Chronic plantar heel pain modifies associations of ankle plantarflexor strength and body mass index with calcaneal bone density and microarchitecture.

Chronic plantar heel pain (CPHP) is associated with calcaneal bone spurs, but its associations with other calcaneal bone features are unknown. This study therefore aimed to determine associations between having CPHP and bone density and microarchitecture of the calcaneus. We assessed 220 participants with CPHP and 100 age- and sex-matched population-based controls. Trabecular bone density, thickness, separation and number, BV/TV, and cortical density, thickness and area were measured using a Scanco Xtreme1 HR-pQCT scanner at a plantar and mid-calcaneal site. Clinical, physical activity and disease history data were also collected. Associations with bone outcomes were assessed using multivariable linear regression adjusting for age, sex, physical activity, BMI and ankle plantarflexor strength. We assessed for potential effect modification of CPHP on these covariates using interaction terms. There were univariable associations at the plantar calcaneus where higher trabecular bone density, BV/TV and thickness and lower trabecular separation were associated with CPHP. In multivariable models, having CPHP was not independently associated with any bone outcome, but modified associations of BMI and ankle plantarflexor strength with mid-calcaneal and plantar bone outcomes respectively. Beneficial associations of BMI with mid-calcaneal trabecular density (BMI-case interaction standardised X/unstandardised Y beta -10.8(mgHA/cm3) (se 4.6), thickness -0.002(mm) (se 0.001) and BV/TV -0.009(%) (se 0.004) were reduced in people with CPHP. Beneficial associations of ankle plantarflexor strength with plantar trabecular density (ankle plantarflexor strength -case interaction -11.9(mgHA/cm3) (se 4.4)), thickness -0.003(mm) (se 0.001), separation -0.003(mm) (se 0.001) and BV/TV -0.010(%) (se 0.004) were also reduced. CPHP may have consequences for calcaneal bone density and microarchitecture by modifying associations of BMI and ankle plantarflexor strength with calcaneal bone outcomes. The reasons for these case-control differences are uncertain but could include a bone response to entheseal stress, altered loading habits and/or pain mechanisms. Confirmation with longitudinal study is required.