periodontitis Flashcards
chronic periodontitis formerly known as….
- pyorhhea
2. adult/adult onset periodontitis
chronic periodontitis
- inflammation of gingiva and adjacent attachment apparatus
- characterized by loss of clinical attachment due to destruction of PDL and loss of adjacent supporting bone
clinical features of chronic periodontitis
- loss of attachment, probe apical to CEJ (CT fibers detach from root cementum)
- gingival inflammation (gingivitis)
- pockets– probe apical to CEJ, depths of 3-4mm
- tooth mobility
- radiographic bone loss
- bleeding, suppuration
most important factor in determining periodontitis
clinicaly measuring attachment loss
clinical patterns of chronic periodontitis
- destructive, relatively common, but less common than gingivitis, majority of cases are mild-moderate
- extent: based on teeth; 30% or less OR clear pattern is localized, over 30% is generalized
- severity based on att.loss: 1-2mm slight, 3-4mm moderate, 5+mm severe
determining severity based on clinical att loss, probing depths, radiographic bone loss
slight: 1-2mm, probe 3-5mm, 2-3mm radiographic loss (less than 15% root length)
moderate: 3-4mm, 5-7mm probe, 16-30% root length or 3-5mm loss radiographically
severe: 5+mm, over 7mm probing, radiographic loss is 5+mm or over 30% root length
ALL BLEED ON PROBING
what does severe chronic periodontitis often have?
-class II or III mobility, class 2 or 3 furcation vertical bony defects
chronic periodontitis - histo changes
- inflammatory changes
- periodontal attachment apical to CEJ (attachment loss)
aggressive periodontitis
- distinct types of periodontitis affecting otherwise healthy individuals
- usually familial aggregation
- usually rapid rate of progression
- both localized and generalized
- usually 25 years old or younger onset age
aggressivev periodontitis formerly known as
- periodontosis
- juvenile periodontitis
- early onset periodontitis
- rapidly progressive periodontitis
- severe periodontitis
- prepubertal periodontitis
age of onset: aggressive vs chronic
aggressive is usually younger than 25
chronic is 50s, 60s, maybe just starting in 40s
clinical features of aggressive periodontitis
- inflammation
- increased probings generally 5mm or more
- probing apical to CEJ, at least 4mm attc.loss
- tooth mobility
- bleeding/suppuration
- radiographic bone loss
**Same as chronic, but mmust be at least 4mm AL
clinical pattern -aggressive periodontitis
- moderate/severe loss at young age (less than 35yo)
- familial
- localized: 1st molar/incisors
- generalized
- prevalence = .5% population
**less than .2% white population, 2.1-2.6% black population (in USA)
specific pattern of aggressive localized periodontitis
1st molars adn incisors (localized)
**generalized is at least 3 more teeth in addition to 1st molars and incisors
**can call it aggressive if only on 1 1st molar (as long as its not from another factor)
localized vs generalized, whites vs balck
blacks - more localized
whites - more generalized
progression of aggressive periodontitis
- might burn out
- might extend to more teeth
- localized might become generalized
- **observe unaffected siblings
- susceptibility for progression/extension might be environmental (both types found in siblings) or if genetic, suggests varying degrees of penetrance for the genes
prevalence of aggressive periodontitis - studies
2 studies of 5,000-11,000 young americans
- *less than .2% whites
- *2.1-2.6% blacks
histology of aggressive periodontitis
same as adult (chronic) periodontits
periodontitis as manifestation of systemic diseases
- hematologic disorders: leukemia, neutropenias, etc
- immune system disorders: HIV, transplant patients
- genetic disorders: cyclic neutropenia, down syndrome (cause reduced immune system)
NOT METABOLIC DISEASES (diabetes, hormonal – you can have periodontitis as a complication of diabetes, but no ‘diabetes assoc. periodontitis’ like in gingivitis)
refractory periodontitis
NO LONGER USED
- still listed in parameters of care
- was not a single disease entity
- destructive perio disease in patients who, when longitudnally monitored, demonstrate additional attachement loss at 1+ sites despite good therapy adn patient efforts to stop disease progression
NUG/NUP
NUP = NUG + attachment loss
NUG = necrotizing ulcerative gingivitis = acute infection of the gingiva which may have a combo of…
- ulceration/ necrosis of gingival margins/papilla
- necrotic gray pseudo- membrane
- severe pain
- bright red marginal gingiva
- spontaneously bleeding gums
- malodor
- possible fever adn lymphadonopathy
difference in NUG and NUP
in NUP, you lose attachment
***these are the ones they check for on college campuses around exam time – smoking, stress, lack of sleep
NUG and NUP
treat with light scaling and chlorhexadine
rare and usually only in HIV+
localized or generalized
clinical patterns of NUG/NUP (soft tissue destruction/necrosis of papillary and possibly marginal gingiva)
- rare
- localized or generalized
- predisposing factors = stress, usually young adults, poor oral hygiene, smoking, poor nutrition
USUALLY HIV+
histology of NUG and NUP
- ulcerated epithelium
- severe inflammation
- areas of necrosis
- FREQUENT PRESENCE OF SPIROCHETES
NUP vs chronic perio
NUP can occur in a matter of weeks, very rapid loss
chronic – 1mm/6months is as fast as it gets
clinical signs of NUP
- NUG superimposed on previously existing or rapidly progressing perio lesions
- might not be separate disease, might just be NUG combined with periodontitis at some sites
gingival abscess
- localized purulent infection that involves the marginal gingiva ir interdental papilla
- clinical features = localized swelling in marginal or interdental gingiva with smooth red shiny surface; no attachment loss; pain; purulent exudate
chronic vs acute (NUG, abscess)
- chronic is slow, more manageable, comes and goes, patient might not even know they have it
- acute is more painful adn exaggerated symptoms
- NUG adn abscesses are more acute than chronic
periodontal abscess
-localized purulent infection in tissues adjacent to periodontal pocket that may lead to destruction of PDL and alveolar bone
periodontal abscess clinical features
- smooth, shiny swelling of gingiva
- pain, area tender to touch
- purulent exudate
- increased probing depth, NOT TO APEX
- tooth sensitive to percussion
- increased tooth mobility
- rapid loss of periodontal attachment
when is periodontal abscess very likely
a few days after scaling in people with deep pockets. get top 4mm very clean, and they tighten up bc clean. so the pus from bottom part is trapped.
combined perio-endo lesion
- localized circumscribed area of infection involving both the perio and/or pulpal tissue.
