INFLAMATORNE BOLESTI
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Transcript of INFLAMATORNE BOLESTI
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284 PDQ ORAL DISEASE
Inflammatory Diseases
Angioedema
Etiology
• Usually triggered by ingested antigens (eg, shellfish, nuts,
fruits, medications)
• Mechanism associated with immunoglobulin E (IgE)-mediated
mast cell degranulation with subsequent histamine release
• Drug reactions resulting in release of inflammatory mediators
(bradykinin)
• Some cases have a genetic basis: C1 esterase inhibitor deficien-
cy or inhibitor dysfunction (autosomal recessive)
• May be correlated with disease states characterized by the
presence of circulating immune complexes
Clinical Presentation
• Soft, diffuse, painless swelling of face, lips, and neck
• Overlying skin and oral mucosa appear noninflamed
• Mucosa may become secondarily erythematous, ulcerative, or,
rarely, vesicular
• Usually short-lived (24–48 hours)
Diagnosis
• Nonspecific histology
• Correlation of history and clinical findings
Differential Diagnosis
• Trauma (physical, cold)
• Cellulitis
• Vascular malformation
• Acute contact stomatitis
• Melkersson-Rosenthal syndrome (early stages)
• Orofacial granulomatosis (early stages)
Treatment
• Elimination of possible etiologic/precipitating factor(s)
• Antihistamines, corticosteroids, adrenaline
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Inflammatory Diseases 285
Prognosis
• Good to excellent
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286 PDQ ORAL DISEASE
Cheilitis Granulomatosa
Etiology
• Isolated, idiopathic, and chronic lip enlargement
• May be an incompletely expressed or oligosymptomatic form
of Melkersson-Rosenthal syndrome
Clinical Presentation
• One or both lips may be diffusely enlarged and nontender.• Episodic swelling initially, with progression to a persistent
enlargement
• Less often, superficial labial exfoliation or surface
weeping/crusting may be noted.
• Lip swelling may herald similar changes of the gingiva, buccal
mucosa, or palate.
• May be associated with Crohn’s disease, sarcoidosis, contactsensitivity, dental abscesses
Microscopic Findings
• Demonstrates noncaseating epithelioid granulomas
• Absence of organisms
Diagnosis
• History of intermittent to persistent asymptomatic lip swelling
• Characteristic appearance
• Lip or soft tissue biopsy (involved gingiva)
• Rule out sarcoidosis (chest radiograph, serum angiotensin-
converting enzyme levels)
• Patch testing for contact allergens
• Dental radiographs to rule out asymptomatic periapical
pathology
Differential Diagnosis
• Angioedema
• Cellulitis/erysipeloid reaction
• Sarcoidosis
• Crohn’s disease
• Melkersson-Rosenthal syndrome
• Cheilitis glandularis
• Contact stomatitis
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Inflammatory Diseases 287
Treatment
• Local intralesional triamcinolone injections under local anes-
thesia• 5 to 10 mg total dose in depot fashion every 3 to 4 weeks to
achieve response
• Local treatment may be coupled with an initial systemic course
of glucocorticoids.
• Clofazimine 100 mg daily for 60 days with reduction to a
maintenance dose of 30 mg on alternate days
• Metronidazole may also be effective at 250 mg three timesdaily for 1 month. This may be coupled with intralesional cor-
ticosteroid placement.
• Dapsone may be effective (as per dermatitis herpetiformis dos-
ing)
• Surgical reduction (cheiloplasty) may be necessary.
Prognosis• Guarded
• Must remain aware of possible neurologic manifestations, oph-
thalmologic involvement, psychological effects
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288 PDQ ORAL DISEASE
Drug-Induced Stomatitis
(Stomatitis Medicamentosa)
Etiology
• Oral changes found in approximately 5% of those with cuta-
neous reaction to drugs
• Mucosal alterations may result from the following:
• Myelosuppression
• Direct cytotoxic or cytostatic effect(s) on dividing epithelialcells
• Xerostomic effects
• Alterations of oral microbial flora
Clinical Presentation
• Painful, erythematous, erosive, or ulcerative lesions
• Nonkeratinized locations often affected initially• Fixed form of drug-associated eruptions relatively uncommon
intraorally
• Pseudomembranous necrotic surface may be noted
Diagnosis
• History
• Clinical appearance
Differential Diagnosis
• Chemical or thermal burn
• Erosive lichen planus
• Pemphigus vulgaris
• Mucous membrane (cicatricial) pemphigoid
• Erythema multiforme
• Acute herpetic gingivostomatitis
• Candidiasis
Treatment
• Identification and withdrawal of offending drug
• Symptomatic management including topical preparations
(see “Therapeutics” section)
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Inflammatory Diseases 289
• Systemic corticosteroids if mucosal reaction is not related to
antineoplastic treatment
Prognosis
• Generally excellent
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290 PDQ ORAL DISEASE
Garré’s Osteomyelitis
Etiology
• Chronic, low-grade, dentoalveolar infection
• Resultant bony inflammation extends to the periosteum, pro-
ducing a reduplication of the cortex (“onion skin” effect).
