Accelerated Knee Osteoarthritis Research Articles

Meniscal degeneration is prognostic of destabilzing meniscal tear and accelerated knee osteoarthritis: Data from the Osteoarthritis Initiative.

The objective of this study was to assess the prognostic potential of magnetic resonance (MR)-detected meniscal degeneration in relation to incident destabilizing meniscal tears (radial, complex, root, or macerated) or accelerated knee osteoarthritis (AKOA). We used existing MR data from a case-control study of three groups from the Osteoarthritis Initiative without radiographic KOA at baseline: AKOA, typical KOA, and no KOA. From these groups, we included people without medial and lateral meniscal tear at baseline (n = 226) and 48-month meniscal data (n = 221). Intermediate-weighted fat-suppressed MR images annually from baseline to the 48-month visit were graded using a semiquantitative meniscal tear classification criterion. Incident destabilizing meniscal tear was defined as progressing from an intact meniscus to a destabilizing tear by the 48-month visit. We used two logistic regression models to assess whether: (1) presence of medial meniscal degeneration was associated with an incident medial destabilizing meniscal tear, and (2) presence of meniscal degeneration in either meniscus was associated with incident AKOA over the next 4 years. People with the presence of a medial meniscal degeneration had three times the odds of developing an incident destabilizing medial meniscal tear within 4 years compared with a person without medial meniscus degeneration (odds ratio [OR]: 3.03; 95% confidence interval [CI]: 1.40-6.59). People with meniscal degeneration had five times the odds of developing incident AKOA within 4 years compared with a person without meniscal degeneration in either meniscus (OR: 5.04; 95% CI: 2.57-9.89). Meniscal degeneration on MR is clinically meaningful as it relates to future poor outcomes.

SUpervised exercise-therapy and Patient Education Rehabilitation (SUPER) versus minimal intervention for young adults at risk of knee osteoarthritis after ACL reconstruction: SUPER-Knee randomised controlled trial protocol

IntroductionAnterior cruciate ligament injury and reconstruction (ACLR) is often associated with pain, functional loss, poor quality of life and accelerated knee osteoarthritis development. The effectiveness of interventions to enhance outcomes...

Abnormal subchondral trabecular bone remodeling in knee osteoarthritis under the influence of knee alignment

This study aimed to investigate the abnormal subchondral trabecular bone (STB) remodeling in knee osteoarthritis (OA) under the influence of knee alignment [hip-knee-ankle (HKA) angle]. Forty-one patients with knee OA underwent radiographic examination before total knee arthroplasty (TKA) for the measurement of HKA angle. Tibial plateau specimens obtained during TKA were used for histomorphometric analyses to assess STB remodeling and cartilage degradation. Tartrate-resistant acidic phosphatase (TRAP) staining was used to test osteoclast activity. Osterix, osteocalcin, and sclerostin expression in the STB were determined using immunohistochemistry. The interaction between HKA angle and side (medial vs lateral of tibial plateau) was the main significant influence factor for STB remodeling and microstructure. The STB with the deviation of the knee alignment was accompanied by obvious abnormal bone remodeling and microstructural sclerosis. Bone volume fraction (BV/TV) was the only significant influence factor for OARSI score, the larger the BV/TV of STB, the higher the OARSI score of cartilage. Moreover, the tibial plateau affected by alignment had more TRAP+osteoclasts, Osterix+osteoprogenitors, and osteocalcin+osteoblasts and fewer sclerostin+osteocytes. The variation of tibial plateau STB remodeling activity and microstructure was associated with HKA angle and cartilage degradation. Knee malalignment may cause abnormal STB remodeling and microstructural sclerosis, which may potentially affect load stress transmission from the cartilage to the STB, thus resulting in accelerated knee OA progression.

Role of adipose tissues in osteoarthritis.

Epidemiologic studies reveal that the link between obesity and osteoarthritis cannot be uniquely explained by overweight-associated mechanical overload. For this reason, much attention focuses on the endocrine activity of adipose tissues. In addition to the systemic role of visceral and subcutaneous adipose tissues, many arguments highlight the involvement of local adipose tissues in osteoarthritis. Alteration in MRI signal intensity of the infrapatellar fat pad may predict both accelerated knee osteoarthritis and joint replacement. In this context, recent studies show that mesenchymal stromal cells could play a pivotal role in the pathological remodelling of intra-articular adipose tissues (IAATs) in osteoarthritis. In parallel, recent findings underline bone marrow adipose tissue as a major player in the control of the bone microenvironment, suggesting its possible role in osteoarthritis. The recent description of adipose tissues of various phenotypes within an osteoarthritic joint allows us to evoke their direct involvement in the initiation and progression of the osteoarthritic process. We can expect in the near future the discovery of novel molecules targeting these tissues.

