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62 Cards in this Set

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Chronic gingivitis
Inflammation of the gingiva
Clinical observations in chronic gingivitis (7)
1) The GINGIVAL PAPILLAE ENLARGE from engorgement of inflammatory fluid and hyperemia and change from a lighter to DARKER color. 2) BLUNTED gingival margins, 3) Loss of gingival stippling occurs. 4) Gingivae frequently BLEED when lightly probed. 5) The attachment apparatus DOES NOT become disrupted (ie. gingival fibers remain attached at the cemento-enamel junction; CEJ). 6) PSEUDO-POCKETS occur due to deepening of the gingival crevice when the inflamed gingivae hypertrophy, ie. swell. 7) Chronic gingivitis is NOT PAINFUL.
Difference between pseudopocket vs true periodontal pocket
1) Pseudopocket: occur due to deepening of the gingival crevice when the inflamed gingivae hypertrophy/swell; creates deep stagnation site which quickly fills with bacteria; 2) Perio pocket: occurs when the gingival attachment apparatus becomes disrupted
Healthy gingival crevice depth
shallow at 0.5 to 1.0 mm in depth.
Gingival crevice fluid (GCF)
Fluid that flows from the tissue through the sulcus into the oral cavity, removing some bacteria and toxic substances. However, GCF stagnates and pools in the crevice when pseudopockets are created, providing protein-rich substrates which enhance proliferation of proteolytic bacteria
NORMAL Microbiota of the crevice
Gram positive and facultative (but less so than supra-gingival plaque) with low numbers of Gram negative and motile bacteria. *Most crevicular residents attach to dental surfaces, however the epithelium is increasingly colonized as it becomes inflamed
Role of By-products of the protein metabolism in the gingival crevice DURING STAGNATION (3)
1) serve as required nutrients for less desirable bacteria, 2) may be directly inflammatory to gingival tissue and 3) being nitrogenous and alkaline (usually), raise the pH of the environment. The high pH enhances anaerobic conditions and selects for certain bacteria, including fastidious anaerobes which may be pathogenic; also enhances calculus formation.
Impact of increased GFC flow DURING STAGNATION
encourages succession of Gram negative, anaerobic and motile species (motile bacteria such as spirochetes and vibrio-like organisms). Many of these bacteria are detrimental to tissue integrity. However, no specific chronic gingivitis pathogens have been identified.
Necrotizing Ulcerative Gingivitis (NUG or “trench mouth”)
a painful gingivitis which affects mainly otherwise healthy YOUNG ADULTS and is believed to be associated with emotional STRESS.
“Trench mouth”
An early name for the disease was “trench mouth” because soldiers in trenches in World War I frequently experienced the disease which was thought to be contagious.
Clinical observations in necrotizing ulcerative gingivitis (4)
1) INTERDENTAL ULCERATION OF THE GINGIVA occurring mostly in the mandibular anterior region, 2) PSEUDOMEMBRANE: Purulent whitish accumulations covering the affected tissue; Made of necrotic epithelium, bacterial debris and pus and when removed, reveals acute inflammation of the gingivae and severe ulceration where interdental papilla previously existed. 3) SEVERE PAIN when eating, brushing teeth or from manipulations by the dentist, 4) STRONG MOUTH ODOR resembling necrosis and putrefaction. THIS ODOR IS AN IMPORTANT DIAGNOSTIC FEATURE OF THE DISEASE
Duration of NUG
SELF-LIMITING and lasts about 2 weeks; Does not usually recur unless the individual is medically compromised.
Predominant bacterial species of NUG
spirochetes which are members of the Treponema genus, primarily T. DENTICOLA, and are strictly anaerobic. However, these are SECONDARY INVADERS and primary invader is unknown
Unique feature of NUG
It is the only periodontal disease in which BACTERUA INVADE invade the local connective tissue. In other periodontal diseases substances from the crevicular biofilm enter the connective tissue, but usually not the bacteria.
Treatment of NUG
Penicillin and metronidazole, which kill spirochetes and will shorten the course of the disease from 14 days to 7 or 10 days; *This is also proof that spirochetes play a role in NUG
Hormonal Gingivitis
Pregnancy gingivitis, esp. in the second trimester
Microflora of hormonal gingivitis
elevated proportions of anaerobic bacteria with high levels of PREVOTELLA INTERMEDIA (Pi), a member of the black-pigmented bacteria, BPB.)
Role of hormones in hormonal gingivitis
Female sex hormones (PROGESTERONE and ESTRADIOL), which are highest in the second trimester stimulate growth rates of Prevotella intermedia (Pi) as the bacteria consumes the hormones; Sex hormones can both directly and indirectly intensify inflammation of gingival tissue.
