Perio

Question 1

Gingival health

Answer 1

Pristine periodontal health
Total absence of clinical inflammation and physiological immune surveillance on a periodontium with normal support

Clinical periodontal health
Absence/minimal levels of clinical inflammation and physiological immune surveillance on a periodontium with normal support

Question 2

Gingivitis

Factors
Process

Answer 2

Gum inflammation induced by biofilm accumulation
Localised gingivitis: BOP 10-30%, Generalised gingivitis: BOP > 30%
Probing discomfort
Oedema, erythema
No radiographic bone loss
Reversible condition

Factors that make gingiva more susceptible to infection: smoking, diabetes, nutritional deficiencies, drugs, sex steroid hormones, hematological conditions
BOP Not good indicator for smokers - reduced blood flow and fibrous gingival tissues
Local: biofilm retention factors, oral dryness

Stages of gingivitis
Stage I: Clinically Healthy gingiva
Biofilm produces metabolites (fatty acids), peptides, LPS
JE stimulated to syn. inflammatory mediators
Perivascular mast cells release histamine → widen capillaries
Endothelium releases IL-8 into vessel, attracts PMNs
PMNs follow chemotactic gradient to sulcus
Complement proteins and antibodies support phagocytosis of bacteria

LPS can either attach directly to the endothelial wall or attach to macrophages that attach to the endothelium, causing receptors to form in blood vessel to which PMNs can bind and exit vessels
Elam1
Pro-inflammatory cytokines IL1a & TNFa, IL8

Stage II: Early Gingivitis
PMNs form dense layer over biofilm aka a palisade (thick wall)
PMNs release proinflammatory cytokines and enzymes
Activation of macrophages
Lymphocytes infitrate CT
Widened intercellular spaces in the junctional epithelium and loss of collagen provides space for infiltrating cells
Increased vasodilation and blood vessel permeability
Lateral proliferation of basal JE cells to make JE thicker against the biofilm→ creates Rete ridges

Stage III: Established Gingivitis
Intense PMN and lymphocyte infiltration in JE/sulcus
T cells activated, coord response by cytokines, plasma B cells produce antibodies
Activated fibroblasts produce MMPs (matrix metalloproteinases) and TIMPs (tissue inhibitors) instead of collagen
Lateral proliferation & Apical migration of junction epithelium → pseudopocket (cannot feel CEJ)

Question 3

Healing of gingivitis

Answer 3

In 4+ days:
Repair of JE
Reduction in PMNs
=> Decreased pus, exudate

In 7-14 days:
Decrease in vascular permeability
Decrease in inflammation
=> Decrease in redness, oedema
Reduction in tissue retractibility

In 2-6+ weeks :
Fibroblasts increase
Collagen production increase
Tissues become firmer
Increased resistance to probing

Question 4

Necrotising Perio diseases

Answer 4

Necrotising Gingivitis
Pain
BOP ++++++++
Central necrosis of interdental papilla - Gums appear different - black, greyish
Halitosis
Fever, malaise → lymphadenopathy (swelling of lymph nodes)
Necrotising Periodontitis
CAL and Radiographic bone loss
Necrotising Stomatitis
Osteonecrosis
Lesions w ulcerations >1cm
Noma
Gangrenous stomatitis
Common among children with severe malnutrition and compromised immunity
Can lead to death if untreated

Treatment:
* Debridement under LA - remove biofilm, calculus, necrotic tissues
* Local irrigation with 0.2% Chlorhexidine
* Antibiotic therapy - metronidazole 400mg, 12hrly, 3-5d
* Analgesics

• OHI, mouthrinse - 0.2% chlorhexidine mouthwash 10ml, 1min 2x day.
• Smoking/stress counselling as req.
  Review after 48-72h
  Review after 14d –> not resolved, refer to GP

Question 5

DIGO

Answer 5

Signs:
Mulberry-shaped gingival overgrowths
Painless, pink and firm, no BOP
Extends to facial & oral gingival margins

Caused by:
Calcium channel blockers
Amlodipine
Immunosuppressants
Cyclosporine, Tacrolimus, sandimmun
Anti-convulsants
Phenytoin
Sodium valproate

Treatment:
Meticulous biofilm control to prevent secondary infection
Surgical excision
Cessation of drug/substitution - but usually not done as prescribed medication keeps other more important conditions stable

Question 6

Periodontitis

Answer 6

Irreversible periodontal tissue destruction resulting in alveolar bone loss
Interdental CAL >= 2mm at more than or equal to 2 non-adjacent teeth
Buccal CAL >= 3mm at more than or equal to 2 teeth
Radiographic bone loss

Diagnostic statement:
Localised/Generalised
Disease
Stage I,II,III,IV - 15%-33%-apical
Grade A,B,C - % bone loss/age 0.25-1->1
Stability
currently unstable (BOP>10, 4mm depths), in remission (BOP>10+4mm or BOP<10+5mm), stable - no BOP at 4mm sites.
Risk factors: smoking/vaping, diabetes, xerostomic medication, stress, alcohol

Question 7

Recession

Answer 7

Apical migration of the gingiva

Causes
Bone loss - like from periodontitis
Trauma
Abrasive brushing
Orthodontic appliances
Occlusal trauma
Anatomical - thin periodontal phenotype
Natural dehiscences or fenestrations
High frenal attachment

Consequences
Dentine hypersensitivity
Impaired OH - Caries
Aesthetics

Question 8

Scalers

Answer 8

Working end - curved or straight
Features: triangular cross section, 2 cutting edges, sharp tip
Common: Sickle, McCall’s
Hand scaler Usage:
Place 2-3mm of the scaler working end slightly below deposit
Tilt surface of blade against tooth to form 85deg angle
Apply lateral pressure towards tooth and pull scaler up

Power scaler
Ultrasonic: Piezoelectric, Magnetostrictive, sonic
Usage: use sides of scaler laterally 0-15deg, very light pressure
Mechanism:
Mechanical vibration
Lavage - water washes away biofilm and debris
Cavitation - water from tip of scaler dissipates heat produced at tip
Acoustic microstreaming - create vibrations in the water, currents help to dislodge biofilm and debris