Meniscal Root Tears and Extrusion Are Significantly Associated with the Development of Accelerated Knee Osteoarthritis: Data from the Osteoarthritis Initiative.

To identify joint structural risk factors, measured using quantitative compositional and semiquantitative magnetic resonance imaging (MRI) scoring, associated with the development of accelerated knee osteoarthritis (AKOA) compared with a more normal rate of knee osteoarthritis (OA) development. From the Osteoarthritis Initiative we selected knees with no radiographic OA (Kellgren-Lawrence grade [KL] 0/1) that developed advanced-stage OA (KL 3/4; AKOA) within a 4-year timeframe and a comparison group with a more normal rate of OA development (KL 0/1 to KL 2 in 4 years). MRIs at the beginning of the 4-year timeframe were assessed for cartilage T2 values and structural abnormalities using a modified Whole-Organ Magnetic Resonance Imaging Score (WORMS). Associations of MRI findings with AKOA versus normal OA were assessed using multivariable logistic regression models. A total of 106 AKOA and 168 subjects with normal OA development were included. Mean cartilage T2 values were not significantly associated with AKOA (odds ratio [OR] 1.06; 95% confidence interval [CI] 0.82-1.36). Risk factors for AKOA development included higher meniscus maximum scores (OR 1.37; 95% CI 1.11-1.68), presence of meniscal extrusion (OR 6.30; 95% CI 2.57-15.49), presence of root tears (OR 4.64; 95% CI 1.61-13.34), and higher medial tibia cartilage lesion scores (OR 1.96; 95% CI 1.19-3.24). We identified meniscal damage, especially meniscal extrusion and meniscal root tears as risk factors for AKOA development. These findings contribute to identifying subjects at risk of AKOA at an early stage when preventative measures targeting modifiable risk factors such as meniscal repair surgery could still be effective.

Composite quantitative knee structure metrics predict the development of accelerated knee osteoarthritis: data from the osteoarthritis initiative

BackgroundWe 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.MethodsWe 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).ResultsPrior 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)].ConclusionsMR-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.

Tibial translation assessed with magnetic resonance imaging does not precede the onset of accelerated knee osteoarthritis: data from the osteoarthritis initiative

Purpose: Accelerated knee osteoarthritis (KOA) is characterized by more pain, impaired physical function, and greater likelihood to receive a joint replacement compared to individuals who develop the typical gradual onset of disease. Prognostic tools are needed to provide earlier discrimination between individuals that develop accelerated KOA compared to people that go on to develop typical KOA. Prior to disease onset, people with accelerated KOA are more likely to present with cruciate ligament degeneration compared to those that develop typical KOA.

Intrameniscal signal alterations strongly predict destabilizing meniscal tears and accelerated knee osteoarthritis: data from the osteoarthritis initiative

Purpose: It is unknown whether early changes in the menisci (e.g., intrameniscal signal alterations) have long-term consequences. We conducted a study to assess the prognostic potential of intrameniscal signal alterations in relation to incident destabilizing meniscal tears (radial or complex tears or macerated menisci) or accelerated knee osteoarthritis (KOA).

The incidence and characteristics of accelerated knee osteoarthritis among women: the Chingford cohort