Puberty gingivitis
Gingivitis triggred by increased sex hormones during puberty that also stimulates overgrowth of Pi
Hormones involved in Puberty gingivitis
Female OR male hormones can be involved (Ex: testosterone, progesterone or estradiol)
Clinical presentation of puberty gingivitis
highly inflamed marginal gingivae which are sometimes PAINFUL, and often is present when PLAQUE ACCUMULATIONS ARE LOW
Chronic Periodontitis (CP)
PERIODONTAL POCKET FORMATION in individuals who are older than about 35 years of age; Disease prevalence and severity INCREASE WITH AGE. NOT PAINFUL
Periodontal pocket (“loss of attachment”)
when the gingival attachment apparatus (connective tissue fibers attached at the CEJ) become disrupted and reattach apically on the root surface. pocket is contiguous with the oral cavity and becomes a deep stagnation site which is rapidly colonized by oral bacteria.
Bone resorption process
If Chronic periodontitis (CP) is untreated, the pocket deepens with time and when it reaches a depth which approximates the level of alveolar bone the bone will resorb resulting in reduced stability of the tooth which may become mobile under chewing forces and eventually will become non-functional.
Duration of CP
may last as long as 20 years from inception to tooth loss and is EPISODIC, meaning it experiences periods of either active or no breakdown and sometimes even healing.
Unique features of chronic periodontitis
CP, in contrast to other periodontal diseases, is associated with high plaque volumes, calculus with staining (often), gingival recession, clearly detectible signs of gingival inflammation and oral malodor.
Microbiota of CP
Similar to gingivitis; As clinical outcomes worsen, oxygen concentrations in the crevicular region decrease and the associated biofilms show shifts to obligate anaerobic species with pathogenic potential. Due to the episodic nature of the disease, however, these compositions may revert to less pathogenic ones when inflammation subsides.
Methods of Measuring progression of CP (2)
1) Define active disease as when at least 2.5 mm bone loss occurred during a 2 month period. 2) Define active disease via measurements of various inflammation mediators or by-products isolated from gingival crevice fluid (GCF).
Common inflammatory mediators/by-products of GCF in CP (3)
1) enzymes such as bacterial arginases, host elastase or cathepsin B, 2) prostaglandins which are inflammation mediators and 3) tissue breakdown products such as glycosaminoglycans.
“Consortia of species” involved in CP
Using above methods of measuring progression of CP, various combinations or consortia of species have been identified with different stages of disease activity. The consortia are designated by the colors, yellow, purple, green, orange and red according to increasing levels of pathogenicity.
Red complex
The MOST PATHOGENIC cluster; consists of Porphyromonas gingivalis (Pg), Treponema denticola (Td) and Tannerella forsythia (Tf).
Horizontal gene transfer in CP
Many virulent periodontal pathogens have “PATHOGENICITY ISLANDS” such as Porphyromonas gingivalis, which indicates HORIZONTAL GENE TRANSFER associated with pathogenic traits most likely developed in periodontal biofilms.
RED COMPLEX SYMBIOSIS
SYNERGISTIC ENHANCED VIRULENCE where there is more pathogenicity when there is a combination of red complex bacteria rather than just one of the species present; Also P. gingivalis (Pg) attachment to a subgingival epithelial surface enabled attachment and biofilm development of Treponema denticola (Td) which would not occur without Pg.
Role of Fusobacterium nucleatum (Fn)
There is a strong symbiotic relationship also develops between Fusobacterium nucleatum (Fn) and P. gingivalis (Pg) and T. forsythia: Fn can 1) DETOXIFY HYDROGEN PEROXIDE which is lethal to Pg and 2) DETOXIFY OXYGEN (despite being an obligate anaerobe). 3) Fn PRODUCES NH3 (an alkali) which permits Pg survival in an acidic environment. (Pg thrives only at a relatively high pHs, eg. 8.0.) 4) Fn also FORMS CO2 which is required by Pg as a nutrient. 5) Furthermore, the periopathogen T. FORSYTHIA (Tf) which otherwise is a weak colonizer of biofilms, readily becomes incorporated into periodontal biofilms when Fn is present.
