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57 Cards in this Set
- Front
- Back
Inflammation |
• A NON_SPECIFIC response to injury by living and non living agents. •Classification is based on: -Nature -Duration -Severity |
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Immune Response |
•A SPECIFIC reaction to cell injury •Humoral Immunity •Cellular immunity |
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Infection |
• Tissue response to invasion and injury by microorganisms |
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Infestation |
•Presense of microorganism •No inflammatory response |
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Why is oral Mucosa highly resistant to infection |
1. Protected by stratified squamous epithelium2. Areas subjected to stress are protected bykeratinized epithelium 3. Enzymes in saliva destroy some types of bacteria 4. Abs in the saliva aid in destruction of bacterialcells |
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The development of an infection will alsodepend on? |
1. Virulence of the agent 2. Number of pathogenic microorganisms 3. Type of microorganism |
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Periodontal Disease |
• Includes conditionsthat affect the gingiva,periodontal ligament,and alveolar bone |
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Simple Gingivitis |
• Inflammation of thegingiva • No loss of attachmentor bone • Usually chronic Clinical Features: -edematous -red and glossy -bleeds easily |
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Necrotizing Ulcerative Gingivitis |
• Ulceromembranous stomatitis • Vincent’s stomatitis (Trench mouth) • Bacterial associated withother factors – Affects individuals with adepressed immune system – Associated with localirritants – NOT contagious |
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Clinical Features of Necrotizing Ulcerative Gingivitis |
• Bad breath (halitosis) • Bad taste • Gingival bleeding • Painful gingivitis (redness, swelling, ulcers) • General malaise, loss of appetite, fever |
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Periodontitis |
• Follows untreatedgingivitis Clinical Features : • Varying degrees of gingivitis with alterations in colour • Epithelial detachment onto cementum forming atrue periodontal pocket • Extensive tooth migration and mobility • Accumulation of pus causes swelling and pain |
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Osteomyelitis |
-• Untreatedperiodontitis results infurther bonedestruction • Formation ofperiodontal abscesses |
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Gonorrhea |
• Caused by Neisseriagonorrhea • Gram negative diplococcus • Primary sites of infection – Genitalia– Anal canal– Pharynx |
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Symptoms of Gonorrhea |
• Burning or itchingsensation • Dryness • Increased salivation • Bad breath • Fetid breath • Fever • Submandibularlymphadenopathy |
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Syphilis |
• Causative agent ->T. pallidum(spirochete) - bacterium • Oral-sexual contact (acquired) • May also be congenital – 1º chancre – 2º fever, rash – 3º gummas (paralysis, insanity) – Congenital syphilis |
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Primary Syphilis |
• Chancre • Occurs at the portal of entry (usualy lips) • Destructive sore • ~20 days after contact • Progression– Macule -> Papule -> Ulcer *The lips are themost commonextragenital sitefor primarysyphilis |
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Secondary Syphilis |
• Generalized maculopapular lesions on the skin• Occurs 6-8 weeks after exposure • Mucous patches on oral mucosa • Multiple, painless, grayish-white plaques cover theerosion • Surface is smooth and opalescent • Highly infectious lesions • Spirochetes can cross the placenta |
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Condyloma Lata |
•Wart- like lesions •Tend to occur around the genitalia •Do not confuse with Condyloma acuminata which iscaused by HPV |
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Tertiary Syphilis |
• 5-20 years after initial infection • Affects ~ 1/3 of untreated patients • Lesions are destructive • Generally non-infective 1. Gumma 2. Diffuse syphilitic glossitis |
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Gumma |
• Granuloma • Characterized byproliferative changes,necrosis and giant cellformation • Palate and tongue arecommon sites • Feels firm and appearsnodular |
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Hutchinsonian Triad OfCongenital Syphilis |
– MULBERRY MOLAR (HYPOPLASIA OF TEETH WITHWIDE SPACING) – RHAGADIS LINEAR SCARS AT CORNER OF MOUTH – SADDLE NOSE – a flat bridge of the nose |
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Tuberculosis |
• Chronic granulomatomatous inflammation •Mycobacterium Reservoirs - Humans -M. Tuberculosis Transmission of TB • Respiratory secretions from patientwith active pulmonary lesions • Consumption of milk or other dairyproducts from tuberculous cattle |
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Types of Lesions in Tuberculosis |
1. Exudative ulcerative lesions 2. Granulomas / Tubercle |
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Factors thatfavor spread of communicable disease |
– Poor living conditions – Low socioeconomic status – Low native resistance – Compromised immunity from debilitating orimmunosuppressed conditions |
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Exudative Ulcerative Lesions |
• Acute inflammatory reaction • Engulfment of the bacilli in an exudate of polysand lymphs • May subside and heal, progress and lead tonecrosis or develop into a granuloma • Tongue is the most common site |
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Granuloma/Tubercle |
• Productive or proliferative lesion • No exudate • Most of the bacilli live in the center • Eventually the tubercle may becomefibrous at the periphery and calcifiedwithin • Bacilli remain viable for years • Tongue is a frequent site |
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Differential Diagnoses |
• Indolent ulceration • Nodular • Granulomatouslesion |
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Primary Tuberculosis |
• Childhood • First infection • As the hypersensitivity develops the exudate isresorbed and heals • Most frequently occurs in the lower 2/3rds ofthe lungs |
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Reinfection Tuberculosis |
