Iran Dental Specialty Board - Periodontics cheat sheet

Gingival epithelium: junctional epithelium has 15–30 cell layers coronally narrowing to 1–3 apically, with long junctional epithelial attachment (hemidesmosomes + internal basal lamina) providing the epithelial seal.

Biologic width (supracrestal attached tissues): junctional epithelium ~0.97 mm, connective tissue attachment ~1.07 mm, sulcus depth ~0.69 mm (Gargiulo); a minimum ~3 mm supracrestal soft tissue is required before restorative margins encroach.

Gingival fiber groups: dentogingival, dentoperiosteal, alveologingival, circular, transseptal, and intergingival/interpapillary fibers; transseptal fibers regenerate earliest after surgery.

Periodontal ligament principal fibers: alveolar crest, horizontal, oblique (most numerous, resists axial load), apical, and interradicular; PDL width 0.15–0.38 mm, narrowest in function.

Gingival crevicular fluid is a serum transudate/inflammatory exudate; flow rate rises with inflammation, and volume is collected with Periopaper for biomarker assays.

Keratinization pattern: parakeratinized oral gingival epithelium; junctional epithelium is nonkeratinized and has fewer desmosomes, explaining greater permeability.

Alveolar bone proper (cribriform plate/lamina dura) is bundle bone, radiographically the lamina dura; it is resorbed first in periodontitis and reformed after therapy.

Blood supply: gingiva from supraperiosteal vessels, PDL from dental artery branches, and alveolar bone from intraosseous vessels; the crestal anastomosis is critical for flap survival.

Plaque biofilm: supragingival biofilm is dominated by Gram-positive facultative cocci/rods (Actinomyces, Streptococcus); subgingival mature biofilm shifts to Gram-negative anaerobes (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola - the 'red complex').

Keystone-pathogen concept: P. gingivalis is a low-abundance keystone pathogen that dysregulates complement (gingipains cleave C3/C5) and drives community dysbiosis rather than acting by bulk biomass.

Virulence factors: fimbriae and gingipains (Arg/Lys-specific cysteine proteases) for adhesion and tissue destruction; leukotoxin (Aggregatibacter actinomycetemcomitans) for neutrophil lysis; LPS for TLR4-driven inflammation.

Host response: neutrophil recruitment via IL-8 and complement C5a; Th1/Th17 axis with RANKL drives osteoclastogenesis, while OPG neutralizes RANKL; the RANKL/OPG ratio predicts bone loss.

Risk factors with strong evidence: smoking (dose-dependent, masks bleeding), poorly controlled diabetes (HbA1c), and dysbiosis; calculus is a plaque-retentive factor, not itself a primary pathogen.

Disease progression models: the older linear model is superseded by the burst model (episodic exacerbations) and the current staging/grading framework that records severity and rate of progression.

Heritability: chronic periodontitis shows roughly 50% heritable variance in twin studies; gene variants (e.g., IL-1 cluster, FcγR) modify susceptibility but are not diagnostic.

Abscess vs. periodontitis: a periodontal abscess follows marginal closure of a deep pocket with purulent exudate; a periapical abscess is pulpally derived - test vitality to distinguish.

Probing depth is measured from the gingival margin to the base of the sulcus/pocket; clinical attachment level (CAL) = probing depth + gingival margin recession (negative if margin is coronal to the CEJ).

Bleeding on probing (BOP) is recorded as present/absent at 6 sites per tooth; full-mouth BOP <10% is consistent with stability, while BOP ≥30% signals active inflammation risk.

2018 classification: Stage I–IV by severity (CAL, radiographic bone loss, tooth loss) and complexity; Grade A–C by progression (bone loss/age ratio, % bone loss, smoking, HbA1c).

Stage III requires CAL ≥5 mm, radiographic bone loss extending to the middle third of root, and ≤4 teeth lost; Stage IV adds ≥5 teeth lost, masticatory dysfunction, or need for complex rehabilitation.

Grade A (slow): <0.25 bone loss/age, no smoking, normoglycemia; Grade B: 0.25–1.0, <10 cigarettes/day, HbA1c <7.0%; Grade C (rapid): >1.0, ≥10 cigarettes/day, HbA1c ≥7.0%.

Radiographic assessment: bitewing/periapical images with a paralleling technique; bone loss is expressed as a percentage of root length and must not be diagnosed from panoramic images alone.

