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Background: We aimed to determine if composite structural measures of knee osteoarthritis (KOA) progression on magnetic resonance (MR) imaging can predict the radiographic onset of accelerated knee osteoarthritis., Methods: We used data from a nested case-control study among participants from the Osteoarthritis Initiative without radiographic KOA at baseline. Participants were separated into three groups based on radiographic disease progression over 4 years: 1) accelerated (Kellgren-Lawrence grades [KL] 0/1 to 3/4), 2) typical (increase in KL, excluding accelerated osteoarthritis), or 3) no KOA (no change in KL). We assessed tibiofemoral cartilage damage (four regions: medial/lateral tibia/femur), bone marrow lesion (BML) volume (four regions: medial/lateral tibia/femur), and whole knee effusion-synovitis volume on 3 T MR images with semi-automated programs. We calculated two MR-based composite scores. Cumulative damage was the sum of standardized cartilage damage. Disease activity was the sum of standardized volumes of effusion-synovitis and BMLs. We focused on annual images from 2 years before to 2 years after radiographic onset (or a matched time for those without knee osteoarthritis). To determine between group differences in the composite metrics at all time points, we used generalized linear mixed models with group (3 levels) and time (up to 5 levels). For our prognostic analysis, we used multinomial logistic regression models to determine if one-year worsening in each composite metric change associated with future accelerated knee osteoarthritis (odds ratios [OR] based on units of 1 standard deviation of change)., Results: Prior to disease onset, the accelerated KOA group had greater average disease activity compared to the typical and no KOA groups and this persisted up to 2 years after disease onset. During a pre-radiographic disease period, the odds of developing accelerated KOA were greater in people with worsening disease activity [versus typical KOA OR (95% confidence interval [CI]): 1.58 (1.08 to 2.33); versus no KOA: 2.39 (1.55 to 3.71)] or cumulative damage [versus typical KOA: 1.69 (1.14 to 2.51); versus no KOA: 2.11 (1.41 to 3.16)]., Conclusions: MR-based disease activity and cumulative damage metrics may be prognostic markers to help identify people at risk for accelerated onset and progression of knee osteoarthritis.

Background: To determine if adults with incident accelerated knee osteoarthritis (KOA) are more likely to have degenerative knee ligaments or tendons compared to individuals with typical or no KOA., Methods: We identified 3 sex-matched groups among Osteoarthritis Initiative participants who had a knee without radiographic KOA at baseline (Kellgren-Lawrence [KL] < 2): 1) accelerated KOA: at least 1 knee had KL grade ≥ 3 in ≤48 months, 2) typical KOA: at least 1 knee increased in radiographic scoring within 48 months, 3) no KOA: both knees had the same KL grade at baseline and 48 months. We evaluated knee magnetic resonance images up to 2 years before and after a visit when the accelerated or typical KOA criteria were met (index visit). Radiologists reported degenerative signal changes for cruciate and collateral ligaments, and extensor mechanism and proximal gastrocnemius tendons. We used generalized linear mixed models with 2 independent variables: group and time., Results: Starting at least 2 years before onset, adults with accelerated KOA were twice as likely to have degenerative cruciate ligaments than no KOA (odds ratio = 2.10, 95% CI = 1.18, 3.74). A weaker association (not statistically significant) was detected for adults with accelerated versus typical KOA (OR = 1.72, 95%CI = 0.99, 3.02). Regardless of time, adults with accelerated (odds ratio = 2.13) or typical KOA (odds ratio = 2.16) were twice as likely to have a degenerative extensor mechanism than no KOA. No other structural features were statistically significant., Conclusions: Degenerative cruciate ligaments or extensor mechanism antedate radiographic onset of accelerated KOA. Hence, knee instability may precede accelerated KOA, which might help identify patients at high-risk for accelerated KOA and novel prevention strategies.

We compared the spatial distribution of tibiofemoral cartilage change between individuals who will develop accelerated knee osteoarthritis (KOA) versus typical onset of KOA prior to the development of radiographic KOA. We conducted a longitudinal case-control analysis of 129 individuals from the Osteoarthritis Initiative. We assessed the percent change in tibiofemoral cartilage on magnetic resonance images at 36 informative locations from 2 to 1 year prior to the development of accelerated (n = 44) versus typical KOA (n = 40). We defined cartilage change in the accelerated and typical KOA groups at 36 informative locations based on thresholds of cartilage percent change in a no KOA group (n = 45). We described the spatial patterns of cartilage change in the accelerated KOA and typical KOA groups and performed a logistic regression to determine if diffuse cartilage change (predictor; at least half of the tibiofemoral regions demonstrating change in multiple informative locations) was associated with KOA group (outcome). There was a non-significant trend that individuals with diffuse tibiofemoral cartilage change were 2.2 times more likely to develop accelerated knee OA when compared with individuals who develop typical knee OA (OR [95% CI] = 2.2 [0.90-5.14]. Adults with accelerated or typical KOA demonstrate heterogeneity in spatial distribution of cartilage thinning and thickening. These results provide preliminary evidence of a different spatial pattern of cartilage change between individuals who will develop accelerated versus typical KOA. These data suggest there may be different mechanisms driving the early structural disease progression between accelerated versus typical KOA. Clin. Anat. 32:369-378, 2019. © 2018 Wiley Periodicals, Inc., (© 2018 Wiley Periodicals, Inc.)

