๐ BMI & Oral Health Risk Results
| Category | BMI Range | Dental Relevance |
|---|
The metabolic-periodontal connection
The relationship between obesity, metabolic syndrome, and periodontal disease is bidirectional and well-documented. Adipose tissue is not metabolically inert - it produces pro-inflammatory cytokines (IL-6, TNF-alpha, leptin) that amplify the systemic inflammatory response to periodontal pathogens. Put simply: an obese patient's body is primed for a more severe periodontal response to the same bacterial challenge that a lean patient handles with less tissue destruction.
Type 2 diabetes makes this worse. Poorly controlled hyperglycaemia impairs neutrophil function, reduces collagen synthesis, and creates advanced glycation end-products that further compromise the periodontal ligament. Patients with BMI >30 and HbA1c >7% are at substantially higher periodontal risk than either factor alone suggests.
For a full periodontal risk assessment, run this alongside the Periodontal Risk Assessment (Lang & Tonetti PRA). For caries risk - which is also elevated in patients with a high-sugar diet contributing to obesity - use the Caries Risk Assessment Tool.
Sleep apnoea and dentistry
Obstructive sleep apnoea (OSA) affects approximately 30% of obese adults. Dentists are often the first clinicians to identify risk: the combination of BMI >35, large neck circumference, retrognathia, and a narrow upper airway is visible in the dental chair. Mandibular advancement devices (MADs) are a first-line treatment for mild-moderate OSA - making OSA screening directly relevant to dental practice.
When this calculator flags elevated sleep apnoea risk, refer to the STOP-BANG questionnaire score as a follow-up and consider referring to the patient's GP for polysomnography if indicated.