periodontal disease- diagnosis Flashcards
what are the symptoms of clinical gingival health?
- coral pink and firm gingivae
- ID papillae exactly fill interdental space
- no signs of inflammation- erythema/ oedema
- good OH
- less than 10% bop
- knife edge margins
- stippling of gingivae
- little inflammatory infiltrate- mainly neutrophils (normal immune surveillance)
- little GCF fluid
what are the symptoms of gingivitis?
INFLAMMATION OF GINGIVAL TISSUES:
- loss of stippling
- overfilled ID papillae
- rolled margins
- erythema
- oedema
- bop
- false pocketing
- plaque at gingival margins
- more inflammatory infiltrate
- increased GCF
- reduced no of fibroblasts
- reduced collagen
what are the clinical signs and symptoms of periodontitis?
- LOA (JE migrates apically)
- radiographic bone loss
- ID papillae recession
- bop
- increased pocketing- true pockets
- mobility
- furcation involvement
- tooth loss
what makes up
LOA?
Pocket?
Recession?
ACJ-base of pocket
GM- base of pocket
ACJ- GM
what happens when the periodontium breaks down?
- JE migrates apically due to underlying PDL and collagen destruction
- collagen breakdown and therefore breakdown of CT ECM, losing tissue support
- bone resorption due to osteoclastic activation due to immune cells such as cytokines and other cells such as fibroblasts, endothelium, osteoblasts releasing host resorption factors
- fibroblast damage and reduction needed for repair
what is the initiating factor for periodontal disease? and what causes the damage
plaque but it is the hosts response to plaque which causes 80% of the tissue damage to avoid bacteria entering deeper tissues
what do people have when they have an increased response to plaque which causes damage?
hyper-reactive immune response
what is the hyper-reactive immune response due to?
increased release of cytokine- IL1- which causes an excessive inflammatory response
discuss the meaning of susceptibility to periodontal disease
- measured by age and OH relative to periodontal destruction
- can be high
- can be low
- high susceptibility relates to genetic factors
can you predict periodontal disease?
no- but can assess susceptibility to understand how it may progress
thorough history should be carried out to assess risk
genetic testing to identify positive PAG- coding for IL1 which means the individual has a hyperactive IR to bacteria by high levels of IL1 which cause excessive inflammatory response
what are the theories of disease progression?
- continuous rate theory
- random burst theory
- multiple burst theory
what is the continuous rate theory?
suggests disease progression is slow and continuous- with affected sites showing constant progressive rates of periodontal destruction
what is random burst theory?
- sites can be active or inactive and undergo random short bursts of destruction at random sites followed by periods of no destruction
what is the multiple burst theory?
- multiple sites undergo destruction within a particular period of time such as during an illness and followed by long periods of no destruction
what are the conclusions from the burst theory ?
- gingivitis does not always progress to periodontal disease
- periodontal destruction does not occur in a gradually or continuously
- pattern of destruction varies between individuals and within the same person (diff sites/diff rates of progression)
what is RAL and Gal?
- rapid attachment loss
- gradual attachment loss
more susceptible individuals will have RAL and low susceptibility will have GAL but can have both occurring at different sites within the same individual e.g RAL in areas harder to clean e.g back of mouth,
how do you screen for periodontal disease?
- risk assessment with thorough history- DH, MH, SH, FM
- clinical assessment- BPE, 6PPC, R/Gs
what is a BPE used for?
screening tool to identify those who need more detailed periodontal assessment