Mobility (Miller 0–III) reflects attachment loss and inflammation; fremitus is assessed by having the patient tap teeth together to detect occlusal traumatism.

Microbiologic/serologic tests (BANA, PCR, ELISA) are adjuncts only; they do not replace probing, radiographs, and the periodontal risk assessment.

Subgingival instrumentation (SRP) targets biofilm and calculus removal; systematic review evidence shows mean CAL gain of ~0.5–1.0 mm in deep pockets and reduced BOP.

Full-mouth disinfection vs. quadrant-wise SRP: meta-analyses show no clinically important difference in CAL or PD at 6–12 months; both are acceptable protocols.

Adjunctive systemic amoxicillin + metronidazole (500 mg each, 3×/day for 7 days) is reserved for Grade C/Stage III–IV patients; it adds ~0.3–0.5 mm CAL gain and reduces need for surgery.

Local delivery of antimicrobials (minocycline microspheres, chlorhexidine chips) provides small short-term PD reduction (~0.2–0.4 mm) and is not a substitute for mechanical debridement.

Host modulation with sub-antimicrobial-dose doxycycline (20 mg twice daily) inhibits matrix metalloproteinases; it is adjunctive and not a primary therapy.

Reevaluation is performed 6–8 weeks after active therapy; persistent pockets ≥5 mm with BOP indicate the need for further therapy or surgical access.

Smoking cessation and glycemic control (HbA1c target <7%) are the highest-yield adjuncts; smoking reduces the CAL gain from SRP by roughly half.

Root surface debridement endpoints: a smooth, hard root surface is not an evidence-based endpoint; clinical outcomes (PD reduction, BOP resolution, CAL gain) define success.

Flap design: sulcular (crevicular) incision preserves keratinized tissue; inverse bevel is used for pocket elimination; vertical releasing incisions must avoid the lingual nerve and mental foramen.

Open flap debridement (OFD) yields greater PD reduction than SRP in deep pockets but little additional CAL gain; it is indicated for access to deep, non-responsive sites.

Resective surgery (gingivectomy, apically positioned flap with osseous surgery) is indicated for pseudopockets and irregular bony contours; it risks recession and root sensitivity.

Crown lengthening: for biologic width violation, osseous resection must re-establish ~3 mm of supracrestal soft tissue; for esthetic crown lengthening, preserve the gingival zenith and interproximal papillae.

Distal wedge procedure removes a wedge of tissue at the distal of terminal molars to eliminate a pseudopocket and improve cleansability.

Guided tissue regeneration (GTR) uses barrier membranes (e.g., collagen, PTFE) to exclude epithelium; best outcomes in intrabony defects with deep, narrow morphology (≥3 mm) and no furcation involvement.

Postoperative care: chlorhexidine 0.12% rinse for 2 weeks, avoid brushing the surgical site, and consider systemic antibiotics only when indicated; suture removal at 7–14 days.

Contraindications to elective periodontal surgery: uncontrolled diabetes, recent myocardial infarction (<6 months), bleeding disorders, and active infection.

Regeneration requires four elements: cells (PDL fibroblasts, osteoblasts), signaling molecules (growth factors), scaffold (graft/matrix), and blood supply; GTR provides the scaffold and cell exclusion.

Bone graft types: autograft (osteogenic, osteoinductive, osteoconductive), allograft (FDBA/DFDBA), xenograft (deproteinized bovine bone), and alloplast (β-TCP, HA); only autograft is truly osteogenic.

Intrabony defect selection: 3-wall defects and deep narrow defects have the best regenerative prognosis; 1-wall and furcation defects respond poorly.

Enamel matrix derivative (EMD) is an amelogenin-based protein that promotes PDL regeneration; meta-analyses show similar CAL gain to GTR for intrabony defects.

Furcation treatment: Grade I - debridement; Grade II - GTR or tunnel preparation depending on anatomy; Grade III - root resection, tunneling, or extraction.

Root coverage procedures: coronally advanced flap (CAF) with connective tissue graft is the reference standard; Miller Class I/II and Cairo RT1 defects have the best prognosis.

Recession classification: Miller I–IV and Cairo RT1–RT3; RT1 = interdental CAL loss ≤1 mm, RT2 = >1 mm, RT3 = severe interproximal loss.

