The primary mechanism by which severe mandibular incisor crowding is hypothesized to independently increase the risk of localized periodontal breakdown, beyond confounding factors like poor hygiene, is:
Severe mandibular incisor crowding causes teeth to displace or rotate within the alveolar housing, violating bone constraints and leading to cortical plate resorption. This results in fenestrations (narrow bone defects exposing root surfaces) and dehiscences (wider marginal defects causing gingival recession and reduced bone support), increasing localized periodontal breakdown risk independently of plaque accumulation or hygiene. Studies, including a 2024 review in the British Dental Journal, highlight that crowded, labially displaced incisors often lack adequate labial gingival coverage, while lingual positioning creates excess tissue and undermined support, predisposing to attachment loss. Proclined incisors in crowded arches show up to a 50% chance of 2 mm bone loss per 8° of proclination, per CBCT analyses. This mechanism differs from hygiene-related plaque retention (option C) or secondary effects like mobility (option B), and while horizontal forces (option A) may contribute, displacement-induced defects are the primary hypothesized pathway in orthodontic literature.

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