perio exam 2 Flashcards
is bop sensitive?
no, b/c trauma could also cause bleeding. it is specific-if no bleeding then there is a great chance pt is healthy
gingivitis ( dental pq only) …
can have local contributing factors
ging w/ systemic disease modification
endocrine association or blood discrasias (ex. leukemia associated)
(which drug from pharm causes that?)
ging w/ systemic disease modification:
endocrine association ex’s:
puberty associated, menstrual cycle, pregnancy, diabetes
ging modified by meds
ging enlargements, oral contraceptives
ging from malnutrition
vit c deficiency or lack of vit A, B2, and B12 complex
summary slide: pq should be there for ging
unless pregnant or medicated
ging around implants
peri-mucositis
6 characteristics to all ging diseases:
- signs/symptoms limited to ging
- precursor-pq
- clinical signs of infmm
- no att loss or on a stable but reduced periodontium
- reversibility of the disease by removing the etiology
- possible role as a precursor of att loss
11 characterists of pq induced ging
- pq @ margin
- margin-start of disease
change in:
3.color 4. contour 5. sucular temp - incresed gingival exudate
- absence of att loss
- absence of bone loss/9.bone loss
9.histological changes
10reversible w/pq removal - bop
color: normal ging v. inflammed v. severly infmm
coral pink, tissue’s vascularity and overlying eli intact v. red and not intact v. red and CYANOTIC; vascular proflieration, decreased keratin and venous stasis
where do the color changes start?
g. margin and interdental papilla then spread to the att g
g bleeding: w/ inc infmm…
chronic/recurrent bleeding
when is there spontaneous bleeding?
inc infmm.. engorged caps, thinning/ulceration of the sulcular epi.
chronic/recurrent bleeding from trauma
spontaneous bleeding=acute/severe cases-maybe related to systemic disease
healthy adjectives
health=firm/resilliant w/dull surface texture (stippling maybe) and scalloped ging fills interdental spaces (papilla there)
what can lead to leathery, firm ging consistency?
chronic g can indue fibrosis and eli proliferation
infmm v. severe infmm descriptions
infmm=extracellular fl and exudate, degeneration of ct & epi, engorged ct/thin epi, and knife edged ging w/loose margins
sometimes clefts (Stillman’s) or festoons (McCalls) may develop
infmm w/ exudate=smooth and shiney,
infmm w/fibrotic changes=nodular and firm
swollen, soft, friable
severe: sloughing w/grayish flake-like debris (necrosis)
mild gingivitis
PD-? mm Plaque ?% BOP ? %
PD-1.5-3 mm Plaque 50% BOP 15 %
moderate gingivitis
PD-? mm Plaque ?% BOP ? %
PD-3-4 mm Plaque 50% BOP 30%
severe gingivitis
PD-? mm Plaque ?% BOP ? %
PD-pseudopockets to 5 mm Plaque 50% BOP 80 %
(no att loss still!)
all had same pq comp-BOP %’s changed
ging enlargement-3 descriptions
- chronic infmm response characteristic w/exudate and proliferative features
- clinically deep red lesions w/soft, friable, smooth, shiny surface and bleeding tendency
- relatively firm resilient and pink lesions w/ greater fibrotic component, abundant fibroblasts and collagen fibers
(3 said “also”, I hope as in “could be this instead” vs. 2 and 3 together….)
What is/are the primary etiological factor(s) for ging?
bacterial plaque
What is/are the secondary etiological factor(s) for ging?
local factors such as 1. calculus 2.marginal deficiencies 3.malocclusion 4.tooth/root anomalies (enamel pearls/cemental tears) 5. BW 6. roots fractures 7. cervical toot reabs
BW=?
histo dimensions of the dento-gingivl junction health .69-sulcus .97=epi attachment 1.07-ct total 2.73
bw = a min of ?mm coronal to alveolar crest?
3 mm
does perio start with gingivitis
YEES!
does gingivitis progress to perio?
not always!
define recurrent periodontitis
return of infmm to the sites treated. recurrent periodontitis may be confined to the ging tissue and may not cause further attachment loss.
with ging modified by endocrine factors, do you need to have plaque?
YES! (page 11)
ex.’s pregnancy, puberty and menstral cycle
pregnancy associated ging-the microbiota is characteristic of what?
microbiota is characteristic of ging
exaggerated localized host response modulated by what hormones?
modified by levels of endogenous hormones (estrogens, androgens, progesterone)
changes with pregnancy associated ging appear in what trimester?
the 2nd trimester and regress upon parturition (birth)
puberty associated gingivitis-what is a secondary factor?
mouth breathing
puberty associated gingivitis: localized host response mediated by…
high hormones, estrogen, testosterone
do clinically detectable changes seem to be associated with the menstrual cycle?
no but and inc in GCF (ging crevicular fl) by 20% described
pyogenic granuloma of pregnancy…
arises from…
presentation timeline…
highly vascularized mass of granuloma tissue
arises from prix ging tissues and has a pedunculated base
2nd or 3rd trimester
ging modified by systemic conditions (5)
diabetes ! & II, leukemias and other blood dysplasias, acute myeloid leukemia associated w/ ging changes, cyclic neutropenia, thrombocytopenia
what are the ging modifications with cyclic neutropenia?
ulcerations (14-36 days per cycle)
what are the ging modifications with thrombocytopenia?
persistent unexplained ging bleeding
now explained lol
what are three drugs associated with ging overgrowth?
1.anticonvulsants (phenytoin or epinutin)
2. immunosuppressants (cyclosporin A)
3.ca2+ channel blockers (Nifedipine)
why didn’t we learn that one in pharm….?
Necrotizing ulcerative ging (nug)
pt’s: adolescents, smokers or psychological stress, have
pain, ulceration and necrosis of interdental papillae*, bleeding
*starts there
Necrotizing ulcerative ging (nug)-what’s often required for resolution?
systemic antibiotics
what’s the differential diagnosis for Necrotizing ulcerative ging (nug)?
primary herpatic gingivostomatitis
Necrotizing ulcerative ging (nug)-predisposing factors
systemic disease ex. ulcerative colitis, blood dyscrasias, nutritional deficiency states
white blood cell function compromised
AIDS pts
is nug associated with peril att loss?
yes
what can nug progress to?
can progress to noma or cancrum oris
noma (wiki): “Noma is a rapidly progressive, polymicrobial, opportunistic infection that occurs during periods of compromised immune function. estimates that 80-90% die from it”
differential diagnosis nug vs herpes (PHS)
nug=bacterial and noncontagious vs.herpes-very contagious
nug NOT in attached ging
herpes=everywhere
symptoms nug v. PHS
ulcerative tissue, yellowish white plaque
mult vesicles burst leaving sm round fibrin covered ulcers (phs)
duration nug vs phs
1-2 days if treated for nug w/anitb’s
1-2 wks phs