Root conditioning (citric acid, EDTA) removes the smear layer and exposes collagen; evidence for added benefit is weak, so it is adjunctive, not mandatory.

Osseointegration: direct bone-to-implant contact without intervening fibrous tissue; success requires primary stability, adequate bone volume, and controlled loading.

Peri-implant mucositis: reversible inflammation confined to soft tissue with BOP and no bone loss; peri-implantitis adds progressive bone loss beyond initial remodeling.

Peri-implantitis diagnostic thresholds: BOP and/or suppuration, increasing probing depth, and radiographic bone loss ≥2 mm or beyond expected crestal remodeling after initial healing.

Risk indicators: history of periodontitis, smoking, poor plaque control, uncontrolled diabetes, and lack of maintenance; patients with treated periodontitis need supportive peri-implant care every 3–6 months.

Implant placement timing: Type 1 (immediate), Type 2 (early, 4–8 weeks), Type 3 (late, 12–16 weeks), Type 4 (delayed, >6 months); immediate placement requires intact socket walls and primary stability.

Peri-implantitis treatment: non-surgical debridement alone is insufficient; surgical access with implant surface decontamination (e.g., air-abrasive, citric acid) and possible resection or regeneration.

Biological width around implants: ~3 mm of soft tissue (epithelium + connective tissue) is needed; platform switching and adequate keratinized tissue reduce crestal bone loss.

Implant maintenance: probing with light force (~0.25 N), radiographic monitoring, and evaluation of occlusion; peri-implant probing is safe and does not damage the seal.

Bidirectional link: periodontitis is associated with diabetes (HbA1c), cardiovascular disease, adverse pregnancy outcomes, and rheumatoid arthritis; the strongest evidence is for diabetes.

Diabetes: hyperglycemia impairs neutrophil function and collagen synthesis; periodontal therapy can reduce HbA1c by ~0.3–0.4% in meta-analyses.

Cardiovascular disease: periodontitis is an independent risk marker; the association is modest and confounded, so causality is not established.

Pregnancy: periodontitis is associated with preterm birth and low birth weight, but randomized trials of periodontal therapy have not consistently reduced adverse outcomes.

Medication-related osteonecrosis of the jaw (MRONJ): risk with bisphosphonates and denosumab; conservative management is preferred, and elective surgery should be deferred in high-risk patients.

Drug-induced gingival overgrowth: phenytoin, cyclosporine, and calcium channel blockers (nifedipine); treatment is plaque control and possible drug substitution.

Infective endocarditis prophylaxis: indicated for high-risk cardiac conditions (prosthetic valve, prior endocarditis, certain congenital heart disease) before invasive dental procedures.

Smoking: nicotine causes vasoconstriction and impairs neutrophil chemotaxis; smoking is the strongest modifiable risk factor for periodontitis progression.

Sequence: emergency care → cause-related (hygiene, SRP) → reevaluation → corrective (surgery, orthodontics, implants) → maintenance; each phase is a decision point.

Prognostic classification: use the 2018 framework (Stage/Grade) plus tooth-level factors (mobility, furcation, endodontic status, restorability) to decide retain vs. extract.

Orthodontic-periodontal interface: orthodontic forces in patients with reduced periodontium require plaque control and controlled force; intrusion in inflamed sites can worsen attachment loss.

Restorative margin placement must respect biologic width (~3 mm); violation causes chronic inflammation, recession, and bone loss.

Endodontic-periodontal lesions: true combined lesions have a poor prognosis; primary endodontic lesions often heal after root canal therapy alone.

Implant vs. tooth decision: consider strategic value, adjacent tooth prognosis, bone volume, and patient factors; a questionable tooth may be retained if it can serve as an abutment.

Esthetic planning: smile line, gingival display, and interdental papilla; crown lengthening or orthodontic extrusion may be needed before restoration.

Maintenance is part of the plan: recall interval 3–6 months based on risk; patients with implants and history of periodontitis need closer monitoring.

Study designs: RCTs provide the strongest evidence for interventions; cohort studies for prognosis; case-control for rare outcomes; cross-sectional for prevalence.

Levels of evidence (Oxford CEBM): systematic reviews of RCTs at the top, then RCTs, cohort, case-control, case series, and expert opinion.

Randomization and blinding reduce selection and detection bias; intention-to-treat analysis preserves randomization benefits.

