Key points P.1 Flashcards
AphthousUlceration
Risk Factors:
- Vitamin micronutrient deficiencies
- Stress
- Drugs
- Allergies
- Bacterial Viral factors?
- Hematologic abnormalities
- Local injury
- Immunologic factors
- Underlying systemic diseases
- Hormonal factors
- Smoking cessation
- Genetic factors
Minor aphthous ulcerations - Clinical Features:
- Arise almost exclusively on nonkeratinized mucosa and may be preceded by an erythematous macule in association with prodromal symptoms of burning, itching, or stinging
- Demonstrate a yellow-white, removable fibrino- purulent membrane that is encircled by an erythematous halo
- Measure between 3 -10 mm in diameter,** demonstrate a variable recurrence rate, and **heal without scarring in 7 to 14 days
- Pain is out of proportion for the size of the ulceration
Major Aphthous Ulcerations- Clinical Features:
- Larger and deeper than minor aphthae with longest duration per episode
- Measure from 1 to 3 cm** in diameter, may have irregular raised borders take from **2 to 6 weeks to heal, and may cause scarring
- Labial mucosa, soft palate, and tonsillar fauces are involved most commonly
Herpetiform Aphthous Ulcerations - Clinical Features
1 to 2 mm** in diameter in **clusters of 10 to 100 in groups** or throughout the mouth, which usually **heal within a few weeks
Aphthous Ulceration
Diagnostic Procedures:
Diagnosis of aphthous stomatitis is clinical, and laboratory testing is usually unnecessary
- Diagnostic testing might be considered in persistent, severe, or recurrent cases
- A CBC demonstrating anemia might suggest hematinic deficiency such as iron, folate, or vitamin B12.
- Neutropenia might prompt consideration of cyclic neutropenia as a cause of ulcerations
- Gluten-sensitive enteropathy (celiac disease) present in fewer than 5% of recurrent aphthous stomatitis cases and can be identified with serum anti- endomysial antibody** and **transglutaminase assay
- The detection of anti-transglutaminase IgA (tTG) and anti-endomysial (EMA) is used for screening of celiac disease (CD) with a sensitivity and specificity of 90 and 99% respectively
- Consider HIV testing in cases with complex or severe involvement, persistent herpetiform or major aphthous stomatitis, or those involving keratinized mucosa (adherent gingival, dorsum of the tongue, hard palate)
AphthousUlceration
Treatment
No definitive curative treatment for RAS has been established to date
The primary objectives of treatment are to:
- relieve pain
- accelerate healing
- reduce the frequency and severity of episodes of RAS
The approach to therapy should be based on:
- the severity of symptoms
- the frequency and duration of the outbreaks
- the clinical history, and
- the patient’s ability to tolerate medication
Adamantiades-Behçet syndrome
Definition
chronic inflammatory multisystemic disorder (with vascular, articular, gastrointestinal, neurologic, urogenital, pulmonary, and cardiac involvement) of unknown etiology with unpredictable exacerbations and remissions
Adamantiades-Behçet syndrome
Etiopathogenesis
- The etiology is unknown
- The most widely accepted theory is that an infectious** or **environmental antigen elicits an abnormal immune response in a genetically susceptible host (presence of HLA-B51 or other susceptibility genes or genetic variations)
- Investigators have correlated attacks to a number of environmental agents, including bacteria (especially streptococci), viruses, pesticides, and heavy metals
Adamantiades-Behçet syndrome
Pathophysiology
- A clinical hypothesis is that infectious agents** and **associated stress proteins found in the oral cavity of patients with BD induce cross- reactivity with host cells and stimulate the proliferation of autoreactive T-cell clones
- Heat shock proteins (HSP) can be recognized by pattern recognition receptors to be an endogenous “danger” signal leading to activation of innate and adaptive immune responses.
- They also increase the expression of adhesion molecules on endothelial cells.