Host contribution to tissue inflammation (2)
1) POOR ORAL HYGIENE: Bacterial accumulation at the gingival margins of teeth as the result of poor oral hygiene can lead to inflammation of the adjacent tissue and serum leakage into the oral cavity and into biofilms. 2) RED BLOOD CELLS: Red blood cells from the host help convert dental plaque dominated by Gram positive organisms into one containing large proportions of anaerobic gram-negative bacteria. PATHOGENIC SYMBIOSIS due to RBCS in the inflammatory fluid acting as a source of HEMIN and IRON for Pg and other periopathogens
Contaminated cementum
Complication of CP where cementum is contaminated by bacteria and debris from the pocket. This makes it impossible for cemental surfaces to be colonized by gingival fibroblasts which is essential for gingival attachment to the tooth. Thus, even during quiescent periods of periodontitis, natural reversal or SHRINKAGE OF THE POCKET IS PREVENTED
Root planning and polishing
Method of reducing pockets by removing contaminated outer layers of cementum so that natural reversal of pocket can occur
Role of endotoxins
Gram negative bacteria release endotoxin from their cell walls upon death; Immunogenic and disrupts tissues; *In addition to endotoxin, bacterial fragments, metabolic by-products and possibly in tact bacterial cells cross the epithelial barrier into connective tissue and directly damage host tissue or stimulate inflammatory responses. Several inflammatory cytokines are present in GFC and their levels positively correlate with severity of CP.
Immune reactions in CP
host reaction to foreign bodies from the periodontal pocket causes the greatest amount of tissue damage in periodontal disease: 1) when polymorphonuclear leukocytes (PMNs) die, they release histolytic enzymes from their LYSOZYMES into the surrounding tissue which leads to BREAKDOWN OF COLLAGEN fibers. 2) Another example is the AUTOIMMUNE DESTRUCTION of fibroblasts or other connective tissue cells following attachment of bacterial fragments to these cells. The contaminated fibroblasts are recognized by the host as foreign and are destroyed by innate immunity.
Predisposing factors (4)
Individualized factors that exacerbate CP including 1) tobacco smoking, 2) emotional stress, 3) diets high in LIPIDS and 4) compromised health (eg. altered immunity, diabetes).
Effect of Calculus on periodontitis (2)
1) calculus intensifies periodontitis because its rough surface constantly IRRITATES GINGIVAL TISSUE. 2) it increases the SURFACE AREA for bacterial colonization. MOST WIDELY BELIEVED hypothesis on how calculus exacerbates periodontitis; *However, calculus alone is not the cause of periodontitis; Animals given antibiotics had perio issues relieved while leaving calculus intact
calculus development
Plaque absorbs calcium and phosphate ions from both saliva and GFC which may crystallize into calculus.
Conditions for calculus development (5)
1) Supersaturated levels of calcium and phosphate in plaque fluid, 2) certain membrane-associated components from Gram negative bacteria, 3) an alkaline environmental pH, 4) natural calculus promoters such as bacteria. 5) ABSENCE of calculus NUCLEATION INHIBITORS
Bacteria in calculus formation
bacteria develop calculus where AMPHIPATHIC MOLECULES exist in the cell membranes. Since these molecules contain both polar and non-polar regions, they attract calcium and phosphate at the polar regions which precipitate into calculus crystals. Mostly Anaerobic/motile Gram negative are involved but one Gram positive, non-motile facultative organism that is strongly calculogenic is CORYNEBACTERIUM (Bacterionema) MATRUCHOTII
Crystal growth inhibitors (4)
positively or negatively charged molecules which either compete with calculus for calcium or phosphate binding or physically block crystal growth sites: 1) pyrophosphate salts, 2) zinc salts, 3) salivary glycoproteins (Ex: statherin, proline-rich proteins (PRP), cystatin and histatin) and 4) IgG and IgA immunoglobulins and albumin. *WEAK ORGANIC ACIDS from bacterial metabolism, like acetic, propionic, butyric and lactic acids, also inhibit calculus formation by mineral dissolution.
Calculus Promoters (3)
act by inhibiting or degrading calculus inhibitors: 1) Proteases - Proteases in saliva and plaque can degrade calcification inhibitors like salivary and pellicle glycoproteins. 3) Acid and alkaline phosphatases - remove phosphate from inhibitor molecules. These are present in oral microorganisms, dental biofilms, calculus, and saliva and will 3) Pyrophosphatases - degrade pyrophosphate.
Other types of calculus promoters (3)
1) Urea and ureases - Production of ammonia from urea breakdown by urease promotes calculus formation by RAISING ENVIRONMENTAL pH. This drives the saturation chemistry of calcium phosphate in plaque fluid toward supersaturation and precipitation. b) Fluoride - catalyzes the precipitation of fluorapatite (a mineral in calculus as well as the tooth). c) Silicon - Silicic acids and silica carry strong negative charges which attract and cause precipitation of calcium molecules. These are notably high in RICE which may, in part, account for prevalence of calculus in populations which consume rice frequently, like INDONESIANS.