Diagnostic test metrics: sensitivity = TP/(TP+FN); specificity = TN/(TN+FP); PPV and NPV depend on prevalence.

Statistical tests: t-test for continuous normal data, Mann-Whitney for non-normal, chi-square for categorical, ANOVA for >2 groups; p<0.05 is conventional.

Systematic review elements: PICO question, explicit search strategy, risk-of-bias assessment, and heterogeneity (I²) evaluation before meta-analysis.

Ethics: informed consent, confidentiality, and declaration of conflicts of interest; research involving human subjects requires IRB approval.

Clinical practice guidelines integrate evidence, patient values, and resources; they are not rigid rules and should be applied with clinical judgment.

Periodontal screening: use the Periodontal Screening and Recording (PSR) or Basic Periodontal Examination (BPE) with a WHO probe; a score of 3 or 4 triggers full periodontal assessment.

Radiographic bone loss is measured from the CEJ to the alveolar crest; >2 mm or >30% of root length indicates periodontitis.

Furcation involvement (Glickman I–IV or Hamp I–III) is assessed with a Nabers probe; Grade III indicates through-and-through involvement.

Occlusal trauma: assess fremitus, mobility, and wear facets; primary trauma occurs in a healthy periodontium, secondary in a reduced one.

Microbiologic testing is not routine; it may be used in aggressive/refractory cases or before antibiotic therapy.

Risk assessment tools (e.g., periodontal risk assessment) combine BOP, PD, tooth loss, bone loss, systemic factors, and smoking to set recall intervals.

Differential diagnosis: gingivitis vs. periodontitis (attachment loss), chronic vs. aggressive (now unified under staging/grading), and periodontal vs. endodontic abscess.

Documentation: record probing depths, CAL, BOP, mobility, furcation, plaque index, and radiographs at baseline and reevaluation.

Plaque control instruction: modified Bass technique with soft brush and interdental cleaning (floss, interdental brushes); interdental brushes are more effective than floss for proximal plaque.

Chemical plaque control: chlorhexidine 0.12% is the gold standard but causes staining and taste alteration; cetylpyridinium chloride and essential oils are alternatives.

Scaling and root planing: use ultrasonic scalers for gross calculus and hand instruments for fine debridement; both are equally effective when well executed.

Antibiotic stewardship: systemic antibiotics are adjunctive, not routine; they should not replace mechanical therapy and require adequate plaque control.

Smoking cessation: brief advice (5 A's) at each visit; quitting improves periodontal outcomes and should be offered before surgical therapy.

Diabetes management: coordinate with the physician; HbA1c <7% improves healing and reduces complications.

Maintenance: recall interval based on risk; high-risk patients every 3 months, low-risk every 6–12 months, with full reassessment annually.

Outcome measures: PD reduction, CAL gain, BOP reduction, and patient-reported outcomes; these define success more than root smoothness.

Flap surgery indications: deep pockets (≥5 mm) with BOP after non-surgical therapy, access for regeneration, and pocket elimination.

Suturing: interrupted sutures for tension-free closure; sling sutures for papilla adaptation; remove at 7–14 days depending on the site.

Osseous surgery: ostectomy and osteoplasty to eliminate bony defects; it reduces pocket depth but causes crestal bone loss and recession.

Mucogingival surgery: free gingival graft (FGG) for keratinized tissue augmentation; connective tissue graft (CTG) for root coverage and esthetics.

Frenectomy: indicated for a high frenum causing recession or diastema; laser or scalpel techniques are both acceptable.

Hemostasis: local anesthesia with vasoconstrictor, pressure, and sutures; avoid excessive epinephrine in cardiac patients.

Postoperative complications: bleeding, infection, flap necrosis, and hypersensitivity; most are managed conservatively.

Reevaluation after surgery at 4–6 weeks; assess healing, plaque control, and need for further therapy.

GTR membranes: non-resorbable (ePTFE, titanium-reinforced) require a second surgery for removal; resorbable (collagen, polylactic acid) degrade over 4–6 months.

Bone graft healing: osteoconduction (scaffold), osteoinduction (growth factors), and osteogenesis (cells); only autograft provides all three.

Growth factors: platelet-derived growth factor (PDGF) and bone morphogenetic protein (BMP) are used in selected regenerative procedures; evidence is limited for routine use.