BackgroundPrior research on accelerated knee osteoarthritis (AKOA) was primarily confined to the Osteoarthritis Initiative, which was enriched with people with risk factors for knee osteoarthritis (KOA). It is unclear how often AKOA develops in a community-based cohort and whether we can replicate prior findings from the Osteoarthritis Initiative in another cohort. Hence, we determined the incidence and characteristics of AKOA among women in the Chingford Study, which is a prospective community-based cohort.MethodsThe Chingford Study had 1003 women with quinquennial knee radiographs over 15 years. We divided the 15-year observation period into three consecutive 5-year phases. Within each 5-year phase, we selected 3 groups of participants among women who started a phase without KOA (Kellgren-Lawrence [KL] < 2): 1) incident AKOA developed KL grade ≥ 3, 2) typical KOA increased radiographic scoring (excluding AKOA), and 3) no KOA had the same KL grade over time. Study staff recorded each participant’s age, body mass index (BMI), and blood pressure at baseline, 5-year, and 10-year study visits. We used multinomial logistic regression models to test the association between groups (outcome) and age, BMI, and blood pressure at the start of each phase. The cumulative incidences and odds ratios (OR) from each phase were pooled using a fixed-effect meta-analysis model.ResultsThe person-based cumulative incidence of AKOA was 3.9% over 5 years (pooled estimate across the three 5-year phases). Among incident cases of KOA, AKOA represented ~ 15% of women with incident KOA. Women with AKOA were older than those with typical (OR = 1.56, 95%CI = 1.16–2.11) or no KOA (OR = 1.84, 95%CI = 1.40–2.43). Women with AKOA had a greater BMI than those without KOA (OR = 1.52, 95%CI = 1.17–1.97). We observed no association between group and blood pressure.ConclusionsIn a community-based cohort, > 1 in 7 women with incident KOA had AKOA. Like the Osteoarthritis Initiative, people with AKOA were more likely to have greater age and BMI.

Adults With Incident Accelerated Knee Osteoarthritis Are More Likely to Use Pharmacological Treatment Options and Receive Arthroscopic Knee Surgery: Data From the Osteoarthritis Initiative.

ObjectiveTo determine if people with incident accelerated knee osteoarthritis (AKOA) were more likely to receive a pharmacological treatment or arthroscopic knee surgery than those with typical knee osteoarthritis (KOA) or no KOA.MethodsWe conducted a nested cohort study using data from baseline and the first 8 years of the Osteoarthritis Initiative. Eligible participants had no radiographic KOA at baseline (Kellgren‐Lawrence [KL] < 2). We classified three groups using KL grades: 1) AKOA: knee progressed to advanced‐stage KOA (KL 3/4) in 4 years or less, 2) typical KOA: knee increased in KL grade by 8 years (excluding AKOA), and 3) No KOA: no change in KL grade by 8 years. The outcome was self‐reported arthroscopic knee surgery or a pharmacological treatment option: nonsteroidal anti‐inflammatory drugs (NSAIDs), hyaluronic acid injections, intra‐articular corticosteroid injections, or prescription analgesics. Between‐group differences in therapeutic use were evaluated with Chi‐square tests.ResultsAdults who developed AKOA (n = 92) were more likely to report arthroscopic knee surgery (AKOA: 32%, KOA [n = 380]: 8%, no KOA [n = 875]: 3%; P < 0.001), hyaluronic acid injections (AKOA: 10%, KOA: 4%, no KOA: 1%; P < 0.001), intra‐articular corticosteroid injections (AKOA: 30%, KOA: 7%, no KOA: 4%; P < 0.001), and NSAID use (over the counter: AKOA: 65%, KOA: 48%, and no KOA: 46%; P = 0.003; prescription: AKOA: 61%, KOA: 43%, no KOA: 41%; P = 0.002).ConclusionAdults with AKOA are more likely to receive pharmacological treatment or arthroscopic knee surgery than their peers. Adults with AKOA are an important patient population that is understudied in clinical research despite their use of greater health care resources.

Accelerated knee osteoarthritis is associated with pre-radiographic degeneration of the extensor mechanism and cruciate ligaments: data from the Osteoarthritis Initiative

BackgroundTo 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.MethodsWe 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.ResultsStarting 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.ConclusionsDegenerative 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.

Longitudinal MRI structural findings observed in accelerated knee osteoarthritis: data from the Osteoarthritis Initiative.

To analyze structural, longitudinal MRI findings during the development of accelerated knee osteoarthritis (AKOA) over 4years. From the Osteoarthritis Initiative (OAI), knees with no radiographic osteoarthritis (KL 0/1) developing advanced-stage osteoarthritis (KL 3/4; AKOA) within a 4-year (y) timeframe were selected. MRIs were graded using the modified Whole-Organ Magnetic Resonance Imaging Score (WORMS) at the beginning of the 4-year timeframe (index visit), at 2-year, and 4-year follow-up. Morphological and clinical findings associated with KL 3/4 onset within 2years compared to 4years were assessed using generalized estimating equations. AKOA was found in 162 knees of 149 subjects (age 63.25 ± 8.3; 103 females; BMI 29.4 ± 3.9). Moderate to severe meniscal lesions WORMS ≥3 were present in 25% (41/162) at the index visit, 64% (104/162) at 2-year and 93% (151/162) at 4-year follow-up. Meniscal extrusion was the most prevalent finding (ranging from 18% at the index visit, 45% at 2-year and 94% at 4-year follow-up) and root tears were the most common types of tears (9% at the index visit; 22% at 2years and 38% at 4years). Risk factors associated with KL 3/4 onset within 2years included root tears at the index visit (adjusted OR, 2.82; 95% CI: 1.33, 6.00; p = 0.007) and incident knee injury (42%, 49/116 vs. 24%, 11/46, p = 0.032). Meniscal abnormalities, in particular extrusion and root tears, were the most prevalent morphological features found in subjects with AKOA. These results suggest that meniscal abnormalities have a significant role in accelerated progression of OA.

