Clinical and imaging factors associated with chronic plantar heel pain

Background & Aims Chronic plantar heel pain (CPHP) is a common clinical condition defined by pain and tenderness under the heel, aggravated by weightbearing. Despite treatment, many individuals with CPHP report persistent symptoms. This may be partly explained by the limited understanding of the factors that contribute to CPHP risk and prognosis.

The goal of this thesis was to better understand these factors with the specific aims of: (1) in a case-control design, to determine associations of clinical factors and imaging biomarkers with CPHP, and (2) in a longitudinal analysis, to determine which clinical factors predict outcomes of pain, foot-related physical function and quality of life in cases 12 months later.

Methods We recruited 220 participants with a clinical diagnosis of CPHP of at least 3 months duration and compared them to 100 age- and sex-matched controls recruited randomly from the electoral roll. Cases and controls were assessed at baseline, and cases were also assessed after 1 year.

Clinical exposures measured in cases and controls were waist girth, body mass index, body composition by bio-impedance analysis, clinical measures of foot and leg function, physical activity via accelerometry, depression and pain catastrophising by validated questionnaire, and symptoms of morning stiffness, night pain and multisite pain. In cases only we also assessed neuropathic symptoms using the painDETECT questionnaire.

Imaging exposures measured in cases and controls were plantar fascia thickness, echogenicity and Doppler vascular signal by US, plantar fascia thickness and signal, plantar fat pad signal, plantar spurs and calcaneal bone marrow lesions (BML) by MRI, and calcaneal trabecular bone density, bone volume fraction (BV/TV), trabecular thickness, separation and number at a plantar and mid-calcaneal site by High-resolution peripheral Quantitative Computed Tomography (HR-pQCT).

These same exposures except for foot posture and QCT were re-assessed in cases a minimum of 12-months later.

Three analyses were performed:

Case-control analysis using conditional logistic regression to assess associations of clinical and US/ MRI exposures with CPHP status.

Cross-sectional analysis using linear regression to assess associations of CPHP as an exposure with HR-pQCT bone outcomes, and

Mixed effects linear model analysis to assess longitudinal associations of clinical exposures with pain and foot-related physical function (by Foot Health Status Questionnaire) and quality of life outcomes (by Assessment of Quality of Life questionnaire).

Results Clinical factors associated with the odds of having CPHP were waist girth (cm) (odds ratio [OR] 1.06 (95% CI: 1.03 to 1.09)), ankle plantar flexor strength (kg) (OR 0.98; 95% CI: 0.97 to 0.99), pain at multiple sites (pain at 4 or more other sites: OR 10.45 (95% CI 3.66 to 29.81)), and pain catastrophizing status (catastrophizer: OR 6.79 (95% CI 1.91 to 24.11)). Univariable associations with morning stiffness, BMI, first metatarsophalangeal joint extension mobility and depression did not persist after adjusting for potential confounders. There were no significant associations with physical activity.

Imaging biomarkers associated with the odds of having CPHP were plantar calcaneal BML size (mm², OR 1.03 (95% CI 1.02 to 1.05)), larger plantar spurs (>5mm, OR 2.15 (95% CI 1.13 to 4.10)), plantar fascia signal (penetrating > 50% of dorsoplantar width, OR 12.12 (95% CI 5.36 to 27.42)), plantar fascia thickness (mm, (MRI) OR 3.23 (95% CI 2.36 to 4.43), (US) OR 3.78 (95% CI 2.69 to 5.32)) and echogenicity (diffusely hypoechoic OR 7.89 (95% CI 4.02 to 15.48), focally hypoechoic OR 24.92 (95% CI 9.60 to 64.69)). Plantar fascia vascularity was uncommon, occurring exclusively in cases (cases with signal n=47(22%)).

At the plantar calcaneus only, in univariable models being a case was associated with higher trabecular density, BV/TV and trabecular thickness. In multivariable models, having CPHP was not independently associated with any HR-pQCT bone outcomes, but modified associations of BMI and ankle plantarflexor strength with mid-calcaneal and plantar bone outcomes respectively. Beneficial associations of ankle plantarflexor strength with plantar trabecular density, thickness, separation and BV/TV were reduced in cases. In the mid-calcaneus, beneficial associations of BMI with trabecular density, thickness and BV/TV were also lower in cases.

At least 12 months later, 95% of participants returned surveys and 90% returned for clinical re-assessment. In longitudinal analyses, worse pain outcomes at 12 months were predicted by higher painDETECT (within-person (WP) β -1.34 (95% CI -1.86 to -0.82)), between-person (BP) β -1.28 (95% CI -2.02 to -0.54)) and pain catastrophising scores (WP β-0.91 (95% CI -1.57 to -0.26)), and for those who reported night pain at baseline (β -4.45 (95% CI -8.51 to -0.39)). Worse foot function was predicted by higher painDETECT scores (BP β-0.96 (95% CI -1.47 to -0.44)), pain catastrophising (BP B-0.937 (95% CI -1.34 to -0.53)), baseline depression (β -1.28 (95% CI -2.22 to -0.34)) and higher baseline BMI (β - 0.60 (95% CI -1.09 to -0.12)). Greater baseline ankle plantarflexor strength was associated with better function at 12 months (β 0.14 (95% CI 0.02 to 0.25)). Worse quality of life was predicted by higher pain catastrophising (BP β -0.36 (95% CI -0.49 to -0.23)), and higher baseline scores for depression (β -1.21 (95% CI -1.54 to -0.89)), multisite pain (β -1.31 (95% CI -2.01 to -0.61)) and BMI (β - 0.27 (95% CI -0.42 to -0.12)). Greater baseline ankle plantarflexor strength (β 0.08 (95% CI 0.04 to 0.11)) and lower baseline foot pain (β 0.04 (95% CI 0.01 to 0.07)) were associated with improved QOL.

Conclusion Systemic, psychological and pain system processes play an important role in CPHP causation and prognosis. We have established that BMLs are a common finding, adding to our understanding of the role of bone in CPHP. Collectively, these results demonstrate the heterogeneity of CPHP, and suggest that different clinical phenotypes exist. These findings could allow clinicians to better target impairments associated with CPHP outcomes that to date have received little attention in CPHP management, such as bone-specific, psychological and pain science interventions.