Perio LOs

Perio Learning Objectives (Isolated)

L1 — Introduction to Periodontal Surgery

• Understand regenerative surgery modalities (GTR, bone grafting, enamel matrix derivative/Emdogain, biologics); distinguish true regeneration (new bone, cementum, PDL) from repair
• Identify clinical indications and contraindications for periodontal surgery: residual pockets ≥5–6 mm with BOP, infrabony defects, furcation grades II–III, mucogingival defects, altered passive eruption, crown lengthening
• Classify periodontal surgical procedures: resective (APF, osseous resection), regenerative (GTR, EMD, bone grafting), access flap (modified Widman, open flap debridement), plastic/mucogingival
• Understand flap design principles: adequate blood supply (wider base), sufficient access, tension-free closure, preservation of interdental papilla
• Perform osseous resective surgery and pocket reduction: osseous resection vs osteoplasty, apically positioned flap, achieve positive bone architecture
• Define and understand the objectives of periodontal surgery within the EFP S3 treatment sequence (Steps 0–4)
• Perform crown lengthening for aesthetic (altered passive eruption / gummy smile) and functional indications (restorative margin placement, supracrestal tissue attachment management)
• Apply GTR barrier membrane principles: prevent epithelium ingrowth, promote PDL and bone cell migration, distinguish resorbable vs non-resorbable membranes
• Apply surgical incision sequence: internal bevel (remove pocket lining), crevicular (release tissue), interdental (separate collar), gentle flap reflection
• Manage furcation defects using root resection, hemisection, tunnelling; understand risks (tunnelling increases caries/sensitivity)

L2 — Gingival Recession and Overgrowth

• Distinguish anatomical, inflammatory, traumatic, and iatrogenic aetiological factors in recession (traumatic occlusion, aggressive toothbrushing, orthodontic movement, iatrogenic margins)
• Select appropriate surgical root coverage procedure per defect: CAF (gold standard RT1), CAF+CTG (most predictable), FGG (keratinised tissue), Tunnel (minimally invasive), Laterally Positioned Flap (isolated defects)
• Apply Miller, Sullivan & Atkins, and Cairo classification systems; recognise Cairo (RT1/RT2/RT3) as post-2017 World Workshop standard
• Manage gingival overgrowth: non-surgical (intensive plaque control, SRP, chlorhexidine, medical liaison) and surgical (gingivectomy, flap surgery, laser) depending on fibrotic component
• Understand drug-induced gingival overgrowth pathogenesis: altered fibroblast function, increased ECM, reduced collagen degradation in phenytoin / cyclosporine / calcium channel blockers; distinguish from inflammatory and systemic causes
• Evaluate prognostic factors for recession treatment success: interproximal attachment (key blood source), tissue thickness, smoking, operator skill, patient compliance
• Identify clinical consequences of gingival recession: root sensitivity, root caries, NCCL, aesthetic concerns, plaque retention, cervical abrasion
• Understand gingival recession definition and epidemiology: apical displacement of gingival margin relative to CEJ; increases with age, periodontitis history, thin phenotype, traumatic toothbrushing

L3 — Endo-Perio Lesions

• Classify endo-perio lesions using modern EFP classification ± root damage (with vs without damage; grades 1–3)
• Sequence treatment for communicating lesions: endodontic first, ≥4-week wait before perio (prevents ankylosis)
• Evaluate Cortellini 2011 regenerative therapy: 92–100% survival, similar complication rate vs extraction in hopeless teeth
• Manage endo-perio with root damage: vertical fracture, perforation, resorption diagnosis and root resection / hemisection
• Apply the Essential Three diagnostic tools (pulp sensibility, full-mouth perio probing, radiographs incl. CBCT) to combined-lesion diagnosis
• Identify anatomical communication pathways: lateral / accessory canals (up to 30% molars), dentinal tubules, palatal grooves, anomalies
• Assess prognosis using multifactorial framework: restorability, attachment loss, furcation involvement, periodontal healing response
• Determine lesion origin via decision tree (Linde): vital tests, radiographic location (apex vs lateral), pocket morphology
• Recognise diagnostic pitfalls: distinguish transient pulpal response (post-deep scaling) from true endo-perio pathology
• Understand bidirectional spread: pulp→perio via accessory canals (common); perio→pulp (rare, requires apical invasion)

