Abstract
Purpose of review
The purpose of this review is to highlight recent studies of osteoarthritis epidemiology, including research on prevalence, disease impact, and potential risk factors.
Recent findings
Osteoarthritis (OA) is highly prevalent in the US and around the globe. It is a leading cause of disability and can negatively impact people’s physical and mental well-being. Healthcare resources and costs associated with managing the disease can be substantial. There is increasing evidence that there are different OA phenotypes that reflect different mechanisms of the disease. Various person-level risk factors are recognized, including sociodemographic characteristics (e.g., female gender, African-American race), genetic predispositions, obesity, diet-related factors, and high bone density/mass. Joint-level risk factors include specific bone/joint shapes, thigh flexor muscle weakness, joint malalignment, participation in certain occupational/sports activities, and joint injury. Recent studies have enhanced our understanding of pre-radiographic lesions associated with OA.
Summary
Application of these new findings may allow us to develop innovative strategies and novel therapies with the purpose of preventing new disease onset and minimizing disease progression.
Keywords: epidemiology, osteoarthritis, impact, phenotypes, risk factors
INTRODUCTION
A number of reviews on the epidemiology of osteoarthritis (OA) have been conducted in the past decade [1–5]. This review highlights new research findings since the middle of 2016. Similar to the other reviews [1–3,5], we will begin by presenting recent data on disease prevalence. We will then discuss recent findings on the impact of OA and the disease’s distinct phenotypes. Finally, we will describe new information concerning systemic- and local-level risk factors associated with OA development and/or progression.
PREVALENCE
The estimated prevalence and incidence of OA vary depending on the definition of OA, the specific joint(s) being evaluated, and the population being studied [1–3]. Using data from the National Health Interview Survey, it was recently estimated that 14 million people in the US have symptomatic knee OA (KOA), including >3 million racial/ethnic minorities [6]. Notably, more than half those with KOA are <65 years of age. Recent cohort and community-based studies have also measured the prevalence of OA of different joints in various communities in South America [7,8], Asia [9–11], and the Middle East [12].
IMPACT OF OSTEOARTHRITIS
OA is a well-known cause of disability around the globe [13]. In a large cohort study of Mexican Americans, the number of activities of daily living impairments was 1.12-1.35 times greater among those with OA, compared to those without it [14]. In a nationwide survey conducted in Korea, the estimated years lived with disability was exceptionally high among elderly males (836 per 10,0000) and females (3039 per 10,0000) with OA [15]. In a population-based study in Sweden, the greater risk for sick leave or disability among those working in female- or male-dominated job sectors was attributed to KOA [16].
Besides affecting people’s physical health, OA may also negatively impact people’s mental health. Data from the Osteoarthritis Initiative (OAI) study demonstrated that those with lower limb OA had greater odds of developing depressive symptoms than those without the disease [17]. OA was also associated with greater odds of suicidal ideation [18]. Another study found a strong relationship between OA and perceived memory loss that was partially mediated by sleep and mood impairments [19].
There is also increasing evidence that OA is a risk factor for cardiovascular disease development. A meta-analysis found that the risk of myocardial infarction was significantly increased in OA and other types of arthritis [20]. Other studies similarly linked coronary heart disease with OA [21,22]. In parallel, the Chingford Cohort study found an increased risk of cardiovascular disease-specific and all-cause mortality among women with symptomatic KOA compared to women without signs/symptoms of OA [23]. Interestingly, there was no relationship found between hand OA and mortality risk. A Swedish study reported no increased mortality in patients with knee and hip OA compared to the general population [24].
In addition, OA consumes a substantial amount of healthcare resources and costs. Studies have demonstrated that OA was associated with higher risk of hospitalization and emergency department charges among those who present in the emergency room for other reasons [25,26]. The average direct cost of OA in Canada increased from $577 to $811 per patient/year between 2003-2010, primarily due to joint replacement surgery costs [27]. In the US, the estimated total annual average direct per-patient cost varied from $1,442 to $21,335 (adjusted to 2015 US$ equivalent) [28]. Observed variations in cost were partly attributed to differences in healthcare resource categories measured between claims data and survey data-based studies.
PHENOTYPES
A phenotype can be defined as a combination of disease attributes that describes differences between patients as they relate to distinct outcomes of interest [29]. KOA is a heterogeneous disease with a very complex pathology. There is growing consensus that these differences are due to the existence of different phenotypes that may represent different mechanisms of the disease [4,30,31]. With different phenotypes, clinicians may tailor their disease management [30]. A recent systematic review identified six variables which represent six clinical phenotypes [31]: 1) chronic pain (with prominent central mechanism), 2) inflammation, 3) metabolic syndrome, 4) bone and cartilage metabolism, 5) mechanical overload, and 6) minimal joint disease. The six phenotypes may represent different disease etiologies with the exception of the minimal joint disease phenotype that classifies subjects based on disease progression.
