L1 Recognising health, gingivitis and periodontitis Flashcards
What percentage of the world’s population will experience gingvitis or periodontitis?
- 95% will experience gingivitis at some point in their life
- 60-65% of the adult population will have periodontitis
What percentage of the population are at a higher risk of periodontitis and what percentage of these will have aggressive disease forms?
- 10% of population are at a higher risk of periodontitis
- 1% of these will have aggressive disease forms
What does gingival phenotype/biotype refer to?
The thickness of the gingivae.
Can be assessed by placing a probe in the sulcus, if the probe can be seen then the gingiva is thin (<1mm).
Is gingival stippling healthy?
Yes, it indicates the attachment of collagen fibres in gingival tissues.
Is a knife edge gingival margin healthy? What is the opposite of this?
Knife edge margin is healthy, if the margin is inflammed and swollen it is described as a “rolled margin”.
What are the main signs of gingival health?
- Pale pink or brown in certain ethnic groups
- Gingival stippling
- Knife edge margin
- Scalloped margin
- Sulcus up to 3mm deep
- Interdental papillae is a triangular shape and fully fills the interproximal space
- No BoP
- No recession
- No mobility
What are the 3 classifications of gingival health according to the 2017 world workshop classification?
- Pristine
- Clinical gingival health on an intact periodontium
- Clinical gingival health on a reduced periodontium
Describe pristine gingival health.
- No attachment loss
- No BoP
- No sulcular probing >3mm
- No redness, swelling or pus
Describe clinical gingival health on an intact periodontium.
- Majority of tissues healthy
- 10% BoP or less
Describe clinical gingival health on a reduced periodontium.
- Periodontium reduced due to previous disease
- Recession
- 10% BoP or less
Define biofilm/dental plaque.
Microbial communities of microorganisms attached to a tooth surface encased within extracellular polymeric substances.
What extracellular polymeric substances are found in dental biofilm?
EPS are products of microbial cells (not from the host).
- Proteins
- Extracellular DNA (eDNA)
- Exopolysaccharides
- Lipids
- Surfactants
- Metals
- Inorganic salts
- Water
What are the 5 microbial complexes found in subgingival dental plaque?
- Yellow complex: found in health
- Purple complex: early colonisers
- Green complex: early colonisers
- Orange complex: gingivitis
- Red complex: periodontitis
What type of relationships do microorganisms in the same complex have with eachother?
Symbiotic relationships.
What microorganisms are found in subgingival dental plaque in health?
- Streptococcus
- S. grodonii
What microorganisms are found in subgingival dental plaque in gingivitis?
- P. intermedia
- F. nucleatum
- C. rectus
- F. periodonticum
What microorganisms are found in subgingival dental plaque in periodontitis?
- P. gingivalis
- T. forsythia (formerly B. forsythus)
- T. denticola
What microorganisms are found in the purple and green complexes (early colonisers)?
- V. parvula
- C. gingivalis
- C. sputigena
- E. corrodens
When do clinical signs of gingivitis present following plaque accumulation?
Within 4-5 days of undisturbed plaque accumulation.
What are the clinical features of gingivitis?
- Erythema
- Oedema
- Loss of stippling (shiny appearance)
- Soft tissues
- Bleeding on probing
- Sulcus depths increased (false pocketing)
- Increased GCF flow
- Painless
What is the difference between localised and generalised gingivitis?
Localised = 30% or less BoP
Generalised = 30% or more BoP
Why is bleeding on probing a significant feature to measure?
- Approx. 30% of sites that bleed from the base of the pocket (not gingival margin) will continue to deteriorate
- 98-99% of sites that don’t bleed remain healthy over time
What are the 4 stages of periodontal disease according to Page and Schroeder (1976)?
1) Initial gingival lesion
2) Early gingival lesion
3) Established gingival lesion
4) Advanced lesion
Describe the first stage of the disease process.
Initial gingival lesion
- Biofilm accumulates over 2-4 days
- Gingivitis not evident clinically
- Increased vascularity and capillary permeability = inflammatory cells able to reach tissues
- Increased GCF = oedema
- Increased polymorphonuclear neutrophils
- 5-10% loss of connective tissue
- Only evident histologically (loss of JE attachment, inflammatory cell infiltrate from fenestrated capillaries)
Describe the second stage of the disease process.
Early gingival lesion (mild gingivitis)
- 4-7 days of plaque accumulation
- Potentially visible clinically
- Change in cell infiltrate from neutrophils to macrophages, and then to lymphocytes
- Continued increased vascularity, angiogenesis, GCF flow
- Damage to fibroblasts reduces collagen production
- Hyperplasia of JE basal cells
Describe the third stage of the disease process.
Established gingival lesion
- 2-3 weeks of plaque accumulation
- Clinically obvious gingivitis
- Continuation of inflammatory processes
- Lymphocytes and plasma cells predominate
- PMNs in sulcus trying to maintain barrier against biofilm
- Rete peg proliferation and elongation
- Production of inflammatory cytokines, destruction of connective tissue
- JE migrates apically, deeper probing
Describe the fourth stage of the disease process.
Periodontitis
- Same inflammtory cells as previous stages, but further destruction due to action of immune system
- Cytokines (IL-1, TNF-α, PGE2) stimulate fibroblasts to produce MMPs
- Loss of collagen and PDL
- JE ulceration and further apical migration
- Extension of anaerobic subgingival plaque (difficult to clean)
- Chronic inflammatory infiltrate
- Osteoclast activity = bone resorption
What microorganisms are present in periodontitis?
- P.gingivalis
- T.forsythia
- T.denticola
- A.actinomycetemcomitans
What type of immunity and cells are involved in periodontitis?
Adaptive immune system (cell mediated immunity)
- Swith from T cells to B cells and plasma cells
The immune system is acting in response to the chronic inflammation.
What inflammatory mediators activate the inflammatory/immune response in periodontitis?
- Cytokines (IL-1/6/8 and TNFα) recruit PMNs and macrophages = initiates tissue destruction
- Prostaglandins (PGE) increase permeability to allow immune cells and complement to reach site = alveolar bone destruction
- MMPs facilitate normal turnover of the CT matrix = collagen destruction
Summarise the reasoning behind periodontal disease progression.
The role of the host response is critical to periodontal disease progression. The immune system is trying to prevent systemic infection, at the expense of oral health.
Host susceptibility is key (genetic risk factors).