Root coverage: CAF + CTG is the reference standard; use a microsurgical approach for better vascularization and esthetics.

Furcation regeneration: GTR in Grade II furcations can improve horizontal defect fill; Grade III furcations have a poor prognosis.

Combined defects: regeneration is less predictable in combined intrabony-furcation defects; consider extraction and implant placement.

Socket preservation: ridge preservation with a graft and membrane reduces dimensional changes after extraction; it does not eliminate the need for later grafting.

Ridge augmentation: horizontal and vertical augmentation with block grafts or GBR; vertical augmentation has higher complication rates.

Implant success criteria: absence of pain, mobility, and radiolucency; bone loss <0.2 mm/year after the first year; function without complications.

Peri-implant mucositis treatment: mechanical debridement, improved plaque control, and professional maintenance; it is reversible.

Peri-implantitis treatment: non-surgical debridement plus adjunctive measures; surgical access with surface decontamination for advanced cases.

Implant surface: moderately rough surfaces (SLA) improve osseointegration; smooth surfaces are associated with more peri-implantitis in some studies.

Implant placement: ensure ≥1.5 mm between implants and ≥1.5–2 mm from adjacent teeth to preserve blood supply and bone.

Loading protocols: immediate loading requires high primary stability; delayed loading is safer in poor bone quality.

Maintenance: assess probing depth, BOP, suppuration, and radiographic bone levels at each recall; peri-implant probing is safe.

Risk factors: history of periodontitis, smoking, and poor plaque control increase peri-implantitis risk; consider these before implant placement.

Diabetes: screen for undiagnosed diabetes in patients with severe periodontitis; coordinate care with the physician.

Cardiovascular: periodontitis is associated with atherosclerosis; patients with cardiovascular disease should receive periodontal therapy as part of overall care.

Pregnancy: periodontal therapy is safe during pregnancy; the second trimester is preferred for elective procedures.

Osteoporosis: bisphosphonate use requires caution; assess MRONJ risk before invasive procedures.

Medication-induced overgrowth: discontinue or substitute the offending drug if possible; plaque control is essential.

Infective endocarditis: prophylaxis for high-risk patients before invasive procedures; follow current AHA guidelines.

HIV: periodontal manifestations include linear gingival erythema and necrotizing ulcerative periodontitis; management includes plaque control and systemic therapy.

Smoking: the strongest modifiable risk factor; cessation should be integrated into periodontal therapy.

Treatment plan phases: emergency, cause-related, corrective, and maintenance; each phase is reevaluated before proceeding.

Prognosis: use tooth-level factors (mobility, furcation, endodontic status, restorability) and the 2018 staging/grading to decide retain vs. extract.

Orthodontic-periodontal interface: control inflammation before orthodontic forces; intrusion in inflamed sites can worsen attachment loss.

Restorative margin placement: respect biologic width (~3 mm); violation causes inflammation and bone loss.

Endodontic-periodontal lesions: true combined lesions have a poor prognosis; primary endodontic lesions often heal after root canal therapy.

Implant vs. tooth: consider strategic value, adjacent tooth prognosis, bone volume, and patient factors.

Esthetic planning: smile line, gingival display, and interdental papilla; crown lengthening or orthodontic extrusion may be needed.

Maintenance: recall interval 3–6 months based on risk; patients with implants and history of periodontitis need closer monitoring.

Study designs: RCTs provide the strongest evidence for interventions; cohort studies for prognosis; case-control for rare outcomes; cross-sectional for prevalence.

Levels of evidence: systematic reviews of RCTs at the top, then RCTs, cohort, case-control, case series, and expert opinion.

Randomization and blinding reduce bias; intention-to-treat analysis preserves randomization benefits.

Diagnostic test metrics: sensitivity = TP/(TP+FN); specificity = TN/(TN+FP); PPV and NPV depend on prevalence.

Statistical tests: t-test for continuous normal data, Mann-Whitney for non-normal, chi-square for categorical, ANOVA for >2 groups.

Systematic review elements: PICO question, explicit search strategy, risk-of-bias assessment, and heterogeneity (I²) evaluation.

Ethics: informed consent, confidentiality, and declaration of conflicts of interest; research involving human subjects requires IRB approval.

Clinical practice guidelines integrate evidence, patient values, and resources; they are not rigid rules.