymphoma Second most common HIV associated malignancy usually B-cell type lymphoma Mouth may be initial presentation Palate and gingiva most common location, but could be anywhere Appear as nodules, growths, painful mass May be non-specific ulcer Prognosis is poor

Squamous Cell Carcinoma Non-healing ulcer anywhere Biopsy any red patch, white patch, or ulcer that is non-responsive to treatment

Thrombocytopenia Intraoral bleeding and/or areas of ecchymosis may be observed with very low platelet counts or ineffective coagulation Requires immediate consultation and treatment

Recurrent Aphthous Ulcers (RAU) No etiologic agent identified Lesions found on buccal mucosa (cheeks) posterior oropharynx, sides of tongue Equal frequency - but more painful and prolonged in HIV infected vs. non-infected

Minor Aphthous Ulcer “canker sores” variable in size - 2-5 mm. diameter surrounded by red halo, may have pseudomembrance covering located on non-keratinized (movable) mucosa often report history of lesions or “canker sores”

Major Aphthous Ulcers greater than 5 mm in diameter, painful, ,and may persist for many weeks biopsy often if non-responsive to treatment and necessary to r/o opportunistic infection may heal with scarring impairment of speech, swallowing and nutrition CDC slide CDC

Aphthous Ulcer Treatment Topical steroids: Fluocinonide 0.05% ointment (Lidex), with 1:1 Orabase Apply qid Clobetasol 0.05% (Temovate) Apply bid ..very potent Dexamethasone elixir (0.5 mg/5 cc) - Hold 1-2 teaspoonfuls in mouth 2 minutes, swish and expectorate, qid Systemic corticosteroid therapy for major lesions – as advised by physician

Sedative Mouth Rinse For temporary relief of pain from oral ulcers Rx: Must be compounded 80 ml 2% viscous xylocaine 80 ml Maalox 100 ml distilled water Disp: 260 ml Sig: Swish for 1 minute and expectorate *Note – gag reflex may be diminished or lost

Xerostomia – “Dry Mouth” Signs and symptoms Xerostomia is the subjective feeling of oral dryness Patient states they can’t eat a meal without water Frequent thirst Often accompanied by objective evidence of hyposalivation Gloved hand will stick to mucosa No “pooling” of saliva observed in floor of mouth Significant dental decay Salivary gland enlargement sometimes observed

Salivary Gland Enlargement Enlargement of major salivary glands, usually parotid gland Lymphocytosis (CD8) and Lymphoproliferative response with cystic lesions May need biopsy and imaging to determine diagnosis

Hyposalivation Inadequate saliva production - common Due to HIV infection and medications which contribute to impaired salivation May occur early in the course of the disease Treatment with fluorides, good oral hygiene, and frequent recalls are essential to avoid tooth loss

Xerostomia Treatment Sugarless gum ( Xylitol ) Sugar-free hard lozenges Artificial saliva products - Optimoist, Oral moisturizer, - Mouth-Kote (OTC)

Unrestored Dental Decay (Caries) Brown areas indicate decay

Result of hyposalivation is tooth loss (patient lost 3 teeth in 2 Result of hyposalivation is tooth loss (patient lost 3 teeth in 2.5 years)

Xerostomia Treatment Fluorides OTC: Gel-Kam (0.4% stannous fluoride) Rx: Prevident Gel or Prevident 5000 Plus (toothpaste plus fluoride)

Basic Oral Care Plan Initial dental exam for every patient Recall every 6 months, sooner if oral conditions include: High caries rate or Xerostomia Periodontal disease Fungal, Viral, or Bacterial infections Neoplastic lesions So assuming we are going to provide comp care – what is the plan Mention care – brush 2-3 x /day with fluoride toothpaste, floss daily Avoid tobacco, snacks

Summary Goal - Maintain maximum health and quality of life for patients Oral assessments Communication among physician, nurse, dental team, and staff is essential

Additional References Patton LL, McKaig R, Strauss R, Rogers D, Eron JJ Jr. Changing prevalence of oral manifestations of human immuno-deficiency virus in the era of protease inhibitor therapy. Oral Surg, Oral Med Oral Pathol Oral Radiol Endod 2000;89:299-304. Tappuni AR, Fleming GJ. The effect of antiretroviral therapy on the prevalence of oral manifestations in HIV-infected patients: a UK study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:623-8. Margiotta V, Campisi G, Mancuso S, Accurso V, Abbadessa V. HIV infection : oral lesions, CD4+ cell count and viral load in an Italian study population. J Oral Pathol Med 1999;28:173-7. Flint S, Glick M, Patton L, Tappuni A, Shirlaw P, Robinson P. Consensus guidelines on quantifying HIV-related oral mucosal disease. Oral Dis 2002;8 Suppl 2:115-9. Patton LL. Sensitivity, specificity, and positive predictive value of oral opportunistic infections in adults with HIV/AIDS as markers of immune suppression and viral burden. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000 Aug;90(2): 182-8. Patton LL, Phelan JA, Ramos-Gomez FJ, Nittayananta W, Shibioski CH, Mbuguye TL. Prevalence and classification of HIV-associated oral lesions. Oral Dis 2002;8 Suppl 2:98-109. Flint S, Glick M, Patton L, Tappuni A, Shirlaw P, Robinson P. Consensus guidelines on quantifying HIV-related oral mucosal disease. Oral Dis 2002;8Suppl 2:115-9. Patton LL. HIV Disease. Dent Clin North Am 2003; Jul 47(3):467-92.