Objectives: To determine whether greater effusion-synovitis volume and infrapatellar fat pad (IFP) signal intensity alteration differentiate incident accelerated knee OA (KOA) from a gradual onset of KOA or no KOA., Methods: We classified three sex-matched groups of participants in the Osteoarthritis Initiative who had a knee with no radiographic KOA at baseline (recruited 2004-06; Kellgren-Lawrence <2; n = 125/group): accelerated KOA: ⩾1 knee progressed to Kellgren-Lawrence grade ⩾3 within 48 months; common KOA: ⩾1 knee increased in radiographic scoring within 48 months; and no KOA: both knees had the same Kellgren-Lawrence grade at baseline and 48 months. The observation period included up to 2 years before and after when the group criteria were met. Two musculoskeletal radiologists reported presence of IFP signal intensity alteration and independent readers used a semi-automated method to segment effusion-synovitis volume. We used generalized linear mixed models with group and time as independent variables, as well as testing a group-by-time interaction., Results: Starting at 2 years before disease onset, adults who developed accelerated KOA had greater effusion-synovitis volume than their peers (accelerated KOA: 11.94 ± 0.90 cm3, KOA: 8.29 ± 1.19 cm3, no KOA: 8.14 ± 0.90 cm3) and have greater odds of having IFP signal intensity alteration than those with no KOA (odds ratio = 2.07, 95% CI = 1.14-3.78). Starting at 1 year prior to disease onset, those with accelerated KOA have greater than twice the odds of having IFP signal intensity alteration than those with common KOA., Conclusion: People with IFP signal intensity alteration and/or greater effusion-synovitis volume in the absence of radiographic KOA may be at high risk for accelerated KOA, which may be characterized by local inflammation., (© The Author(s) 2018. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

We aimed to determine if knees with incident accelerated knee osteoarthritis (AKOA) were more likely to receive a knee replacement (KR) than those with common knee osteoarthritis (KOA) or no KOA. We conducted a nested cohort study using data from baseline and the first 9 years of the Osteoarthritis Initiative (OAI). Eligible knees had no radiographic KOA at baseline (Kellgren-Lawrence [KL] < 2). We classified 3 groups using KL grades from the first 8 years of the OAI: 1) AKOA: knee progressed to advance-stage KOA (KL 3/4) in ≤ 4 years, 2) common KOA: knee increased in KL grade (excluding AKOA), and 3) No KOA: no change in KL grade by 8 years. The outcome was a KR (partial or total) at or before the 9-year OAI visit. We conducted a logistic regression with generalized linear mixed model and adjusted for age, body mass index, and sex. Overall, 14% of knees with AKOA received a KR by the 9th year compared with 1% and < 1% of those with common or no KOA, respectively. Knees that developed AKOA were > 80x and ~ 25x more likely to receive a KR than knees with no KOA or incident common KOA (adjusted odds ratio = 25.08; 95% confidence interval = 9.63-65.34). In conclusion, approximately 1 in 7 knees that develop AKOA received a KR; however, KRs were rare in the OAI among other knees with no radiographic KOA at baseline. Urgent steps are needed to identify adults at high-risk for AKOA and develop prevention strategies regarding the modifiable risk factors.

We examined the association between previously reported modifiable risk factors for accelerated knee osteoarthritis (AKOA) at the Osteoarthritis Initiative's (OAI) baseline and 48-month visits among adults who develop AKOA between the 48- and 96-month visits. We conducted a case-control study using data from the OAI baseline to the 96-month visit. Participants had no radiographic knee osteoarthritis (KOA) in the index knee at OAI baseline and 48-month visits [Kellgren-Lawrence (KL) <2]. We classified 2 groups: (1) AKOA: >1 knee developed advance-stage KOA (KL = 3 or 4) between 48- and 96-month visits and (2) No KOA: no KOA and no change in radiographic severity bilaterally over 96 months. We used logistic regression models to evaluate the association between the outcome of AKOA (versus no KOA) and several modifiable risk factors collected at OAI baseline and 48-month visits [body mass index (BMI), systolic blood pressure, comorbidity score, and NSAID use]. We also explored a new injury from baseline to 48 months and from 48- to 96 months. Adults with greater baseline and 48-month BMI were more likely to develop AKOA. Injury was only associated with AKOA onset when it occurred within 4 years of developing AKOA [prior 2 years: odds ratio = 6.21; 95% confidence interval (CI) 3.40, 11.35; 2-4 years prior: odds ratio = 4.42, 95% CI 2.06, 9.50]. BMI may consistently predispose an adult to AKOA, but certain injuries are likely a catalyst for AKOA.