Early pre-radiographic structural pathology precedes the onset of accelerated knee osteoarthritis

BackgroundAccelerated knee osteoarthritis (AKOA) is characterized by more pain, impaired physical function, and greater likelihood to receive a joint replacement compared to individuals who develop the typical gradual onset of disease. Prognostic tools are needed to determine which structural pathologies precede the development of AKOA compared to individuals without AKOA. Therefore, the purpose of this manuscript was to determine which pre-radiographic structural features precede the development of AKOA.MethodsThe sample comprised participants in the Osteoarthritis Initiative (OAI) who had at least one radiographically normal knee at baseline (Kellgren-Lawrence [KL] grade < 1). Participants were classified into 2 groups based on radiographic progression from baseline to 48 months: AKOA (KL grade change from < 1 to > 3) and No AKOA. The index visit was the study visit when participants met criteria for AKOA or a matched timepoint for those who did not develop AKOA. Magnetic resonance (MR) images were assessed for 12 structural features at the OAI baseline, and 1 and 2 years prior to the index visit. Separate logistic regression models (i.e. OAI baseline, 1 and 2 years prior) were used to determine which pre-radiographic structural features were more likely to antedate the development of AKOA compared to individuals not developing AKOA.ResultsAt the OAI baseline visit, degenerative cruciate ligaments (Odds Ratio [OR] = 2.2, 95% Confidence Interval [CI] = 1.3,3.5), infrapatellar fat pad signal intensity alteration (OR = 2.0, 95%CI = 1.2,3.2), medial/lateral meniscal pathology (OR = 2.1/2.4, 95%CI = 1.3,3.4/1.5,3.8), and greater quantitative knee effusion-synovitis (OR = 2.2, 95%CI = 1.4,3.4) were more likely to antedate the development of AKOA when compared to those that did not develop AKOA. These results were similar at one and two years prior to disease onset. Additionally, medial meniscus extrusion at one year prior to disease onset (OR = 3.5, 95%CI = 2.1,6.0) increased the likelihood of developing AKOA.ConclusionsEarly ligamentous degeneration, effusion/synovitis, and meniscal pathology precede the onset of AKOA and may be prognostic biomarkers.

Accelerated Knee Osteoarthritis Is Characterized by Destabilizing Meniscal Tears and Preradiographic Structural Disease Burden.

To determine whether accelerated knee osteoarthritis (KOA) is preceded by, and characterized over time by, destabilizing meniscal tears or other pathologic changes. We selected 3 sex-matched groups of subjects from the first 48 months of the Osteoarthritis Initiative, comprising adults who had a knee without KOA (Kellgren/Lawrence [K/L] radiographic grade <2) at baseline. Subjects in the accelerated KOA group developed KOA of K/L grade ≥3, those with typical KOA showed increased K/L radiographic scores, and those with no KOA had the same K/L grade over time. An index visit was the visit when the radiographic criteria for accelerated KOA and typical KOA were met (the no KOA group was matched to the accelerated KOA group). The observation period was up to 2 years before and after an index visit. Radiologists reviewed magnetic resonance (MR) images of the index knee and identified destabilizing meniscal tears (root tears, radial tears, complex tears), miscellaneous pathologic features (acute ligamentous or tendinous injuries, attrition, subchondral insufficiency fractures, other incidental findings), and meniscal damage in >2 of 6 regions (3 regions per meniscus: anterior horn, body, posterior horn). In addition, bone marrow lesions (BMLs) and cartilage damage on MR images were quantified. Linear mixed regression models were performed to analyze the results. At 1 year before the index visit, >75% of adults with accelerated KOA had meniscal damage in ≥2 regions (odds ratio 3.19 [95% confidence interval 1.70-5.97] versus adults with typical KOA). By the index visit, meniscal damage in ≥2 regions was ubiquitous in adults with accelerated KOA, including 42% of subjects having evidence of a destabilizing meniscal tear (versus 14% of subjects with typical KOA). These changes corresponded to findings of larger BMLs and greater cartilage loss in the accelerated KOA group. Accelerated KOA is characterized by destabilizing meniscal tears in a knee compromised by meniscal damage in >2 regions, and also characterized by the presence of large BMLs and greater cartilage loss.