L4 — Perio-Resto Interface

• Explain biologic width (supracrestal tissue attachment, SCAT) dimensions: epithelial attachment 0.97 mm + connective tissue 1.07 mm + sulcus 0.69 mm (Gargiulo 1961); note Schmidt 2013 variability 0.2–6.73 mm
• Identify consequences of biologic width violation: chronic inflammation unresponsive to hygiene, uncontrolled bone loss, microflora shift to virulent gram-negative anaerobes, gingival recession
• Apply crown lengthening assessment: bone sounding under anaesthesia; rule: <3 mm soft tissue from bone to planned margin → surgery indicated
• Distinguish crown lengthening surgical techniques by BW invasion × KT adequacy: gingivectomy (no BW invasion, adequate KT), gingivectomy+osteotomy (BW invasion + adequate KT), apically repositioned flap (inadequate KT)
• Apply Carvalho clinical management guidelines for subgingival margins: measure margin-to-bone distance, preserve ≥2 mm keratinised tissue, ensure smooth margins, avoid BW breach via gingivectomy vs osteotomy decision
• Explain prerequisites for successful comprehensive dentistry: achieve biofilm control, resolve inflammation, reduce pocket depth, stabilise attachment, prevent post-restoration tissue shift
• Classify restorative margin locations by periodontal consequences: supragingival (ideal, no SCAT violation), equigingival (at crest), subgingival (2× attachment loss risk per Broadbent 2006, Schatzle 2000)
• Evaluate restorative design for plaque retention: precise marginal fit (CLSM biofilm at sub-mm gaps); overcontouring risks; surface finish (glazed porcelain least retentive)
• Understand interdisciplinary foundation: perio prepares healthy substrate → prostho achieves correct margins / contours / shapes (Hsu 2015)
• Manage overhanging / defective restorations: recognise microflora shift to gram-negative anaerobes (Lang 1983); correction difficulty (specialised handpieces vs replacement)

L5 — Wound Healing and Regeneration

• Explain the four phases of periodontal wound healing (clot/vascular, inflammatory, granulation, maturation) with timeline and cellular dynamics; epithelial migration rate (4–7 days) “wins the race” unless blocked by GTR
• Apply the Melcher hypothesis (1976): epithelial → LJE (repair), gingival CT → root resorption (repair), alveolar bone → ankylosis (repair), PDL → true regeneration
• Classify bone graft materials by mechanism: autogenous (osteogenic), allograft (osteoinductive), xenograft (osteoconductive), alloplast (scaffold); match to defect morphology and clinical goals
• Explain GTR membrane function: physical barrier preventing epithelial migration, allowing PDL/bone cells to repopulate; resorbable (collagen, polylactic acid, calcium sulfate) vs non-resorbable (ePTFE)
• Describe Emdogain (EMD, porcine amelogenin gel): inducing cementum/PDL/bone regeneration; indications (intrabony ≤5 mm, recession), contraindications (uncontrolled diabetes, bisphosphonate, immunosuppression, smoking)
• Classify intrabony defect morphology (3-wall > circumferential > 2-wall > 1-wall) and predict regeneration potential by depth (≥3 mm), width (narrow preferred), soft tissue quality
• Synthesise three intentions of wound healing: first (sutures, regeneration), second (granulation, fibrosis), third (delayed closure, infection risk); apply to periodontal site closure
• Identify patient and defect factors affecting regeneration: local (plaque <15%), behavioural (smoking, compliance), systemic (diabetes control mandatory, bisphosphonate caution); stratify controllable vs not
• Distinguish long junctional epithelium (LJE, satisfactory repair) from true regeneration (new cementum + PDL + alveolar bone); explain why histology (not clinical alone) defines regeneration
• Explain critical surgical elements supporting regeneration: blood supply, clot stabilisation, wound coverage, technique, space maintenance; early clot formation and dry-socket prevention

L6 — Occlusion in Periodontal Therapy

• Define occlusal trauma (primary, secondary, acute, chronic); explain tissue injury mechanisms and clinical presentation per 2017 World Workshop classification
• Identify clinical and radiographic signs of trauma from occlusion: fremitus, mobility (Miller scale), PDL widening, angular bone loss, wear facets, tooth migration
• Explain jiggling forces mechanism: bidirectional loading, PDL space widening, funnel-shaped crest, increased mobility without attachment loss in healthy periodontium
• Assess pathological tooth mobility: distinguish physiological from pathological; use Periotest / periodontometer ranges; recognise progressive mobility as TFO sign
• Differentiate primary occlusal trauma (excess force on healthy periodontium) from secondary (normal/reduced force on compromised periodontium); explain treatment implications
• Explain relationship between occlusal trauma and periodontitis: trauma alone does not initiate disease; aggravates inflammatory response if plaque present; co-destructive in periodontitis
• Describe occlusal adjustment and splinting modalities: enameloplasty, bite raising, extracoronal splinting, joint crowns, occlusal splints (hard vs soft); indications for Miller grade 1/2/3 mobility
• Analyse histological responses to traumatic forces: pressure side (resorption, haemorrhage, necrosis), tension side (fibre elongation, bone formation); pressure/tension zones under unidirectional vs jiggling forces
• Discuss 2017 World Workshop evidence on abfraction and gingival recession: limited evidence for abfraction as clinical entity; conflicting recession causation; no evidence TFO causes attachment loss
• Explain PDL physiology and adaptive capacity: mechanoreceptors, viscoelastic absorption, adaptive changes to force magnitude / direction / duration / frequency; reversibility in healthy vs diseased periodontium