Aggressive Periodontitis (AgP)
Also called EARLY ONSET PERIODONTITS (EOP); a PAINLESS periodontal diseases in young adults (under 30)
AGGREGATIBACTER ACTINOMYCETEMCOMITANS (Aa)
Gram negative facultative rod bacteria Present in in AgP biofilms; Elaborates LEUKOTOXIN, a substance which kills white blood cells. Contributes to LACK OF INFLAMMATION associated with AgP
Clinical observations in AgP (6)
1) rapid attachment loss, 2) disease severity which is inconsistent with microbial deposits in the pockets, 3) predilection for FEMALES 3:1, 4) frequent presence of AGGREGATIBACTER ACTINOMYCETEMCOMITANS, 5) FAMILIAL associations, eg. disease occurence in family lines and 6) genetically-mediated CHEMOTACTIC DEFECTS which prevent leukocyte migration into disrupted tissue. The chemotactic defects, along with leukotoxin, are at least partially responsible for the ABSENCE OF INFLAMMATION in AgP.
Prevalence of AgP
AgP affects less than 1% of Caucasians and 7.6% of Indonesians and populations of North African descent.
Sub-categories of AgP (3)
This disease can by sub-categorized by presence of localized or generalized bone loss, type of dentition affected, ie. permanent, primary or mixed and disease progression rate: 1) Localized aggressive periodontitis (LAP) - affects ADOLESCENTS, 2) Generalized aggressive periodontitis of the PRIMARY DENTITION (up to age 12) that affects BOTH SEXES EQUALLY, 3) Generalized aggressive periodontitis in YOUNG ADULTS
Clinical observations of Localized aggressive periodontitis (LAP)
1) localized pocketing associated with MOLARS AND INCISORS ONLY, 2) RAPID bone loss, 3) low dental caries rates, 4) low plaque levels in pockets and generally healthy appearing gingival tissue with scant inflammation, 5) PMN chemotactic defects, 6) familial association and 7) high colonization by Aa.
Generalized aggressive periodontitis of the primary dentition (5)
1) localized or generalized periodontal pocketing and low incidence of dental caries, 2) generally healthy (appearing) gingival tissue with low dental plaque levels, 3) PMN chemotactic defects and 4) familial component to the disease, as it tends to occur in other family members. 5) Role of Aa bacteria is less pronounced than in LAP
Generalized aggressive periodontitis in young adults
RESEMBLES CP clinically with some tissue INFLAMMATION and crevicular PLAQUE, but it affects a younger population, roughly 20 to 35 years old, and is rapidly progressive. It shows BOTH generalized and localized bone loss and affects FEMALES more than males 3:1. *A familial association and host immune defects are suspected, but not confirmed. Specific pathogens have not been identified and involvement of Aa has been inconsistent.
Refractory periodontitis
any periodontitis which becomes refractory to usual treatment approaches. RESISTANCE TO ANTIBIOTICS is a common finding
Microbiota of refractory periodontitis (2)
1) non-oral Gram negative rods such as Enterobacter, Klebsiella and Pseudomonas species (species normally found in the gut) may be involved in some cases. 2) Candida species, enterococci and/or staphylococci also have been isolated from disease sites and are difficult to eradicate.
HIV gingivitis
characteristic gingivitis seen in HIV infected individuals of all ages whereby a “BAND-LIKE” marginal gingivitis appears on buccal surfaces along with diffuse REDNESS extending toward the vestibule. CANDIDA ALBICANS is involved.
Treatment of HIV gingivitis
NYSTATIN (an anti-fungal agent)
HIV Periodontitis
HIV associated periodontitis that is often severe and rapid with CRATERED GINGIVAL PAPILLAE, loss of attachment and tissue ULCERATION and NECROSIS like NUG.
Links between Periodontal disease and general health
statistical association between periodontal disease and incidence of cardiovascular disease, stroke, diabetes mellitus, pre-term labor and low birth weight infants possibly due to entry of LIPOPOLYSACCHARIDES from periodontal pockets into the systemic circulation. Increased vascularity of inflamed tissue may enhance systemic uptake of LPS
Lipopolysaccharides (LPS)
endotoxin from the Gram negative microbiota. LPS is a potent inducer of immune responses, and adverse sequelae may result from systemic over- production of prostaglandins and inflammatory cytokines caused by periodontal LPS.