Diffuse tibiofemoral cartilage change prior to the development of accelerated knee osteoarthritis: data from the osteoarthritis initiative

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.

One in seven cases of incident knee osteoarthritis is accelerated knee osteoarthritis: data from the Chingford cohort

One in seven cases of incident knee osteoarthritis is accelerated knee osteoarthritis: data from the Chingford cohort

Novel composite knee structure metrics of disease activity and cumulative damage predict the development of accelerated knee osteoarthritis: data from the osteoarthritis initiative

Novel composite knee structure metrics of disease activity and cumulative damage predict the development of accelerated knee osteoarthritis: data from the osteoarthritis initiative

Association Between Declining Walking Speed and Increasing Bone Marrow Lesion and Effusion Volume in Individuals with Accelerated Knee Osteoarthritis.

To determine whether a decline in walking speed during the year prior to disease onset is associated with concurrent changes in cartilage, bone marrow lesions (BMLs), or effusion in adults who develop common knee osteoarthritis (OA), accelerated knee OA, or no knee OA. We identified 3 groups from the Osteoarthritis Initiative based on annual radiographs from baseline to 48 months: accelerated knee OA, common knee OA, and no knee OA. We used the cartilage damage index (CDI) to assess tibiofemoral cartilage damage and used a semiautomated program to measure BML and effusion volume. Walking speed was assessed as an individual's habitual walking speed over 20 meters. One-year change in walking speed and structural measures were calculated as index visit measurements minus measurements from the year prior visit. Logistic regression models were used to determine whether change in walking speed (exposure) was associated with change in each structural measure (outcome) for the overall group and then separately for the accelerated knee OA, common knee OA, and no knee OA groups. Adults who slowed their walking speed were almost twice as likely to present with increased BML volume, with a significant association (odds ratio 3.04 [95% confidence interval (95% CI) 1.03-8.95]) among adults with accelerated knee OA. Adults with accelerated knee OA who slowed their walking speed were approximately 3.4 times (95% CI 1.10-10.49) more likely to present with increased effusion volume. Walking speed change was not significantly associated with CDI change. A change in an easily assessable clinical examination (i.e., 20-meter walk test) was associated with concurrent worsening in BML and effusion volume in adults who developed accelerated knee OA.

Diffuse tibiofemoral cartilage change prior to the development of accelerated knee osteoarthritis: Data from the osteoarthritis initiative.

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.

Age but not BMI Predicts Accelerated Progression of KOA: Data from the Osteoarthritis Initiative

Background/Objectives: Knee osteoarthritis (KOA) accounts for about 35% of the arthritis burden among adults. Most adults with KOA have slowly-progressing, common knee osteoarthritis (CKOA); however, some individuals experience accelerated KOA (AKOA), rapid progression to end-stage disease within 48 months. This study analyzed individuals without radiographic evidence of KOA at baseline to determine which (baseline) characteristics were associated with progression to CKOA and/or AKOA status 48 months later.Methods: Data (n = 1,561) from the Osteoarthritis Initiative (OAI) were utilized. Multinomial logistic regression was employed to determine the magnitude of association between baseline risk factors and 48-month KOA status (AKOA and CKOA, compared to no KOA).Results: Older age (p = 0.032), greater baseline BMI (p &lt; 0.001), female gender (p = 0.009), and greater baseline PASE score (p =0.036) were significantly associated with CKOA (11.9% of participants) and/or AKOA (3.5% of participants) at 48 months. Age, BMI, andPASE were all more strongly associated with greater risk of AKOA compared to risk of CKOA (Age: OR = 1.59 vs. 0.97; BMI: OR = 1.62vs. 1.28; PASE: OR = 1.21 vs. 1.08). Of these, only BMI was significantly associated with greater risk of both AKOA and CKOA.Conclusion: Certain factors impact the risk of AKOA and CKOA differently. Age did not increase the risk of CKOA, but among thosewith CKOA or AKOA, the proportion with AKOA increased with age. Thus, older age at onset is associated with more rapid KOA progression.