- infection can arise from pulpal inflammatory disease and express itself through the PDL or alveolar bone to oral cavity
- or can arise from perio pocket communicating through accessory canals of tooth and/or apical communication and secondarily infect the pulp
- can arise as sequela of fractured tooth
endo lesion
periapical = chronic apical periodontitis
clinical features of combined perio-endo lesion
- sever perio attachment loss that often can be probed to apex of tooth
- non responsive/ necrotic pulp
- may have clinical appearance of perio abscess or endo abscess
- signs may vary whether acute or chronic
- smooth, shiny swelling of gingiva/mucosa
- possible pain with area of swelling tender to touch
- purulent exudate often noted
- increased probing depth
- tooth sensitive to percussion
- increased tooth mobility
- fistulous tract possible
- rapid perio. att. loss
- facial swelling, cellulitis possible
does perio-endo lesion have to have fiistula
no. can drain through sulcus
tooth related factors
- defective restorations
- anatomic (enamel pearl)
- fracture
mucogingival deformaties
- deviations from normal anatomic relationship between gingival margin and mucogingival junction
- recession
- probing beyond MGJ
- loss of keratinized tissue
mucogingival deformaties - gingival recession
- relatively common, most often on facial surfaces
- preexisting thin facial gingiva/bone
- toothbrush abrasion, ortho, restorative
- can be localized or generalized
- periodontitis — you do have attachment loss but might not be periodontitis if overall healthy mouth with exact casue of recession known
mucogingival deformaties - lack of keratinized gingiva
- may occur in absence of disease
- generally narrowest on buccal of mandibular PMs
common mucogingival conditions
- recession
- absence/reduction of keratinized gingiva
- probing depths beyond MGJ
* *anatomic variations can complicate management – tooth position, frenulum inerstions, vestibular depth
gingivitis on a reduced periodontium
- resolution of periodontitis so prexisting attachment loss/bone loss possible
- plaque at gingival margin
- disease starts at gingival margin
- change in gingival color and contour
- increased gingival exudate
- bleeding on provocation
- inflammatory histo changes
- reversible with plaque removal
problems with ‘gingival health on reduced periodontium’ or ‘plaque induced gingivitis on reduced periodontium’
- impossible to determine disease activity in single appt, so patient could have episodic periodontitis (whetehr or not there is bleeding)
- if there is bleeding on probing, impossible to tell if it is gingivitis on reduced periodontium or active periodontitis
- patients with thin periodontium may have active periodontitis that caises attachment loss and recession of gingiva, possibly ywithout deep pockets
perio case types
I: gingivitis– inflammation of gingiva, no att.loss, hyperplasia/ edema/ shallow pocket (unless hyperplasia)
II: slight periodontitis– moderate pockets = 3-5mm; minor-moderate att loss = 1-2mm; no tooth mobility; satisfactory topography
III: moderate periodontitis– mod to deep pockets = 5-7mm; mod-severe att loss = 3-4mm; unsatisfactory topography; slight mobility
IV: severe periodontitis– deep pockets = 7+mm; severe att loss = 5+mm; advanced mobility, usually missiing teeth, may become prosthetic reconstruction cases
V = refractory — NOT USED– destructive periodontitis in patients who, when longitudnally monitored, demonstrate attachment loss at one or more sites despite well executed efforts to slow progression
what are AAP case types used for?
- initially to describe adult periodontitis for insurance companies
- not used frequently now but still in use for disaes severity
limitations of AAP case types
- not applicable to NUP, abscesses, aggressive periodontitis – really only for chronic periodontitis
- more easily applied to sextants than whole mouth bc it goes by worst area, and you could have localized severe and generalized slight
difference between diagnosis adn AAP case type
- diagnosis can be much more discriminating
- such as “localized severe with generalized moderate chronic perio” vs case type 4
broad overview of case types
I = gingivitis II-IV = periodontitis V = refractory perio, NOT USED
AAP Case Type I
GINGIVITIS: inflammation of gingiva characterized clinically by gingival hyperplasia, edema, shallow pocket formation (unless hyperplasia/gingival enlargement) and NO BONE/ATT LOSS
AAP Case Type II
SLIGHT PERIODONTITIS: moderate pockets (3-5mm) and attachment loss of 1-2mm; minor-moderate bone/att loss; satisfactory topography; no tooth mobility
AAP Case TYpe III
MODERATE PERIODONTITIS: moderate to deep pockets (5-7mm) and att.loss 3-4mm; moderate-severe bone loss; unsatisfactory topography; slight mobility of teeth
AAP Case Type IV
SEVERE PERIODONTITIS: deep pockets (7+mm) and 5+mm att loss, severe bone loss, advanced mobility - usually missing teeth
*may become prosthetic reconstruction cases
AAP Case Type V
REFRACTORY – NO LONGER USED
Destructive periodontal disease(s) in patients who, when longitudinally monitored, demonstrate attachment loss at one or more sites, despite well-executed therapeutic and patient efforts to stop the progression of disease