- Overexpression of pro- inflammatory cytokines**, mainly T-helper (Th)1 and Th17 cells appear to be **responsible for the enhanced inflammatory reaction. Increased neutrophil activity and neutrophil infiltration in the affected organs may be caused by increased interleukin (IL)-17 response
- The immune system activated at the end of all these complex inflammatory processes is thought to eventually induce tissue damage and vasculitis
Adamantiades-Behçet syndrome
Symptoms
The International Study Group for Behçet’s disease criteria, is the most commonly used and internationally recognized diagnostic criteria requires the presence of oral ulcer plus any two of recurrent genital ulcer, typical eye lesions, typical cutaneous lesions**, or a **positive skin pathergy test
Adamantiades-Behçet syndrome
Management:
No curative therapy is currently available for BD
- The ultimate goals of treatment are to prevent irreversible organ damage, which occurs especially in the early stage and active phases of the disease, and to alleviate symptoms
Mucocutaneous involvement:
- No curative therapy
- Topical corticosteroids, lidocaine containing creams, or sucralfate suspension can be used for most minor orogenital lesions
- For severe or refractory mucocutaneous lesions, colchicine, dapsone, thalidomide, methotrexate, prednisone, or interferon-alpha can be considered
As for RAS, the treatment of oral ulcers and other mucocutaneous lesions consists mainly in the use of topical agents**, particularly **steroids
Granulomatosiswith Polyangiitis (WegenerGranulomatosis)-GPA
Classification
- Classic GPA**: With classic Wegener granulomatosis, patients initially show involvement of the **upper and lower respiratory tract; if the condition remains untreated, then renal involvement often rapidly develops (generalized Wegener granulomatosis)
- Limited GPA: is diagnosed when there is involvement of the respiratory system without rapid development of renal lesions
- Superficial GPA: One subset of patients exhibits lesions primarily of the skin and mucosa, a condition termed superficial Wegener granulomatosis. In this form of the disease, systemic involvement develops slowly
Granulomatosis with Polyangiitis (Wegener Granulomatosis)-GPA
Clinical features:
- The reported prevalence of oral lesions varies widely with oral involvement representing the initial presentation in 2% of affected patients - but when present is characteristic
- The most characteristic oral manifestation is strawberry gingivitis
- This distinctive but uncommon pattern of gingival alteration appears to be an early manifestation of GPA and has been documented before renal involvement in most cases
- The surface forms numerous short bulbous projections, which are hemorrhagic and friable; this red, bumpy surface is responsible for the strawberry-like appearance
- Oral ulceration also may be a manifestation
GPA
Other less common orofacial manifestations:
- include facial paralysis, labial mucosal nodules, sinusitis-related toothache, arthralgia of the temporomandibular joint (TMJ), jaw claudication, palatal ulceration from nasal extension, oral-antral fistulae, and poorly healing extraction sites
- Enlargement of one or more major salivary glands from primary involvement of the granulomatous process also has been reported
GPA
Oral Management
- Intralesional steroid injections (triamcinolone acetonide 10 mg/ mL) may assist in the prompt resolution of gingival disease
- During induction therapy, only emergency dental treatment should be performed
- Antibacterial prophylaxis** and **corticosteroid supplementation should be employed as required
- If oral lesions suggestive of relapse appear, immediate specialist referral is indicated
Lichenoid Contact Reactions from Dental Restorative Materials
Type of reaction?
- The vast majority of hypersensitivity reactions to dental restorative materials are to dental amalgam**, usually associated with the **mercury content, but sometimes with copper, zinc, or tin and is also known as Amalgam Contact Hypersensitive Lesions (ACHL)
- Reactions have been seen much less frequently to other dental restorations containing materials such as gold, beryllium, chromium, cobalt, or composite resins
- Represent chronic type IV hypersensitivity reactions
Lichenoid Contact Reactions from Dental Restorative Materials
The diagnosis of a lichenoid contact reaction is made from:
- the clinical appearance of the lesion
- the lack of lesional migration, and
- the correlation to adjacent dental metal