Clinical Presentation
• Usually an asymptomatic, unilateral, mandibular, bony hardasymmetry
• Limited to children and young adults
Radiographic Findings
• Medullary mottling with (lucent and opaque) ill-defined margins
• Periosteal-cortical expansion
• Occlusal radiograph shows concentric or parallel layering of cortex
Diagnosis
• Carious mandibular tooth, usually first permanent molar
• Radiographic features
• Biopsy results showing periosteal osteoblastic reaction, mini-
mally inflamed fibrous marrow
Differential Diagnosis
• Ewing’s sarcoma
• Langerhans cell disease (histiocytosis X)
• Osteosarcoma
• Fibro-osseous lesion
• Metastatic disease
Treatment
• Elimination of the infected focus (carious tooth to be extracted
or filled)
• Antibiotic administration early in treatment phase
Prognosis
• Good
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Inflammatory Diseases 291
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292 PDQ ORAL DISEASE
Gingivitis
Etiology
• Variable
• Most are microbiologic or plaque associated (simple marginal
gingivitis).
• Some are modified by hormonal changes, such as those in
pregnancy (pregnancy gingivitis).
• Fusospirochetal gingivitis plus poor oral hygiene and poor nutri-tion are associated with acute necrotizing ulcerative gingivitis.
• Rarely, some forms are associated with contact allergy (“plasma
cell gingivitis”).
Clinical Presentation
• Dependent on etiology, as follows:
• Plaque associated: marginal inflammation to moregeneralized erythema and blunting of interdental papillae
with rolled margins
• Hormonally related: diffuse erythema and hyperplasia
• Fusospirochetal: necrotic, blunted, ulcerated interdental
papillae with spontaneous bleeding; foul odor
• Allergy based: hyperplastic and bright red, granular to
velvety surface alteration
Diagnosis
• Identification of cause
• Patch testing for contact allergens
Differential Diagnosis
• Acquired immunodeficiency syndrome–associated periodontaldisease
• Oral lichen planus
• Mucous membrane (cicatricial) pemphigoid
• Acute herpetic gingivostomatitis
• Pemphigus vulgaris
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Inflammatory Diseases 293
Treatment
• Local débridement and chlorhexidine rinses in cases of bacterial
origin• Reduction of hormonal dosage
• Elimination of allergen
Prognosis
• Excellent
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294 PDQ ORAL DISEASE
Median Rhomboid Glossitis
Etiology
• A benign, inflammatory condition
• Often related to yeast colonization (erythematous candidiasis)
• Inflammatory process noted in response to overlying Candida
population
• Exact mechanism is unclear
Clinical Presentation
• Well-defined, asymptomatic erythematous patch on dorsum of
tongue
• Paramedian erythema, usually with focal atrophy of filiform
papillae
• Chronic forms may become multinodular.
• Rarely may be hyperkeratotic• May be mistaken for a benign or malignant tumor
Microscopic Findings
• Papillary, atrophic or hyperplastic epithelium
• Candidal colonization of surface
• Heavy, chronic inflammatory infiltrate
Diagnosis
• Clinical appearance, location
Treatment
• Topical and/or brief course of systemic antifungal therapy
(optional)
• Observation
Prognosis
• Excellent
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Inflammatory Diseases 295
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296 PDQ ORAL DISEASE
Osteomyelitis
Etiology
• An acute or chronic inflammatory process within the
medullary space or along the cortical surface of bone
• Usually due to extension of a periapical abscess
• Other common causes include physical trauma (fracture) or
bacteremia.