• Chronic disease • Formation of tubercules/granulomas • Caseous necrosis |
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Lupus Vulgaris |
• TB of the skin • Reddish-brownnodules on the face • Nodules may becomescaly or ulcerate • Scarring |
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Scrofula |
• Tuberculous CervicalLymphadenitis • TB infection of thesubmaxillary and cervicallymph nodes • Large firm masses • Extension of TB in the oralcavity |
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Control of Active Infection |
• Isolation • Precautions (private room, ventilation) • Treatment (multi-drug treatment) • Control of contacts– Quarantine not indicated– BCG • Epidemic controls– Cases must be documented– X-ray screening of immigrants |
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Actinomycosis |
• Caused by Actinomycesisraeli • Fungus-like bacterium • Anaerobic •Most cases involve the cervical facial area •Lumpy Jaw |
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Clinical Features of Actimomycosis |
• Painless, hard reddish-bluenodules appear over the upperpart of the neck, under the earor in the submandibular area • Abscesses burrow toward the surface • Discharge yellow purulent exudate (pus) -> contains foul smelling sulfur granules |
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Candidiasis |
• Yeast Infection • Normal flora of skin,mouth, and GI tract • Candida albicans |
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Several Forms Of Oral Candidiasis |
• Pseudomembranous Candidiasis • Erythematous Candidiasis • Denture Stomatitis (chronic atrophiccandidiasis) • Chronic Hyperplastic Candidiasis (Candidalleukoplakia) • Angular cheilitis |
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PSEUDOMEMBRANOUS CANDIDIASIS |
• A white curdlike material ispresent on the mucosalsurface • Underlying mucosa iserythematous • A burning sensation canoccur • Patient may complain of ametallic taste in the mouth |
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ERYTHEMATOUS CANDIDIASIS |
• A red painful mucosa is the presentingcomplaint • May be localized or generalized |
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DENTURE STOMATITISCHRONIC ATROPHIC CANDIDIASIS |
• MOST COMMON TYPE AFFECTINGTHE ORAL MUCOSA • Presents as erythematous mucosabut is limited to the mucosacovered by the full or partialdenture • Lesions vary from petechiae-like tomore generalized and granular • Asymptomatic and often discoveredduring routine examination |
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CHRONIC HYPERPLASTIC CANDIDIASISCANDIDAL LEUKOPLAKIA |
• Appears as a white lesion that does not wipeoff • Will respond to antifungal medication |
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ANGULAR CHEILITIS |
• Candida organisms are often the cause ofangular cheilitis • Erythema and fissuring at the corners of themouth •"Perlche" |
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Virus |
• Nucleoprotein particle • May produce tissue necrosisor inflammation • May produce tissuehyperplasia, warts orneoplasia |
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Herpes Virus |
• Enveloped icosahedralDNA virus • Member of theherpesviridae family • 8 known human herpesviruses • Life-long latentinfection with periodicreactivation |
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Herpes Simplex Virus Type 1 VS. Type 2 |
Type 1 • Enveloped icosahedralDNA virus • Member of theherpesviridae family • 8 known human herpesviruses • 3 sub families Type 2 • Causes genital andanal lesions |
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Herpes Simplex 1 |
• Cold sores or fever blisters • Represents recurrentdisease • Occurs when the host’sresistance is lowered • Oral mucosa is rarelyinvolved • Vesicles • Ulcers • Crusting •"Herpes Labialis" |
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Herpes Simplex 2 |
• Causes genital and anal lesions Differential Diagnosis(Include any condition that presents with vesicles orulcers) • Aphthous stomatitis– no fever, no vesicles • Herpangina– Confined to the oropharynx (Coxsackie virus) • ANUG– no vesicles |
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Herpetic Keratitis |
• Serious • Ulceration of the cornea due to repeated infection may lead to blindness |
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Herpetic Whitlow |
A whitlow or felon is an infection of the tip of the finger |
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Shingles |
•Varicella-Zoster Virus(Human herpes virus 3) •Affects Adults •Unilateral 1.Small bumps 2. Turns to blisters 3. Crust over 4. Disappears 5. Last weeks to years after the rash disappears •Very painful |
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Herpangina |
• An acuteoropharyngitis causedby a Coxsackie virus • Affects children andyoung adults • Uniform vesicles with redmargins on the palate andposterior oral tissues • Ulceration • Erythema |
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Epstein Bar Virus |
• Human herpes virustype 4• Attacks B-lymphocytesand epithelial cells Example: Infectious Mono • Relationship between EBV and oncogenesis – Burkitt’s lymphoma – Nasopharyngeal carcinoma |
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Hairy Leukoplakia |
• Opportunisticinfection related toEBV • Found primarily in HIVinfected patients • Lateral surface of thetongue is the mostcommon site |
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Human Herpes Virus-8 |
• The gene of HHV-8 acts as a vascular switch • Turns ON the synthesis of angiogenic factors • RESULT: Kaposi’s Sarcoma |
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Human Papilloma Virus |
• Formationof a benign outgrowthof cells wart/papilloma •Skin warts •Genital Warts (condylomas) |
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Condyloma acuminatum |
• Infectious lesion • Verrucous or papillary growth • Keratinized cells act as the host for the virus • Characteristically located in the anogenitalregion |
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Hand, Foot and Mouth Disease |
• Common illness in infants andchildren • A viral infection of the skin and oralmucosa characterized by vesiculareruptions restricted to the hands andfeet and in the mouth. |
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Measles |
• Measles virus is a RNAparamyxovirus • Highly infectious • Immunization is necessary • "Koplik’s spots" (pathognomic) |