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King's Year 3 BDS: Periodontology · Meedu
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Dentistry
King's Year 3 BDS: Periodontology
Revision of Classification & Overview of Steps of Periodontal Therapy
Risk Factors in Periodontal Disease
Stepwise Approach for Periodontal Treatment: Focus on Steps 1 & 2
Gingival Enlargement: Systemic & Drug-Influenced Causes
Role of Host Response & Mechanisms of Periodontal Tissue Destruction
Role of Adjunctive Antimicrobials in Managing Periodontal Diseases
Clinical & Histological Outcomes Following Non-Surgical Therapy
Periodontal Reassessment After Non-Surgical Treatment & Supportive Care
Acute Periodontal Conditions & Necrotising Periodontal Diseases
Diagnosis & Management of Halitosis
Perio 1: History Taking & Clinical Assessment (Periodontal & Peri-Implant)
Perio 2: Practical Aspects of Steps 1 & 2 of Periodontal Therapy
Perio 3: Systemic Risk Factors — Diabetes & Smoking
Perio 4: Systemic Risk Factors — Medications, Pregnancy & Others
Perio 5: Self-Applied Antimicrobials
Perio 6: Professionally-Administered Adjunctive Antimicrobials
Perio 7: Reassessment & Care Planning After Non-Surgical Treatment
Perio 8: Acute Periodontal & Necrotising Conditions
King's Year 3 BDS: Periodontology
Year 3 Periodontology module at King's College London Dental Institute. Lecture block (risk factors, stepwise therapy Steps 1 & 2, gingival enlargement, host response, adjunctive antimicrobials, non-surgical outcomes, periodontal reassessment, necrotising conditions, halitosis) plus clinical perio tutorials (history taking, practical Steps 1–2, diabetes/smoking, medications & pregnancy, self-applied & professional antimicrobials, reassessment and acute conditions).
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A patient with chronic periodontitis is found to have high levels of Porphyromonas gingivalis in subgingival plaque. Despite low absolute numbers of this organism, the polymicrobial community persists and drives progressive alveolar bone loss.
Select the correct answer
A.
P. gingivalis produces potent exotoxins that directly lyse osteoblasts, reducing bone formation capacity independently of immune modulation.
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B.
P. gingivalis outcompetes commensal organisms for iron, creating a nutrient-depleted niche that selectively favours pathogenic species.
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C.
P. gingivalis stimulates excessive neutrophil recruitment via upregulation of IL-8, causing bystander tissue destruction through oxidative burst.
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D.
P. gingivalis subverts complement activation and toll-like receptor signalling to impair bacterial clearance, allowing a dysbiotic community to sustain chronic inflammation and osteoclast-mediated bone resorption.
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E.
P. gingivalis secretes collagenases that directly degrade the periodontal ligament, with subsequent bone loss occurring passively due to loss of mechanical support.
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