Classifications
● Gingivae = masticatory mucosa, covers alveolar process & cervical part of teeth
● Outcomes of perio tx: control risk factors, stop progression, eliminate infective microorg,
tissue healing
Health
● Pristine
● Well-maintained
● Stability & reduced periodontium → successful tx
● Remission & reduced periodontium → improvement but not optimum risk
factor ctrl)
● Incipient gingivitis
● Stability = <10% BoP, no probing depths >3mm that bleed
Gingivitis
● Biofilm only / biofilm & modifying factors / necrotising
● Reversible
Modifying Factors
● Systemic = smoking, hyperglycaemia
● Oral = subgingival restorations, xerostomia, drug-induced enlargement
Extent: localised (<30%) / generalised (>30%)
Severity
● Mild (papillae, minor colour change)
● Moderate (papillae & marginal gingivae, red, oedema, IF, BoP)
● Severe (incl attached gingivae, BoT)
Biofilm-induced gingivitis Necrotising gingivitis
● No age ● Young adults
● Less evident in smokers ● Sudden onset
● No ulceration/pain ● Smokers/stress
● T. denticolea, F. nucleatum, P. ● Ulcers along gingival margin
intermedia ● Marked halitosis
● No AB required ● Mixed infection (incl spriochetes)
● Responds to OH & AB
Gingival overgrowth
● Manage w OHI
● Tx: surgical correction (gingivectomy/flap surgery), drug substitution
● Consider yellow carding
Periodontitis
● Stage: 1 (initial, <15%), 2 (moderate, 15-33%), 3 (severe, mid ⅓), 4 (v severe, apical ⅓)
- max CAL / max bone loss on RG
● Grade: A, B, C (progression speed)
- % bone loss of root length divided by age, RF
, ● Pathogenesis: breakdown of PD fibre bundles @ cervical margin, resorption of alveolar
bone, apical proliferation of JE beyond CEJ
● Dx: 6PPC, BoP, subgingival calculus, mobility, vitality, RG
● Tx: plaque control, NSM, maintenance
Histology
Health
● Features: knife-edge gingivae, stippled, scalloped, sulcus <4mm, triangular IDP, no BoP,
different biotypes (thick/thin)
● Histology: JE attached to tooth surface, GCF contains NP & MP, collagen aids
attachment
Initial Lesion
● 2-3d
● Increased capillary perm / GCF /LC & NP
● Collagen starts to break down
● Not seen clinically
Early Lesion
● 6-10d
● Increased capillary perm / GCF / T & B lymphocytes / MP
● Collagen destruction & FB damage
● Hyperplasia of JE basal cells
Established Lesion
● 10-14d
● Increased IF infiltrate & rete peg prolif
● Host & bacteria products → collagen destruction, deepend gingival crevice (JE
tries to maintain barrier)
Advanced Lesion
● Extended subgingival anaerobic plaque
● Breakdown of CT fibres attaching root to gingival CT & alveolar bone
● JE ulceration & apical migration
● Chronic IF infiltrate
● Alveolar bone resorption
Plaque & PDD
● Lack of OH measure → plaque accumulation
● Attracts PMNLs → enz & degranulation → tissue damage
● G-ve bacteria → endotoxin → cell damage & complement
● Direct complement = opsonic, IF, lysis. Indirect complement = increase Ig response
● CLEAR link = plaque extent & gingivitis
● WEAK link = plaque extent & periodontitis → multifactorial
, Radiology
● OPT: + lower dose than FMIOPA. - distortions, less clear md incisor region
● BW: + good detail, additional disease dx. - less teeth than OPT, no apical info
● IOPA: + apical zone, least distortion. - increased dose if FM
● OPT if generalised, IOPA/BW if localised
● Limits = superimposition, underestimate bone loss, no morphology of pocket, represents
past activity
BPE
● Sextant only incl if 2 or more teeth
● Ignore 8s unless 7s/6s missing
● Probing depth 20-25g
● Angle probe near contact points
● 1 = OHI & S&P
● 2 = OHI, S&P, treat PRF
● 3 = OHI, S&P, allow resolution of false pockets, 6PPC in that sextant
● 4 = OHI, S&P, full 6PPC, RG, RSD, 3m review of probing depths
- Continue to examine all sites to ensure don’t miss ptl furcation
● Drawbacks: screening only, no dx/TP, cant monitor tx, no info within sextants
● Probing errors: op variability (force, position, angle), obstacles (blood, calculus)
- Reproducibility w automatic probes / constant pressure probe