• Most common organisms include staphylococci and streptococci
Clinical Presentation
• Pain, swelling, fever, lymphadenitis
• Sequestrum formation
• Lower lip paresthesia, occasionally with acute disease in
mandible
• Associated soft tissue swelling
Radiographic Findings
• Acute phase may be unremarkable
• Ill-defined, patchy radiolucency (“moth eaten”)
Diagnosis
• Presentation and radiographic findings
• Microscopic evidence of intrabony inflammation, marrow
fibrosis, osteoclastic resorption, reduced osteoblastic activity,
nonviable bone
Differential Diagnosis
• Osteosarcoma
• Local extension of malignant tumor
• Metastatic tumor• Osteoradionecrosis
Treatment
• Drainage and antibiotics for acute disease
• Débridement, sequestrectomy, antibiotics for chronic disease
• Reconstruction if necessary after disease is resolved
Prognosis
• Good
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Inflammatory Diseases 297
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298 PDQ ORAL DISEASE
Osteoradionecrosis
Etiology
• A serious complication of tumoricidal doses of radiation to
the head and neck, usually > 60 Gy (6,000 rads)
• Radiation produces damage to the microvasculature, permit-
ting a hypoxic state, which, in turn, leads to a hypocellular
bony environment.
• Minor damage to the irradiated bone produces a nonhealingwound, forming dead bone—necrosis.
Clinical Presentation
• Usually affects the mandible
• Bone pain
• Exposed necrotic bone within radiation portal
• External fistula formation• Pathologic fracture
Radiographic Findings
• Irregular zones of mixed radiopacity and radiolucency
• Separation of nonvital bone (sequestrum) from remaining
viable bone
Diagnosis
• Radiographic and clinical features
• Biopsy results show nonvital bone.
Differential Diagnosis
• Metastatic tumor
• Locally recurrent tumor• Osteomyelitis
• Osteosarcoma
• Radiation-induced sarcoma
Treatment
• After biopsy, débridement of bone preceded and followed by
hyperbaric oxygen therapy• If necessary, resection and reconstruction
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Inflammatory Diseases 299
• Necessary tooth extraction and elimination of focal infection
within radiation portal 21 days prior to treatment
• Excellent preventive dental care
Prognosis
• Guarded
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300 PDQ ORAL DISEASE
Periapical Granuloma
Etiology
• A mass of inflamed granulation tissue
• Forms secondary to pulp necrosis of the associated tooth
• May develop following periapical abscess formation or may
form as pulpal death eventuates without abscess precursor
Clinical Presentation• Usually asymptomatic
• With acute exacerbation, pain and sensitivity develop.
• Tenderness at root apex on palpation
• Pain on biting or percussion of tooth
Radiographic Findings
• Radiolucency at apex of tooth• Size ranges up to 1 to 2 cm in diameter
• Root resorption not uncommon
Diagnosis
• Radiographic features
• Demonstration of nonvital pulpal component
Differential Diagnosis
• Periapical cemental dysplasia
• Periapical cyst
Treatment
• Conventional endodontic therapy
• Apical curettage/root end amputation if above measures fail• Extraction of involved tooth
Prognosis
• Excellent
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Inflammatory Diseases 301
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302 PDQ ORAL DISEASE
Sarcoidosis
Etiology
• Unknown; granulomatous disease process
• May represent a systemic response to a single provoking agent;
mycobacteria has been suggested but not proven
• Possible role of genetic factors coupled with disordered reac-
tions to foreign antigens
Clinical Presentation
• Mucocutaneous
• Red to brown nodules/plaques with erythema nodosum
features
• Minor salivary glands of the lips and palate may be involved.
• Erythematous, hyperplastic gingiva
• Salivary/lacrimal• Parotid, submandibular, and lacrimal glands may be
enlarged.
• Multiple organ systems, such as the following, may be involved:
• Particularly the lung, but also liver, endocrine glands, the
heart, and the reticuloendothelial and musculoskeletal
systems
• Heerfordt’s syndrome may be related to sarcoidosis (uveitis,parotid gland enlargement, fever, cranial nerve palsies).
Diagnosis
• Demonstration of sarcoidal (noncaseating epitheloid) granulo-
mas in at least two organ systems
• Elevated serum angiotensin-converting enzyme levels are
usually present.• Over 90% of cases have abnormal chest radiograph.
• Other causes of granulomatous inflammation must be ruled out.
Differential Diagnosis
• Tuberculosis
• Lymphoma (non-Hodgkin’s, Hodgkin’s)
• Deep fungal infection• Crohn’s disease
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Inflammatory Diseases 303
Treatment
• Corticosteroids, if symptoms demand
• Severe or unresponsive cases: methotrexate• Cutaneous lesions only: hydroxychloroquine
• Intralesional corticosteroids
Prognosis
• Generally good