13.3 Periodontal Assessment, Non-Surgical Therapy & Periodontal Surgery

13.3 Periodontal Assessment, Non-Surgical Therapy & Periodontal Surgery

Periodontics is the specialty of dentistry dedicated to the prevention, diagnosis, and treatment of diseases affecting the supporting and surrounding tissues of the teeth—the periodontium (comprising the gingiva, periodontal ligament [PDL], cementum, and alveolar bone proper). Periodontal diseases are among the most widespread chronic infectious inflammatory conditions globally and represent the leading cause of tooth loss in adult populations.

In Canadian dental assisting practice, the chairside assistant must be thoroughly versed in periodontal terminology, diagnostic probing interpretation, specialized hand and ultrasonic instrumentation, surgical assisting protocols, and post-operative surgical wound dressing management.

Etiology & Pathogenesis: Gingivitis vs. Periodontitis

1. Microbial Etiology & The Red Complex

Periodontal disease is an infectious condition initiated by polymicrobial subgingival plaque biofilm. While over 700 bacterial species can inhabit the oral cavity, Socransky's microbial complexes classify periodontal microflora according to their pathogenicity. The most destructive periodontal progression is driven by the Red Complex—a consortium of obligate anaerobic, Gram-negative, highly virulent pathogens that dominate late-stage, active periodontal pockets:

• Porphyromonas gingivalis: Produces potent proteolytic enzymes (gingipains) that degrade host collagen, cleave immunoglobulins, disrupt complement cascades, and invade gingival epithelial cells.
• Tannerella forsythia: Produces proteolytic enzymes, induces host apoptotic cell death, and arrests host tissue repair mechanisms.
• Treponema denticola: A highly motile spirochete that travels through viscous pocket environments, degrades host extracellular matrices, and suppresses host neutrophil activity.

2. Host Immuno-Inflammatory Response

Although bacterial biofilm is the primary initiating agent, the bacteria themselves do not cause the majority of tissue destruction. Rather, the host's own immune response to bacterial antigens and endotoxins (lipopolysaccharides, LPS) drives tissue breakdown. Macrophages, polymorphonuclear neutrophils (PMNs), and fibroblasts secrete destructive inflammatory biochemical mediators:

• Pro-inflammatory Cytokines: Interleukin-1 (IL-1), Interleukin-6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α).
• Prostaglandin E2 (PGE₂): Stimulates osteoclasts to resorb alveolar bone.
• Matrix Metalloproteinases (MMPs, especially MMP-8 / Collagenase): Cleave and destroy collagen fibers of the periodontal ligament and gingival connective tissue matrix.

3. Biological Distinction: Gingivitis vs. Periodontitis

                         [ Periodontal Disease Spectrum ]
                                        │
         ┌──────────────────────────────┴──────────────────────────────┐
         ▼                                                             ▼
[ Gingivitis ]                                                [ Periodontitis ]
  • Confined to free & attached gingiva                         • Involves all periodontium structures
  • Erythema, edema, BOP present                               • Apical migration of junctional epithelium
  • NO clinical attachment loss (CAL = 0)                       • Clinical Attachment Loss (CAL ≥ 1 mm)
  • NO alveolar bone resorption                                 • Irreversible alveolar bone destruction
  • 100% REVERSIBLE with hygiene                                • IRREVERSIBLE anatomical loss

• Gingivitis: A plaque-induced, reversible inflammatory lesion strictly confined to the free and attached gingival soft tissues. Clinically presents with erythema (redness), edema (swelling), loss of surface stippling, and bleeding upon gentle probing. Crucially, there is NO apical migration of the junctional epithelium, NO loss of connective tissue attachment (CAL = 0), and NO radiographic alveolar bone resorption. Professional prophylaxis and meticulous home care restore the tissues to complete health.
• Periodontitis: An irreversible, destructive chronic inflammatory condition where the infection extends beyond the gingiva into the deeper periodontal structures. Characterized by the apical migration of the junctional epithelium, destruction of periodontal ligament Sharpey's fibers, resorption of alveolar bone crest, and formation of true periodontal pockets with progressive Clinical Attachment Loss (CAL).

Comprehensive Periodontal Clinical Examination

Accurate diagnosis requires systematic data collection recorded in the patient's periodontal chart.

1. Periodontal Probing & Six Recorded Sites

A calibrated periodontal probe with a blunt, rounded tip is used to measure the depth of the gingival sulcus or pocket. The probe is gently walked circumferentially around the sulcus using light probing force (approximately 20 to 25 grams, or 0.2 to 0.25 N of force, sufficient to blanch a thumbnail without causing pain).