The purpose of this study was to examine if adults who develop accelerated knee osteoarthritis (KOA) have greater knee symptoms with certain activities than those with or without incident common KOA. We conducted a case-control study using data from baseline and the first four annual visits of the Osteoarthritis Initiative. Participants had no radiographic KOA at baseline (Kellgren-Lawrence (KL) <2). We classified 3 groups as follows: (1) accelerated KOA: > = 1 knee developed advance-stage KOA (KL = 3 or 4) within 48 months, (2) common KOA: > = 1 knee increased in radiographic severity (excluding those with accelerated KOA), and (3) no KOA: no change in radiographic severity by 48 months. We focused on individual items from the WOMAC pain/function subscales and KOOS pain/symptoms subscales. The index visit was a year before a person met the definition for accelerated, common, or no KOA. To examine group difference in knee symptoms, we used ordinal logistic regression models for each symptom. Results are reported as odds ratios (OR) and 95% confidence intervals (CI). Individuals who developed accelerated KOA were more likely to report greater difficulty with lying down (OR = 2.10, 95% CI = 1.04 to 4.25), pain with straightening the knee fully (OR = 2.04, 95% CI = 1.08, 3.85), and pain walking (OR = 2.49, 95% CI = 1.38, 4.84) than adults who developed common KOA. Individuals who develop accelerated KOA report greater symptoms with certain activities than those with common KOA. Our results may help identify individuals at risk for accelerated KOA or with early-stage accelerated KOA.

Background: Patellofemoral osteoarthritis (PFOA) is associated with pain and decreased self-reported function. The impact of PFOA on actual physical performance is currently unknown., Objective: To investigate the impact of PFOA on physical performance and pain., Methods: Eight participants aged 40-65 years with bilateral, symptomatic, radiographic PFOA and 7 age- and gender-matched pain-free control participants without radiographic PFOA were studied. Physical performance was measured with the Timed-Up-and-Go (TUG) and 50-foot Fast-Paced-Walk (FPW) tests. Dependent variables included time to complete the TUG and FPW; pretest-posttest change in pain intensity (TUG and FPW); and self-reports of perceived knee pain, stiffness, and physical function. Data were analyzed with nonparametric statistics., Results: The PFOA group TUG time was longer than the control group (p=0.01). No difference between groups was found for FPW time. Pretest-posttest pain increased for the TUG and FPW in PFOA participants (p< 0.05). The PFOA group reported greater knee pain, stiffness, and less physical function than controls (previous 48 hours) (p < 0.01)., Conclusions: Symptomatic, radiographic PFOA is associated with increased pain during the TUG and FPW tests and longer time required to complete the TUG. The TUG may be a more sensitive test of physical performance in PFOA.

Increased joint stress and malalignment are etiologic factors in osteoarthritis. Static tibiofemoral frontal plane malalignment is associated with patellofemoral osteoarthritis (PFOA). Patellofemoral joint stress is increased by activities such as sit-to-stand (STS); this stress may be even greater if dynamic frontal plane tibiofemoral malalignment occurs. If hip muscle or quadriceps weakness is present in persons with PFOA, aberrant tibiofemoral frontal plane movement may occur, with increased patellofemoral stress. No studies have investigated frontal plane tibiofemoral and hip kinematics during STS in persons with PFOA or the relationship of hip muscle and quadriceps strength to these motions. Eight PFOA and seven control subjects performed STS from a stool during three-dimensional motion capture. Hip muscle and quadriceps strength were measured as peak isometric force. The PFOA group demonstrated increased peak tibial abduction angles during STS, and decreased hip abductor, hip extensor, and quadriceps peak force versus controls. A moderate inverse relationship between peak tibial abduction angle and peak hip abductor force was present. No difference between groups was found for peak hip adduction angle or peak hip external rotator force. Dynamic tibiofemoral malalignment and proximal lower extremity weakness may cause increased patellofemoral stress and may contribute to PFOA incidence or progression.

Background: Co-contraction is an impairment commonly reported in children with cerebral palsy. However, co-contraction has not been investigated during passive movements which may be used to assess spasticity in children with cerebral palsy. The purpose of this study was to examine the frequency of co-contraction and the relationship between reflex activity and co-contraction during passive movements of the knee joint in children with cerebral palsy., Methods: Twenty children with cerebral palsy participated in this study. One set of ten continuous passive movements from 90 degrees of knee flexion to 25 degrees of knee flexion and from 25 degrees of knee flexion to 90 degrees of knee flexion was completed at 15 degrees /s, 90 degrees /s, and 180 degrees /s. The mean percentage of the range of motion of each movement and mean percentage of the number of movements which exhibited electromyographic activity of the vastus lateralis, medial hamstrings, and co-contraction were calculated for each set of movements., Findings: The number of the movement repetitions and the percentage of the range of motion which exhibited co-contraction were considerable regardless of the direction and speed of motion. Significant positive correlations were found between the percentage of the passive range of motion with medial hamstrings activation, vastus lateralis activation, and co-contraction during passive movements into both knee flexion and knee extension at a velocity of 15 degrees /s, 90 degrees /s, and 180 degrees /s (P<0.001)., Interpretation: Co-contraction commonly occurs during passive movements of the knee in children with cerebral palsy. The presence of co-contraction may influence measurements of spasticity which use passive movements to assess spasticity.