DENT 267: LO3 LS3 & LS4- Plan Perio Care of Viral Infections of the Gingiva, and Gingival Manifestation of Inflammatory & Immune Conditions and Lesions

viral origin

-Coxsackie virus (hand foot and mouth disease)

-herpes simplex

-varicella-zoster (chicken pox, shingles)

-Molluscum contagiosum virus

-Human papilloma-HPV (squamous cell papilloma condyloma acuminatum, verruca vulgaris, and focal epithelia hyperplasia)

herpes virus

-herpes simplex virus (HSV) type 1 and 2

-Varicella Zoster (chicken pox)

primary herpetic gingivostomatitis

-acute herpetic gingivostomatitis

-herpes simplex virus type I

-small percentage (1%) of individuals on first contact w/ the HSV 1 develop severe signs and symptoms of a primary infection

-contagious

-virus binds to nerve terminals within epithelial tissues of the mouth & skin

-in most ppl, primary infection is asymptomatic, 10-20% may show some signs of initial infection and may go unnoticed)

primary herpetic gingivostomatitis: most contagious when

-vesicular stage

primary herpetic gingivostomatitis: spread how

-by kissing and contact w/ open sores or by contact w/ infected saliva, contaminated surfaces

-from saliva to fingers (herpetic whitlow) to eye

clinical characteristics of primary herpetic gingivostomatitis

-prodrome: tingling, itching, pain at site prior to blisters developing

-acute

-last 7-10 days

-vesicles that rupture to form ulcers (intraoral, skin, lips)

-bleeding

-fever

-malaise

-lymphadenopathy

-headache/irritability

-painful

HSV-1 and HSV-2 stages

1. prodromal stage: early stage with redness, swelling and a burning or tingling sensation at the sight of infection

2. Blister stage: outbreak of tiny blisters filled w/ clear to whitish-yellow fluid

3. eruptive stage: blisters break open and leak fluid, leaving painful open sores that crust over

4. healing stage: crusted sores start to scab and heal

HSV-1

-more commonly associated w/ oral herpes (cold sores)

HSV-2

-more commonly linked to genital herpes

mild reaction to initial HSV infection

-a single herpes vesicle

moderate reaction to initial HSV infection

-multiple widespread lesions

severe reaction to initial HSV infection

-severe widespread lesions

histopathology of AHGS (acute herpetic gingivostomatitis)

-vesicles located within the epithelium

-ballooning degeneration

-ulcers

-diagnosis usually based on hx and clinical findings

-virus can become latent in the body and can be reactivated later

etiology of AHGS (acute herpetic gingivostomatitis)

-by mid age, about 70% have been infected w/ HSV-1 without any symptoms during primary infection

-small percentage (1%) of the population will develop the acute signs

-virus ascends through the sensory & autonomic nerves

-most causes of AHGS are caused by HSV 1 but may also result from initial infection by HSV 2

prognosis of acute herpetic gingivostomatitis

-persists as latent HSV in neuronal ganglia that innervate the site

-once infected, most ppl develop immunity

-in some, virus is latent and will hide in trigeminal nerve ganglion and recur as recurrent herpes simplex (only 15%-40% of seropositive patients/clients experience recurrent mucuocutaneous lesions)

-sunlight, trauma, fever, stress may trigger recurrence

-contagious (in vesicular stage)

acute herpetic gingivostomatitis: nutritional implications

-fluid intake to avoid dehydration, nutritional drinks (Boost, Ensure) Gatorade, Pedialyte

-well-balanced diet low in retentive sugars, process foods in blender

-7-10 days resolution

care planning for acute herpetic gingivostomatitis

-diagnosis by clinical symptoms & history

-systemic antiviral meds such was acyclovir

-analgesics and antipyretics (to prevent/reduce fever), fluids, close observation, biofilm control

-rinse/coating agent (Benadryl/Maalox suspension) by prescripton

-topical anesthetic (mouthrinse) w/ caution on children

-usually runs its course in 10-20 days

-dentist/physician may prescribe antivirals if very recurrent

-postpone dental treatment

if someone with acute herpetic gingivostomatitis has a fever of higher than 38.3 degrees celsius, what should be done

-patient is septic w/ oral bacteria that have entered the bloodstream through the open sores on the gingiva or mucosa

-systemic antibiotics to control secondary bacterial infection (Penicillin V or Clindamycin)

recurrent herpes

-no elective dental treatment when client has herpes lesions

-lesions could progress if tissue is manipulated

-virus can spread to clothing through aerosols & then be transmitted

herpetic whitlow

An infection caused by herpes simplex virus infection that involves the finger

varicella-zoster infections

-headache, pharyngitis, maculopapular eruptions, fever, vesicles, ulcers

-in the oral cavity, the vesicles that breakdown form ulcers

-neurotropic virus so can recur as Herpes Zoster causes shingles

-shingles more common in elderly and the immunocompromised

care plan for varicella-zoster infections

-postpone elective dental treatment

-palliative (manage pain, fever, skin lesions, Benadryl, antiviral drugs)