• Six Recorded Measurement Sites per Tooth:
  1. Distobuccal (DB)
  2. Mid-buccal / Facial (B)
  3. Mesiobuccal (MB)
  4. Distolingual (DL)
  5. Mid-lingual (L)
  6. Mesiolingual (ML)
• Sulcular Depth Interpretation:
  • Healthy Sulcus: Probing depth of 1 mm to 3 mm, with firm tissue adaptation and zero bleeding.
  • Periodontal Pocket: Probing depth of 4 mm or greater, indicating pathological deepening of the sulcus.

2. Bleeding on Probing (BOP)

Bleeding on probing occurs when the probe tip contacts the ulcerated, inflamed sulcular epithelial lining of the pocket wall. BOP is the most reliable clinical indicator of active inflammatory periodontal disease. While the presence of BOP indicates active inflammation, the consistent absence of BOP is an exceptional prognostic indicator of periodontal health and stability (exhibiting a 98% negative predictive value).

3. Clinical Attachment Loss (CAL) Calculation

Probing depth alone can be clinically deceptive:

• In gingival hyperplasia (e.g., drug-induced overgrowth), deep probing depths exist despite intact alveolar bone—creating a pseudopocket (false pocket) with zero attachment loss.
• In gingival recession, severe bone loss can be present despite shallow 2 mm to 3 mm probing depths.

Clinical Attachment Loss (CAL) measures the true, irreversible destruction of periodontal support from a fixed anatomical landmark—the Cementoenamel Junction (CEJ)—to the base of the pocket:

CAL = Probing Depth + Gingival Recession

• Case 1 (Recession Present): A tooth has a probing depth of 4 mm, and the gingival margin has receded 3 mm apical to the CEJ.
  CAL = 4 mm + 3 mm = 7 mm of attachment loss
• Case 2 (Margin at CEJ): Probing depth is 5 mm, and the gingival margin rests exactly at the CEJ.
  CAL = 5 mm + 0 mm = 5 mm of attachment loss
• Case 3 (Gingival Overgrowth / Pseudopocket): Probing depth is 6 mm, but the inflamed gingival margin is located 3 mm coronal to the CEJ (covering the enamel).
  CAL = 6 mm - 3 mm = 3 mm of attachment loss

4. Furcation Involvement: Glickman Classification

In multi-rooted teeth (mandibular molars, maxillary molars, and maxillary first premolars), bone loss can expose the anatomical bifurcation or trifurcation where roots separate. Furcations are examined using a curved, blunt-ended Nabers furcation probe.

• Class I (Incipient): The probe tip detects the fluting or concavity of the furcation entrance. Bone loss is minimal; the probe cannot enter the furcation roof horizontally. No radiographic changes.
• Class II (Cul-de-Sac): The probe penetrates horizontally into the furcation roof, but cannot pass completely through to the opposite side.
• Class III (Through-and-Through, Submerged): The probe passes completely through the furcation between the roots (from buccal to lingual in mandibular molars, or between mesiobuccal, distobuccal, and palatal roots in maxillary molars). However, the furcation entrance remains covered and concealed by gingival soft tissue.
• Class IV (Through-and-Through, Clinically Visible): The probe passes completely through between the roots, and the furcation tunnel is clinically visible to the naked eye due to severe gingival recession.

5. Tooth Mobility: Miller Classification

Mobility is evaluated by applying alternating horizontal force using the rigid metal handles of two dental instruments (e.g., mirror handle and blunt explorer handle). Never test mobility using fingers, as the compressibility of finger pads masks true movement.

• Class 0: Normal physiological mobility (0.1 mm to 0.2 mm).
• Class I: Perceptible horizontal crown movement up to 1 mm in a faciolingual direction.
• Class II: Moderate horizontal crown movement exceeding 1 mm in a faciolingual direction, but without vertical movement.
• Class III: Severe horizontal movement exceeding 1 mm combined with vertical depressibility (the tooth can be depressed apically into the alveolar socket).

Summary Comparison of Periodontal Clinical Indices

Non-Surgical Periodontal Therapy (Phase I Therapy)

Phase I periodontal therapy (cause-related therapy) is the initial clinical standard for arresting active periodontal infection and restoring tissue equilibrium.

1. Scaling & Root Planing (SRP) Defined

• Scaling: The mechanical removal of supragingival and subgingival plaque biofilm, cellular debris, and calcified calculus deposits from crown and root surfaces.
• Root Planing: The definitive smoothing of altered, necrotic root cementum impregnated with bacterial toxins (endotoxins/LPS) to produce a glassy, biologically acceptable root surface that facilitates the reattachment of junctional epithelium.

