MOUTH NF path Flashcards
saliva contains
- lysozyme: attacks bac cell walls
- lactoperoxidase: prod. hypohalides (antimicrob.)
- lactoferrin: chelates iron–>restricts microbe access to iron
- IgA: appear in saliva thru transudation not active sec.
- sec. blood group Ag (glycolipids): blocks microbial attachment
- buffering capacity
persons with this have higher #s of bac, more probs with oral cavity infections, dental caries, gum recession, etc.
saliva production deficiency (Sjogren’s syndrome, radiation-ind., drug-induced xerostomia)
the gingival sulcus contains
IgG and other transudated imm.globs, complement, PMNs, exp. during inflamm. states
factors which alter oral NF
sig. change in diet presence/absence of teeth absence of saliva Ab tx hospitalization: G+-->G-rods change in immune status (suppress.) overall health
clin sig oral NF: aerotolerant anaerobes: G+ a-hemolytic streptococci:
s. mutans, s. sanguis, s. salivarius, s. mitis
* also etiologic agents of endocarditis (disp. NF), dental caries (OG @ origin)!
clin sig oral NF: facultative anaerobes
Eikenella corrodens (G-rod): causes skin/soft tissue ing/abscesses (mouth/hd), bite wounds
(@ origin or disp. NF)
Actinomycetes israelii: (G+, thin, branching filaments w/ clubbed ends): soft tiss. absc. in mouth/head(@ origin) and bronchial-pulm inf. by direct tiss extension and aspiration of saliva/oral fluids w/ org. (disp. NF)
anaerobes present on teeth, saliva, gingival crevices (can spread to lungs, blood)
Treponema denticola, T. vincentii (spirochetes)
Fusobacterium spp. (G-rod)
Porphyromonas gingivalis (G-rod)
Prevotella intermedia (G- rod)
Bacteroides forsythus (G-rod)
Aggregaitbacter (form. Actinobacillus)- actinomycetemcomitans (G- coccobacillus)
*all can cause periodontal disease (OG @ origin)
faculative anaerobes
yeast : Candida spp, C. albicans
oral thrush, dental stomatitis, pharyngitis (OG @ origin)
dental caries
demineralization at tooth
endogenous origin, mixed NF–>cariogenic orgs
e.g. S. mutans (G+ cocci)–>acid prod. via fermentation
dental caries risk
high sucrose diets, high simp. sugars, carbs
non fluoridated water
accum. of plaque from not cleaning
DC transmission
Streptococcus mutans: trans. in family units/close contacts
humans: resevoir
DC not freq. observed in
the v. young (it’s a chronic process)
DC pathogenesis
chronic, slow, not self-limiting biofilm formation (mult. genera)-->calcifies (tartar)-->chronic, slowly prog.
DC mechanism
bac ferment sugar–>org. acid (lactic)–>solubilize hydroxyapatite–>demineralize enamel/dentin–>caries
DC mech depends on pres. of bac that
produce organic acids (ferm. of sugars) and water INSOLUBLE glucans (via glycosyltransferase)
fermentation results in..which lead to..
cracks, fissures, erosions, pits w/ calculus/tartar
dentoalveolar inf.
immunitity to DC
adaptive imm. is Ab mediated : prev. binding of cariogenic orgs. to tooth surface
-vaccine not need due to water fluoridation
DC s/s
cracks, fissures, erosions, pits w/ calculus/tartar–> tooth ache
DC tx
removed dis. tissue, replace w/ inert restoration
prev/control of DC
change diet: avoid ref. sugar
inc. oral hygiene
fluoride (hyroxyapatitie–>fluorohydroxyapatite)
sealants
future prevention: sp. targeted antimicrob. pep: STAMP: C16G2
dentoalveolar infections
pyogenic infections of tooth and surrounding tissues
agents: oral and carious flora that have gained access to inner tooth tissue
risk: those w. dental caries or traumatic injury
dentalv inf. pathogenesis
via caries or trauma, orgs. get to inner tooth tissue–>microb. invasion of pulp w/ pulpits–>if drainage blocked–>pulpal necrosis, invasion of alveolar bone–>
end result of dentalv. inf
periapical or acute alveolar abscess and osteomyelitis
dentalv. inf immunity
Ab mediated
dentalv. s/s
tooth sensitive to pressure, percussion, heat, cold, etc. +/- drainage
dentalv dx
clinical s/s + caries or enamel compromise
radiographs to detect silent lesions, esp. in interproximal caries (btw teeth)
dentalv tx
dep. on severity
- elim of inf. pulp, deep periodontal scaling, drainage if abscesses, tooth extraction if req, analgesics
ppx, prevention of dentalv. inf
avoid sugar, inc. hygiene, fluoride, sealants, C16G2 STAMP (same as caries)
Gingivitis–>Periodontal disease
NF induce inflamm. via imm system to attack tooth and supporting structures (gingival, period. lig, alv. bone, cementum) s/s: painless gum bleeding–>sig. pain, pungent breath and reabsorption of bone and tooth loss
gingivitis
plaque builds on teeth and gingival margins/crevices and calcifies–>inflamm. and friability of gingiva
orgs of chronic gingivitis
Prevotella intermedia, Bacteroides sp., Fusobacterium spp. (G- rod)
orgs of acute ulcerative gingivitis (Vincent’s disease, trench mouth)
Treponema denticola, T. vincentii (Spirochetes)
Prevotella intermedia, Fusobacterium spp (G-rod)
Periodontitis
inflamm. and invol of deeper tissue, involvement of periodontal lig. and alv. bone (chronic)–>tooth loss
destruction of supp. structs is
irreversible
bac invade and cause inflammation thru niche in plaque–>neutros stim to rel. lysosomal contents (mettalprot/elastases)–>tiss destr.–>bac. hide from imm sys. in tooth and in supra/sub gingival plaque (biofilm) and inhib. neutrophil phagocytosis
this org. subverts norm cell surface rec-IC sig to cause imm. dysfunc
Porphyromonas gingivalis
P. gingivalis can colonize gum via…
and can be sustained via..
