Gingivitis and Periodontitis Flashcards
What is the main difference between gingivitis and periodontitis?
Gingivitis = reversible inflammation to the gingiva
Periodontitis = irreversible infection associated with all parts of the periodontium
What are the 4 stages of gingival inflammation?
- Healthy / Prsitine gingiva
- Initial lesion
- Early lesion
- Established lesion
What are the key features of healthy gingiva?
No plaque
Shallow gingival sulcus
JE fimrly attached to root, sulcular epithelium, and connective tissue
Some gingival crevicular fluid (GCF)
What are the clinical characteristics of healthy gingiva?
Pink or pigmented
Firm
No bleeding
What are the histological characteristics of healthy gingiva?
JE coronal to cemento-enamel junction
Supragingival fibres intact
Alveolar bone intact
Periodontal ligament intact
What are the clinical characteristics of gingivitis?
Erythemic (redness)
Inflamed
Bleeding present
Pain
What are the histological characteristics of ginigivitis?
JE located at CEJ
Supragingival fibre destruction
PDL intact
Alveolar bone intact
What changes occur during the inital lesion phase?
Within 2 - 4 days, bacteria colonise the tooth near the gingival margin, initiating host response
PMNs pass from bloodstream into the gingival conenctive tissue and release cytokines that destroy gingival connective tissue, allowing PMNs to move quickly through tissue
PMNs migrate into the sulcus and phagocytose bacteria, this process causes peri-vascular collagen loss
What are prostaglandins (PG) and matrix metalloproteinase (MMP)?
PG = biochemical mediators, E series are crucial to perio bone destruction
MMP = family of enzymes that work together to break down connective tissue, causes extensinve destruction to collagen in pero tissues
What changes occur during the early lesion (early gingivitis) phase?
Within 4 - 7 days, abcteria penetrate connective tissue and more PMNs are attracted to the site, releasing more cytokines and causing more localised destruction of connective tissue
Macrophages are recruited to the connective tissue and release cytokines, PGE2, and MMPs (more destruction)
JE and sulcus become densely infiltrated by neutrophils and begin to show development of rete pegs/ridges
Increased collagen destruction (70% around infiltrate destroyed), affecting circular and dentoginigval fibre groups, collagen production decreases
What changes occur diring the established lesion phase?
Within 14 - 21 days, plaque biofilm extends subgingivally and disrupts the attachment of the most coronal portion of the JE
Macrophages and lymphocytes are most numerous in the connective tissue, PMNs continue to fight bacteria in the sulcus, so host cells continue to produce more toxic chemicals (cytokines, PGE2, and MMPs)
Blood vessels engorged and congested as venous return is impaired, blood flow is sluggish and localised gingival anoxemia gives bluish hue
Moderate / severely inflammed gingiva and deepening of gingival sulcus, but NO LOA
What is periodontitis?
Bacterial infection of the periodontium associated with the body’s response to bacterial invasion of the JE and connective tissue
Process is usually pain free, patient present to the clinci after noticing bleeding gums or mobile teeth
Eventually bony socket of the tooth is compromised adn the tooth becomes mobile
What are the clinical characteristics of periodontitis?
- Colour varies from red and purplish-blue
- Bleeding on probing
- Inflammed or fibrotic gingiva
- Increased pocket depths > 3mm
- Recession
- Bone resoprtion
- Drifiting of teeth
- Tooth mobility
- Suppuration on probing (pus formation)
What are the histological characteristics of periodontitis?
- Coronal portion of JE detaches from root surface
- Apical portion fo JE moves apically along surface of root creating a periodontal pocket
- Collagen fibres are destroyed
- Permanent destruction of alveolar bone and periodontal fibres
- Cementum is exposed to oral environment
What is the mechanism of alveolar bone destruction?
Macrophages produce cytokines, PGE2, and MMPs which stimulate fibroblasts and secrete more PGE2 and MMPs
Mediators from macrophages and fibroblasts result in destruction of the connective tissue and PGE2 stimualte osetoclasts and resorb the crest of the alveolar bone