2. Periodontal Hand Instrumentation Armamentarium

                       [ Periodontal Scalers & Curettes ]
                                       │
         ┌─────────────────────────────┴─────────────────────────────┐
         ▼                                                           ▼
[ Sickle Scalers ]                                          [ Curettes (Cylindrical Back) ]
  • Triangular cross-section                                  • Semicircular cross-section
  • Sharp pointed tip & back                                  • Smooth rounded toe & back
  • STRICTLY SUPRAGINGIVAL                                    • Subgingival & supragingival
                                                                     │
                                      ┌──────────────────────────────┴──────────────────────────────┐
                                      ▼                                                             ▼
                           [ Universal Curettes ]                                        [ Gracey Area-Specific ]
                             • 2 parallel cutting edges                                    • 1 offset cutting edge
                             • Face 90° to lower shank                                     • Face 70° to lower shank
                             • All surfaces / entire mouth                                 • Specific tooth surfaces

A. Sickle Scalers (e.g., Jacquette, Towner, H6/H7)

• Geometry: Triangular cross-section, two cutting edges that converge to a sharp pointed tip, flat face angled 90° to the terminal shank, and a sharp pointed back.
• ABSOLUTE CLINICAL RULE: Sickle scalers are strictly restricted to supragingival calculus removal!
• Hazard: Inserting a sickle scaler subgingivally causes severe laceration of the delicate pocket epithelium and gouges the root surface with its sharp tip and sharp back.

B. Universal Curettes (e.g., Columbia 13/14, Barnhart 5/6)

• Geometry: Semicircular cross-section, rounded toe, smooth rounded back, two parallel cutting edges on each blade, and a face angled at 90° to the lower terminal shank.
• Application: Can be adapted on both anterior and posterior teeth throughout the entire mouth, utilizing both cutting edges for supra- and subgingival scaling.

C. Gracey Area-Specific Curettes

• Geometry: Semicircular cross-section, rounded toe, rounded back, and an offset blade angled at 70° to the lower terminal shank. This design creates only one lower working cutting edge (the outer, longer curved edge). When the lower shank is held parallel to the long axis of the root, the cutting edge is automatically aligned at the perfect 70° operating angulation to the root surface.
• Area-Specific Distribution:
  • Gracey 1/2 and 3/4: Anterior teeth (all surfaces).
  • Gracey 5/6: Anterior teeth and premolars.
  • Gracey 7/8 and 9/10: Posterior teeth, facial (buccal) and lingual surfaces.
  • Gracey 11/12: Posterior teeth, mesial surfaces.
  • Gracey 13/14: Posterior teeth, distal surfaces.
  • Gracey 15/16: Posterior mesial modification with extreme shank bend.
  • Gracey 17/18: Posterior distal modification with deep accentuation.

3. Ultrasonic Scaling Instrumentation

• Magnetostrictive Units (e.g., Cavitron): Operates at 20,000 to 45,000 Hz using a stack of ferromagnetic metal strips or ferrite rods. Tip movement is elliptical, meaning all surfaces of the tip (back, face, lateral sides) are active.
• Piezoelectric Units: Operates at 25,000 to 50,000 Hz using ceramic crystals. Tip movement is linear (back-and-forth), meaning only the two lateral edges of the tip are clinically active.
• Mechanisms of Action:
  • Mechanical Action: High-frequency micro-vibrations shatter and fracture tenacious calculus.
  • Cavitation: High-speed water flow forms microscopic vapor bubbles that implode violently, producing localized shock waves that lyse bacterial cell walls.
  • Acoustic Microstreaming: Intense hydrodynamic swirling forces within the fluid disrupt tenacious biofilm and flush debris out of the pocket.
• Safety & Infection Control: Continuous water cooling is mandatory to prevent thermal pulpal necrosis. Aerosols generated during ultrasonic use harbor high concentrations of bacteria; pre-procedural 0.12% chlorhexidine rinses and continuous high-volume evacuation (HVE) are mandatory.

Surgical Periodontal Procedures

When periodontal pockets persist at depths of 5 mm or greater with bleeding on probing following Phase I non-surgical therapy, surgical access is indicated to achieve definitive root debridement and re-establish biological architecture.