-effective biofilm control

types of hypersensitivity reactions

-contact allergy

-plasma cell gingivitis

-erythema multiforme

types of autoimmune diseases

-pemphigoid

-lichen planus

-lupus erthematosis

types of granulomatous inflammatory conditions

-Crohn's

-sarcoidosis

what is recognized as a clinical manifestation of certain autoimmune/immunopathologic

-desquamative gingitivis

oral features of mucocutaneous disorders

-oral mucosa can be affected by a variety of mucocutaneous diseases (skin and mucosal surfaces- eye, oral cavity, genital mucosal surfaces)

what is desquamative gingivitis

-erosive lesions associated with vesiculobullous diseases such as lichen planus, pemphigoid and pemphigus

oral lichen planus

-intense redness of the gingiva

-ulcerations

-interlacing white lines may be present

-raised white lesions may be present

-normally chronic condition with oral form

-6 types of clinical manifestations

oral lichen planus: what are the 6 types of clinical manifestations (lesions)

-papular

-reticular

-plaque type

-erythematous

-ulcerative

-bulbous

clinical characteristics of MILD and MOD desquamative gingivitis

-mild forms

-mod

-burning sensation irritated by thermal changes, air, spicy foods, and carbonated drinks

-local irritants exaggerate response

clinical characteristics of SEVERE desquamative gingivitis

-lesions may also involve alveolar, buccal and palatal mucosa

-extreme pain that can be aggravated by spicy foods, air, temp, carbonated frinks

etiology of desquamative gingivitis

-related to systemic immunologic (Autoimmune) abnormalities that often show skin lesions as listed in the AAP classification (systemic mucocutaneous conditons)

-allergic reactions, food allergy related, drug induced, potentially vit deficiency, potentially in menopausal women

histopathy/pathogenesis of desquamative gingivitis

-atrophy and thinning of the epithelium

-separation of epithelium from CT

-direct or indirect Immuno-fluorescence testing of tissue may show antibody/antigen involvement

nutritional implications/prognosis

-nutritional: may have problems eating due to soreness

-prognosis: periods of remission/exacerbation is typical for the mucocutaneous disorders

diagnosis of desquamative gingivitis related to a mucocutaneous disorder

-client history

-clinical signs & symptoms

-biopsy of the affected tissue

-biopsy may reveal the antibody/antigen complexes involved

-bloodwork may be involved to detect autoantibodies (such as w/ lupus)

if diagnosis supports the findings of a mucocutaneous disorder, what should be done

-referral to dentist/periodontist/oral surgeon for biopsy

-referral to dermatologist

care plan gingival manifestations of mucocutaneous reactions

-client education: discuss nature of disease and important of biofilm control in eliminating biofilm as a source of irritation

-debridement

-well-balanced diet

-topical corticosteroids may be prescribed by the dentist of physician

-use a splint if needed

-systemic treatment may include systemic corticosteroids

-eval

-frequent CC intervals

-warm water rinses

-avoid spicy, carbonated drinks, and alcohol

-avoid stressful situations

client case: 23 year old female has a history of recurent desquamative gingivitis over last several years in localized areas. A biopsy was done previously with no specific diagnosis made. What should we do?

-refer client to a periodontist for assessment

allergic reactions

-result from contact sens to certain mouthwashes, toothpastes, dental restorative materials (acrylic, nickel)

-carvone- terpenoid found in essential oils of caraway seeds, dill, spearmint

-more common in ppl who have multiple allergies

-flavouring agents/additives in "tartar-control" toothpastes

signs of allergic reaction

-fiery red, edematous with ulcerations

-bleeding

-sloughing

-cheilitis

erythema multiforme

-uncommon acute inflammatory disorder

-causes large, symmetrical erythematous papules resembling target in circular pattern

-unknown cause

plasma cell gingivitis

-rare

-characterized by a massive infiltration of plasma cells into the sub-epithelial gingival tissue

-clinically presents as a diffuse enlargement with edematous swelling of the gingiva in the max and mand anterior segments

-exact mechanism behind this is unknown

-presence of plasma cells suggests an allergic origin

-diagnosis is by biopsy

non-biofilm induced traumatic lesions: physical/mechanical insults

-frictional keratosis

-toothbrushing-induced gingival ulceration

-factitious injury (self harm)

-can be self-inflicted, accidental, or iatrogenic

-commonly appears as abrasions, ulcerations, burns

chemical insults

-etching

-chlorhexidine

-ASA

-hydrogen peroxide

-dentifrice detergents

-paraformaldehyde or calcium hydroxide