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35 Cards in this Set
- Front
- Back
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Perio pocket |
pathologically deepened gingival sulcus |
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Healthy probing depth |
1-2mm (other lecture on Clinical Exam says 1-3mm); *If we were sterile, it would be 1mm but this does not usually occur |
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Characteristic of sulcus |
360 degree “moat” around the tooth |
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2 ways of transitioning from sulcus to pocket |
1) Coronal movement of gingival margin, 2) Apical displacement of gingival attachment (junctional epithelium) |
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3 Classifications of Perio pockets |
1) Gingivitis (caused by the actual bulk of plaque pushing against gingiva to make a pocket but no actual loss of bone or attachment; Junctional epithelium/collagen is still at CEJ vs in periodontitis it is on the root surface), 2) Suprabony periodontal pocket: missing alveolar crest and its attachments (PDL); bottom of pocket is coronal to bone; involves horizontal bone loss , 3) Intrabony/Infrabony periodontal pocket: bottom of pocket is apical to the bone; involves vertical bone loss |
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Simple pocket |
Involves one wall of tooth |
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Compound pocket |
Involves more than one wall |
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Spiral pocket |
Involve the root furcation of the tooth |
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How does inflammation affect accuracy of perio probe measurements? |
NON-INFLAMED: Probe usually stops coronal to apical termination of the junctional epthelium (ATJE) due to resistance from CT and bone; INFLAMED: Probe meets little resistance so rests apical to ATJE by about 0.45 mm; *However, perio probe measurements pretty accurate at +/- 1mm |
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Effect of gingivitis on developing periodontitis |
Having gingivitis did not necessarily predict that a patient will develop periodontitis (positive predictive value less than 0.25); However, LACK OF GINGIVITIS is a strong predictor that the patient will NOT get periodontitis (negative predictive value 0.98) |
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Effect of Bleeding on probing (BOP) on developing periodontitis |
Patients with BOP at least 50% of the time were 3x more likely to develop periodontitis (lose at least 2mm clinical attachment); Important to see if perio treatment has also stopped the bleeding; *Also strong negative predictor b/c LACK of BOP predicts not getting periodontitis |
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What should be recorded on a perio chart? |
1) Probing depth (PD), 2) Presence of supragingival plaque (recorded as blue dot above PD site), 3) Positive or negative distance from CEJ to FGM, 4) CAL calculation (Probing depth + CEJ to FGM), 5) Presence of BOP as red dot above CAL at the site; *Top part of chart refers to buccal sites and bottom part is lingual sites |
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BOP |
Earliest sign of gingivitis (increase in gingival crevicular fluid production is also a sign); signifies inflammatory lesion in BOTH the epithelium AND CT |
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Effect of smoking on BOP |
Smoking suppresses BOP and can mask it (dose-dependent effect) |
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Why does bleeding occur? |
Due to chronic inflammation, there is vascular changes to underlying tissue: dilation and engorgement of the capillaries and thinning of the sulcular epithelium (making capillaries closer to the surface); *Spontaneous bleeding is rare and usually only happens with mechanical trauma like probing that causes temporary rupture of capillaries |
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What causes gingival wall of pocket to be red, flaccid, with smooth shiny surface and pitting on pressure? |
RED COLOR: Circulatory stagnation; FLACCID: Destruction of gingival fibers and surrounding tissues; SMOOTH/SHINY: Atrophy of epithelium and edema; PITTING ON PRESSURE: Edema and degeneration |
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Why is the gingival wall pink and firm in some cases of periodontitis? |
Fibrotic changes have predominated over exudation and degeneration; However, inner wall of pocket will have degeneration and often be ulcerated |
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What causes painful probing? |
Ulceration on inner aspect of pocket wall |
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What causes pus? |
Suppurative inflammation of inner wall |
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Types of bacteria in healthy gingiva |
Coccoid and straight rods; facultative aerobic |
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Types of bacteria in diseased gingiva |
Increased spirochetes and motile rods; *However, type of bacteria is not predictive of disease; *Mentions P. gingivalis |
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What causes pocket formation? |
Inflammatory change in CT wall of gingival sulcus |
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2 Mechanisms associated with collagen loss |
1) Collagenases and other enzymes secreted by various cells in healthy and inflamed tissue, 2) Fibroblasts phagocytize collagen fibers; *PMNS invade coronal end of JEand JE loses cohesiveness and detaches more and more apically; In attempt to restore health, host’s neutrophils, macrophages, fibroblasts, epithelial cells, etc. produce proteinases, cytokines, and prostaglandins that damage/destroy tissue – INFLAMMATORY RESPONSE (non-specific processes) |
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Where does the most degenerative damage occur? |
Lateral wall of pocket |
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Areas within the pocket |
1) Area of quiescence: flat minor depressions where there is shedding of epithelial cells, 2) Bacterial accumulation, 3) Bacterial-leukocyte interaction, 4) Intense cellular desquamation (possible b/c JE allows things in and out) |
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Edematous vs fibrotic pockets |
Products of the same disease process and subject to constant modification depending on relative predominance of exudative and constructive changes (dynamic due to “wound healing” that never actually completely heals; In some cases, fibrotic outer layer of pocket with inner layer inflamed and ulcerous (can appear normal from the outside) |
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6 Pocket contents |
1) Debris of microorganisms and their products (enzymes, endotoxins, metabolic products, etc.), 2) Gingival fluid, 3) Food remnants, 4) Salivary mucin, 5) Desquamated epithelial cells, 6) Leukocytes; *Sometimes there is purulent exudate |
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Purulent exudate |
Living and dead leukocytes and bacteria, serum, and small amount of fibrin; Pus is only a secondary sign of perio disease |
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Where is pus formation more extensive? |
In SHALLOWER pockets |
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Abscess |
Localized accumulation of pus |
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gingival abscess |
a localized purulent infection that involves the marginal gingiva or the interdental papilla. |
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pericoronal abscess |
involves the soft tissues associated with the crown of a partially erupted tooth. |
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periodontal abscess |
localized purulent infection within the tissue which is adjacent to the periodontal pocket that may lead to the destruction of the PDL and alveolar bone. |
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How does the root surface wall of the periodontal pocket change? |
With deepening of the pocket the collagen fibers that once formed attachment into the cementum are destroyed. Cementum becomes exposed now to the oral environment. |
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Decalcification and remineralization of cementum |
Hypermineralized zones; Also areas of demineralization due to root caries; Areas of cellular resorption of cementum and dentin are common in root surface unexposed by perio disease |