1. Excisional Surgery: Gingivectomy & Gingivoplasty

• Gingivectomy: The surgical excision and removal of diseased, fibrous, or hypertrophic gingival tissue. Indicated for eliminating pseudopockets resulting from drug-induced gingival enlargement (caused by calcium channel blockers such as nifedipine or amlodipine; anticonvulsants such as phenytoin; and immunosuppressants such as cyclosporine). Contraindicated when the pocket base extends apical to the mucogingival junction.
• Gingivoplasty: The surgical recontouring and reshaping of healthy gingival margins to recreate physiological scalloped contours and knife-edge papillae.

2. Periodontal Flap Surgery (Open Flap Debridement)

• Elevation of a full-thickness mucoperiosteal flap (e.g., Modified Widman Flap) using a periosteal elevator.
• Provides direct visual access to deep root surfaces, furcation invasions, and complex alveolar bone defects for thorough ultrasonic and hand debridement.

3. Osseous Surgery: Resective vs. Regenerative

• Resective Osseous Surgery: Modifies alveolar bone architecture to eliminate pockets:
  • Ostectomy: The surgical removal of tooth-supporting alveolar bone (bone in direct contact with root attachment) to eradicate deep osseous craters.
  • Osteoplasty: The surgical recontouring and thinning of non-supporting bone (e.g., thick ledges, tori, exostoses) without sacrificing tooth attachment.
• Regenerative Osseous Surgery: Reconstructs lost bone, PDL, and cementum:
  • Bone Graft Materials: Autografts (harvested from the patient's own oral sites, e.g., symphysis or ramus; gold standard for osteogenesis); Allografts (freeze-dried demineralized cortical bone from human cadaver donors); Xenografts (deproteinized inorganic bone matrix from bovine or porcine sources); and Alloplasts (synthetic ceramics such as hydroxyapatite or beta-tricalcium phosphate).
  • Guided Tissue Regeneration (GTR): A biocompatible resorbable (collagen) or non-resorbable (e-PTFE) barrier membrane is surgically positioned over the bone graft, interposed between the mucoperiosteal flap and the root surface. The membrane physically blocks fast-proliferating gingival epithelial cells and connective tissue fibroblasts from growing downward into the healing defect, allowing slow-migrating pluripotential cells from the periodontal ligament and alveolar bone to repopulate the root surface, regenerating true functional cementum, PDL Sharpey's fibers, and alveolar bone.

4. Periodontal Dressings (Periodontal Packs)

A periodontal dressing functions as an intraoral surgical bandage placed over sutured wounds.

• Functions: Mechanically protects the surgical wound from masticatory trauma and food impaction, splints mobile flaps against underlying bone, minimizes post-operative hemorrhage, prevents dead space, and improves patient comfort. The pack possesses no intrinsic healing or curative agents.
• Material Types:
  • Zinc Oxide-Eugenol (ZOE) Packs: Traditional powder/liquid; sets firm, but can cause burning mucosal sensations and allergic contact dermatitis.
  • Non-Eugenol Chemical-Cure Packs (e.g., Coe-Pak): The modern clinical standard. A two-paste system (base containing zinc oxide and vegetable oil; catalyst containing rosin, chlorothymol, and fatty acids). Pliable, non-irritating, and easily adapted.
• Clinical Placement Protocol:
  • The pastes are mixed on a paper pad until uniform in color, allowed to rest for 2 to 3 minutes until non-sticky, and rolled into pencil-thick ropes with lubricated gloves.
  • Ropes are adapted across cervical thirds and gently pressed into interproximal embrasures, interlocking mechanically from facial to lingual.
  • Placement Restrictions: Must never extend onto occlusal tables (masticatory forces will fracture and dislodge the pack) and must never impinge upon the active vestibular mucosa or frenum attachments (movement will cause severe friction ulcerations and dislodge the pack).
• Removal: The dressing is carefully removed in 7 to 10 days post-operatively using a blunt plastic instrument or scaler, followed by gentle irrigation with warm water or 0.12% chlorhexidine.

Complications and Post-Operative Instructions

Competencies 5.10.5 and 5.10.6 cover managing complications and giving instructions after periodontal procedures.

Instructions after scaling, root planing or periodontal surgery:

• Avoid eating until the anesthetic wears off. Then choose soft foods and chew on the other side for the first days.
• Avoid smoking, which delays healing.
• Rinse gently with the prescribed antimicrobial rinse (for example, chlorhexidine) or warm salt water, starting when the dentist directs.
• Brush and floss all other areas normally. Clean around the surgical site gently, as instructed.
• Keep the dressing removal and re-evaluation appointments, and keep regular periodontal maintenance visits.