Ultrasound-detected osteophytes predict the development of radiographic and clinical features of hand osteoarthritis in the same finger joints 5 years later

Background Structural pathology may be present in joints without radiographic evidence of osteoarthritis (OA). Ultrasound is a sensitive tool for early detection of osteophytes. Our aim was to explore whether ultrasounddetected osteophytes (in radiographically and clinically normal finger joints) predicted the development of radiographic and clinical hand OA 5 years later. Methods We included finger joints without radiographic OA (Kellgren-Lawrence grade (KLG)=0; n=301) or no clinical bony enlargements (n=717) at baseline and examined whether ultrasound-detected osteophytes predicted incident radiographic OA (KLG ≥1, osteophytes or joint space narrowing (JSN)) or incident clinical bony enlargement (dependent variables) in the same joints 5 years later. We applied logistic regression with generalised estimating equations adjusted for age, sex, body mass index and follow-up time. Results Ultrasound demonstrated osteophytes in 86/301 (28.6%) joints without radiographic OA and 392/717 (54.7%) joints without clinical bony enlargement. These osteophytes were confirmed in the majority of joints where MRI assessment was available. Significant associations were found between ultrasound-detected osteophytes and development of both radiographic OA (OR=4.1, 95% CI 2.0 to 8.1) and clinical bony enlargement (OR=3.5, 95% CI 2.4 to 5.1) and also incident radiographic osteophytes (OR=4.2, 95% CI 2.1 to 8.5) and JSN (OR=5.3, 95% CI 2.1 to 13.4). Conclusion Ultrasound-detected osteophytes predicted incident radiographic and clinical hand OA 5 years later. These results support the use of ultrasound for early detection of OA

The Maternal and Paternal Effects on Clinically and Surgically Defined Osteoarthritis

Objective: It is currently unknown whether osteoarthritis (OA) is inherited mainly from the mother, father, or both. This study was undertaken to explore the effect of maternal and paternal factors on hip, knee, and hand OA in offspring. Methods: Participants from the Musculoskeletal Pain in Ullensaker Study (MUST) (69% female; mean ± SD age 64 ± 9 years) and a Norwegian OA twin study (Nor‐Twin) (56% female; 49 ± 11 years) reported whether their mother and/or father had OA. Using a recurrence risk estimation approach, we calculated whether maternal and paternal OA increased the risk of 1) surgically defined hip and knee OA (i.e., total joint replacement) and 2) clinically defined hip, knee, and hand OA (i.e., the American College of Rheumatology criteria) using logistic regression. Relative risks (RRs) with 95% confidence intervals (95% CIs) were calculated. Results: Maternal OA consistently increased the risk of offspring OA across different OA locations and severities. Having a mother with OA increased the risk of any OA in daughters (RR 1.13 [95% CI 1.02–1.25] in the MUST cohort; RR 1.44 [95% CI 1.05–1.97] in the Nor‐Twin cohort) but not (or with less certainty) in sons (RR 1.16 [95% CI 0.95–1.43] in the MUST cohort; RR 1.31 [95% CI 0.71–2.41] in the Nor‐Twin cohort). Having a father with OA was less likely to increase the risk of any OA in daughters (RR 1.00 [95% CI 0.85–1.16] in the MUST cohort; RR 1.52 [95% CI 0.94–2.46] in the Nor‐Twin cohort) and sons (RR 1.08 [95% CI 0.83–1.41] in the MUST cohort; RR 0.93 [95% CI 0.35–2.48] in the Nor‐Twin cohort). Conclusion: OA in the mother increased the risk of surgically and clinically defined hip, knee, and hand OA in offspring, particularly in daughters. Our findings imply that heredity of OA may be linked to maternal genes and/or maternal‐specific factors such as the fetal environment

The Maternal and Paternal Effects on Clinically and Surgically Defined Osteoarthritis

Objective - It is currently unknown whether osteoarthritis (OA) is inherited mainly from the mother, father, or both. This study was undertaken to explore the effect of maternal and paternal factors on hip, knee, and hand OA in offspring. Methods - Participants from the Musculoskeletal Pain in Ullensaker Study (MUST) (69% female; mean ± SD age 64 ± 9 years) and a Norwegian OA twin study (Nor‐Twin) (56% female; 49 ± 11 years) reported whether their mother and/or father had OA. Using a recurrence risk estimation approach, we calculated whether maternal and paternal OA increased the risk of 1) surgically defined hip and knee OA (i.e., total joint replacement) and 2) clinically defined hip, knee, and hand OA (i.e., the American College of Rheumatology criteria) using logistic regression. Relative risks (RRs) with 95% confidence intervals (95% CIs) were calculated. Results - Maternal OA consistently increased the risk of offspring OA across different OA locations and severities. Having a mother with OA increased the risk of any OA in daughters (RR 1.13 [95% CI 1.02–1.25] in the MUST cohort; RR 1.44 [95% CI 1.05–1.97] in the Nor‐Twin cohort) but not (or with less certainty) in sons (RR 1.16 [95% CI 0.95–1.43] in the MUST cohort; RR 1.31 [95% CI 0.71–2.41] in the Nor‐Twin cohort). Having a father with OA was less likely to increase the risk of any OA in daughters (RR 1.00 [95% CI 0.85–1.16] in the MUST cohort; RR 1.52 [95% CI 0.94–2.46] in the Nor‐Twin cohort) and sons (RR 1.08 [95% CI 0.83–1.41] in the MUST cohort; RR 0.93 [95% CI 0.35–2.48] in the Nor‐Twin cohort). Conclusion - OA in the mother increased the risk of surgically and clinically defined hip, knee, and hand OA in offspring, particularly in daughters. Our findings imply that heredity of OA may be linked to maternal genes and/or maternal‐specific factors such as the fetal environment