INFLAMATORNE BOLESTI

8/3/2019 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

Inflammatory Diseases 285

Prognosis

• Good to excellent

Cheilitis Granulomatosa

Etiology

• Isolated, idiopathic, and chronic lip enlargement

• May be an incompletely expressed or oligosymptomatic form

of Melkersson-Rosenthal syndrome

• 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

• Angioedema

• Cellulitis/erysipeloid reaction

• Sarcoidosis

• Crohn’s disease

• Melkersson-Rosenthal syndrome

• Cheilitis glandularis

• Contact stomatitis

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-

• Surgical reduction (cheiloplasty) may be necessary.

Prognosis• Guarded

• Must remain aware of possible neurologic manifestations, oph-

thalmologic involvement, psychological effects

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

• 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

• 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)

• Systemic corticosteroids if mucosal reaction is not related to

antineoplastic treatment

Prognosis

• Generally excellent

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).

• 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

• 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

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”).

• 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

• Acquired immunodeficiency syndrome–associated periodontaldisease

• Oral lichen planus

• Mucous membrane (cicatricial) pemphigoid

• Acute herpetic gingivostomatitis

• Pemphigus vulgaris

Treatment

• Local débridement and chlorhexidine rinses in cases of bacterial

origin• Reduction of hormonal dosage

• Elimination of allergen

Prognosis

• Excellent

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

• 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

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

• Pain, swelling, fever, lymphadenitis

• Sequestrum formation

• Lower lip paresthesia, occasionally with acute disease in

mandible

• Associated soft tissue swelling

• 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

• 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

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.

• Usually affects the mandible

• Bone pain

• Exposed necrotic bone within radiation portal

• External fistula formation• Pathologic fracture

• 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.

• 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

• Necessary tooth extraction and elimination of focal infection

within radiation portal 21 days prior to treatment

• Excellent preventive dental care

Prognosis

• Guarded

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

• 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

• Periapical cemental dysplasia

• Periapical cyst

Treatment

• Conventional endodontic therapy

• Apical curettage/root end amputation if above measures fail• Extraction of involved tooth

Prognosis

• Excellent

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

• 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.

• Tuberculosis

• Lymphoma (non-Hodgkin’s, Hodgkin’s)

• Deep fungal infection• Crohn’s disease

Treatment

• Corticosteroids, if symptoms demand

• Severe or unresponsive cases: methotrexate• Cutaneous lesions only: hydroxychloroquine

• Intralesional corticosteroids

Prognosis

• Generally good

INFLAMATORNE BOLESTI

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