C5a rec
C3
(comp cascade can be damaging!)
forms of periodontitis: classic periodontitis
retract. of gums, plaque pres., calculi abundant, bone resorption**
chronic periodontitis
periodontitis + loosening and sep. of teeth–>tooth loss
abscess can form and involve period. lig and alv. bone
*major cause of tooth loss in adults
localized juvenile periodontitis
severe, rapid progression, destructive *not plaque associated (no bone resorption?)
org: Aggregaitbacter actinomycetemcomitans
others: P. gingivalis, P. intermedia
periodontitis orgs
Porphyromonas gingivalis* keystone
Prevotella intermedia
Bacteroides sp.
Fusobacterium spp. (G-rod)
periondontitis tx
remove plaque/tartar, antimicrob. tx (lose teeth by 30, 40 if untx)
necrotizing ulcerative gingivitis and periodontitis
(Vincent’s dis, trench mouth)
like periodontitis, but more acute
NUGP orgs
Treponema spp. (spirochetes)
Fusiform bac
P. intermedia
NUGP affects
males 18-30
risks: poor hygiene, malnutr., fatigue/stress, smtms mouth trauma
NUGP path/clin manif
like gingivitis +
pt. more compromised
s/s: 4 P’s: papillae (irreg. necrotic ulcers), pseudomem. in aff. area (gray), pain, pungent breath
+ reg. lymphadenopathy, fever, malaise (syst.)
NUGP tx
syst. abx (PCN, metronidazole) top. antimicrobs and antiseptic rinse (3% H202)
* thorough pro cleaning and good oral hygiene
loc. juv. periodontitis pop.
neutropenic kids, or have chemotaxis defects
Afr. Am, host factors
loc. juv. periodontitis path, s/s
not plaque assoc., immuncomp is the prob.
“lazy leuk. syndrome”, leuk adh. def
s/s: gums look norm, X-rays show loss of alv. bone (1st molars and incisors)–>loss of perm teeth
loc. juv. period. tx
surg root debridement and resections of aff. tissue
tx w/ abx (metro, tetra)
cervicofacial actinomycosis org
Actinomyces isrealii
cervfac act risks
poor hyg (etOH), trauma, dent extra, orthodontics, hd/nk surg
cervfac act path
pyogenic abscesses w/ tiss fibrosis
compromise in muc. integ–>org gets to submuc. tiss–>spreads by extension along fascial planes
cervfac act s/s
slowly progress., chronic (wks, mod)
low grade/no fever
painful/unilat indurated lesion in peri/submandib. reg w. soft tiss. edema and erythema +/- cervical lymphad.
mult. draining sinus tracts w/ “sulfur granules”
(small yellow/white grains w/ macros + org. filaments @ periphery) (NOT pathognom.)
Histoplasma capsulatum and Nocardia can also have “sulfur granules”
cervfac act dx
Gs of sulfur granule–>G+ thin branching filament (sulf. grans not always observed)
cervfac act tx
PCN, tetra
remove source of inf.: disrupt abscess, drain pus, debride dead tiss, remove tooth/root canal
Ludwig’s Angina
cellulitis, involves subling, submax, submand soft spaces–>airway compromise, asphyxiation, death
Ludwig’s org
Actinomyces israelii (& other Actins)
Ludwig’s risks
adults w/ caries, dentalv inf., trauma to enam/dent
Ludwig’s path
dentalv inf–>spreads via facial planes to subs spaces (2nd/3rd molars often originating source)
Ludwig’s s/s
bilateral**
sub spaces
rapid (w/in 24 hrs) spreading indurated cellulitis +/- abscess or lymp. involvement (nk lymphadenitis)
inf. on floor of mouth–>swell. elevation of floor, pushes tongue to roof, swollen hard nk, diff eating/swallowing/breathing, mouth held open
edema of nk and glottis–>airway obstr/asphyx
+/- fever/syst. signs
Ludwig’s tx
systemic abx (PCN, amox, metro) maintain airway (intub, trach) surg debridement/drainage
Stomatitis
inflammation of oral mucosal membranes (pharyngitis (sore throat))
Oral candidiasis- “thrush” and dental Stomatitis caused by
Candida albicans (yeast, euk fungi)
3 forms: yeast, pseudohyphae, hyphae
biofilms in CV caths, dentures
NF of mouth: fungal spores germ as sing. round cells–>oval/elong., repr. by budding
form moist or mucoid colonies (resemb. bac colonies)
Oral candidiasis pop
newborns, Ca pts., abx therapy, AIDs pts, dentures (65%!)
oral candidiasis pres/s/s
white–>yellow “cottage cheese” patches in mouth
oral pain–>don’t try to remove patches–>exc. bleeding
inflamm: eryth, edema, sore throat, gums, tongue, etc
friable & tender under lesions
if have oral candidiasis and immuncomp(T cell suppr)
can present w/ candidal esophagitis
oral cand. dx
s/s, wet mount microscopy of saline or KOH prep: yeast w/ pseudohyphae, Gs
oral cand. tx
anti fungal drugs/rinses: ketoconazole
