CO:09:4 | Erosive hand osteoarthritis: the impact of comorbidities in the context of joint disease

Sara Bindoli¹, Clarissa Benvoluti¹, Giacomo Cozzi¹, Marta Favero¹, Mariagrazia Lorenzin¹, Andrea Doria¹, Paolo Sfriso¹, Roberta Ramonda¹. | ¹UOC Reumatologia, Dipartimento di Medicina , Università degli studi di Padova, Italy

Background. This study aimed to determine whether cardiovascular and osteometabolic comorbidities are associated with the radiographic hallmarks of erosive hand osteoarthritis (EHOA), specifically osteophytes, joint space narrowing (JSN), malalignment, central erosions, sclerosis, and subchondral cysts. We also evaluated how these comorbidities relate to clinical and serological measures of disease activity, including pain (VAS), validated disease questionnaires, swollen and tender joint counts, and inflammatory markers.

Materials and Methods.  We enrolled patients exhibiting at least one central erosion in a proximal (PIP) or distal (DIP) interphalangeal joint, excluding any with metacarpophalangeal erosions. Each participant underwent a comprehensive clinical assessment by an expert rheumatologist and completed the VAS for pain, the AUSCAN index, and the DREISER algo-functional scale. We collected demographic, clinical, metabolic, and bone-metabolic data such as BMI, blood pressure, laboratory values, and bone-densitometry results. Radiographs were scored using the Altman system after specific training to ensure inter-reader reliability; we graded osteophytes, JSN, malalignment, central erosions, sclerosis, and cysts. Comorbidities were quantified with the Charlson Comorbidity Index (CCI), metabolic syndrome defined per Adult Treatment Panel (ATP) III criteria, and ten-year fracture risk estimated via the DeFRA score.

Results. Eighty-seven patients (77% female; mean age 63.2 ± 8.9 years) were analysed. Radiographic scores of the different joints analysed are detailed in Table 1 . Cardiovascular risk factors were present in 76.8% of subjects: 48.2% had total cholesterol > 200 mg/dL, 9.1% were obese (BMI > 30 kg/m²), 6.9% had fasting glucose > 126 mg/dL, and 28.7% were hypertensive (>140/90 mmHg). Sixteen patients (18.4%) had osteoporosis, and 28.3% (17/60) of those with DEXA data available had lumbar T-scores <–2.5. Pain (VAS) correlated with swollen (r=0.44, p < 0.01) and tender (r=0.47, p < 0.01) joint counts. AUSCAN and DREISER scores correlated strongly with VAS (r=0.63 and r=0.52, p < 0.01). Disease duration correlated with total radiographic score (r=0.57, p < 0.01). In regression analyses, osteoporosis was associated with increased osteophyte formation (p=0.013), and JSN was associated with diabetes (p=0.043).Osteoporosis was also associated with higher DREISER (p0.018) and AUSCAN (p=0.024) scores; lower lumbar T-scores correlated with worse VAS (p= 0.045), AUSCAN (p=0.0009), and DREISER (p=0.015), and inversely correlated with inflammatory markers.

Conclusions.  Our findings indicate that individual cardiovascular and osteo-metabolic comorbidities contribute to structural joint damage and disease progression in EHOA. The association between osteoporosis and increased osteophyte formation suggests that reduced bone density may induce an osteoprolipherative response. Furthermore, lower T-scores correlate with worse hand-function scores, underscoring the detrimental impact of bone-density loss on daily activities. A multidisciplinary strategy with rigorous risk-factor control may improve long-term outcomes for EHOA patients.