Another systematic review reported on which characteristics are most relevant in distinguishing KOA phenotypes [32]. Clinical phenotypes are the KOA phenotypes most frequently investigated, followed by laboratory and imaging phenotypes (Table 1). Authors of the review concluded that pain sensitization, psychological distress, radiographic severity, body mass index (BMI), muscle strength, inflammation, and comorbidities (especially metabolic syndrome) were most associated with clinically distinct phenotypes. They also reported that gender, metabolic abnormalities, pattern of cartilage damage, and inflammation were most relevant in distinguishing structural phenotypes.
Table 1.
Category | Distinguishing Characteristics |
---|---|
Clinical | Pain sensitization profile |
Psychological profile | |
Comorbid symptoms profile | |
Clinical characteristics | |
Knee joint alignment | |
Metabolic | |
Gait parameters | |
Mechanistic factors | |
Imaging | Knee chondrocalcinosis |
MRI-detected denuded bone areas | |
Imaging features and clinical symptoms | |
Knee joint compartment (patellofemoral, tibiofemoral) | |
Laboratory | Biochemical marker patterns |
Inflammatory profile | |
Cytokine/chemokine profile (synovial fluid) | |
Serum biochemical markers of bone metabolism | |
Serum biochemical markers of cartilage metabolism | |
Profile of gene expression in peripheral blood leukocytes |
RISK FACTORS: SYSTEMIC
The World Health Organization defines risk factor as any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease [33]. Current evidence on person-level risk factors associated with OA disease development and/or progression follows below.
Sociodemographic
Older age is a well-known risk factor for OA [1–3]. Compared to men, women are more likely to develop hand, foot, and KOA but are less likely to develop cervical spine OA [1]. A new study of incident diagnoses of OA among US service members comparably found that the rates of shoulder and cervical spine OA were higher among men than women [34]. Another found that lower levels of endogenous sex hormones were associated with increased knee effusion-synovitis only in women and not in men with symptomatic OA [35].
Compared to other races, African-Americans are also more likely to develop symptomatic knee and hip OA [2,5]. There are known racial/ethnic differences in radiographic OA features [5]. In a longitudinal study, it was recently discovered that African-American males had higher risk of medial knee joint space width (JSW) loss over time than African-American females and whites [36]. Controlling for other known risk factors for KOA attenuated these differences, however.
Genetic
Approximately 30%-65% of the risk of OA is genetically determined [1,3]. A recent review by Warner et al [37] highlighted the main findings from genetic association studies on OA to date. They reported that genome-wide associated scan (GWAS) studies have so far identified 21 independent susceptibility loci for OA. Since this review’s publication, the single nucleotide polymorphism (SNP) rs4238326 in the ALDH1A2 gene was linked with KOA risk in a Chinese sample study [38]. This is relevant, as genetic variants within the ALDH1A2 gene was only previously linked with hand OA in European populations [37]. Data from the Chingford study also found that the SNP rs11688000 in the neurokinin 1 receptor gene (TACR1) was associated with decreased risk of symptomatic OA [39].
An issue with conducting genetic association studies for OA is the heterogeneity of phenotypes used. Using endophenotypes, which can be more reliably quantified (e.g., minimum JSW), can help reduce this problem [37,40]. Four distinct loci were recently associated with minimum JSW in a hip OA study [41].
Obesity and Metabolic Syndrome
Obesity has long been identified as a risk factor for KOA [1–4]. An updated meta-analysis also showed that increased BMI moderately contributed to increased susceptibility to radiographic and/or clinical hand OA [42]. Although the association between obesity and hip OA had been weak based on previous studies [1,2], a cross-sectional study from Japan [43] and a prospective cohort study from Spain [44] recently found an independent association between weight gain and hip OA diagnosis. Conversely, weight loss has been consistently associated with improved arthritis symptoms in a dose-response manner and slower knee cartilage degeneration in two different study populations [45,46].
Very few previous studies have investigated the relationship between hyperlipidemia and OA [2]. A recent case-control study from the UK demonstrated that hyperlipidemia was in independent risk factor for new onset hand OA [47]. In the Chingford study, higher levels of high-density lipoprotein cholesterol were protective against the incidence of radiographic hand OA [48]. In parallel, use of antilipemic agents (primarily ezetimibe, and excluding statins and fibric acid) was associated with fewer structural and better knee pain changes among OAI participants [49]. Statin use was not associated with reduced risk of consultation or surgery for hip or KOA in a pooled analysis of four cohort studies done in Sweden, however [50].
Examination of the OAI data found an association between higher systolic blood pressure and increased incidence of radiographic KOA [51]. A recent report does not support an association between diabetes mellitus and hand/knee OA [52–54]. There was also no significant association found between metabolic syndrome and radiographic hand OA using Framingham data [55].
Vitamins/Diet
As vitamin D plays a major role in cartilage and bone metabolism, it has been hypothesized that low levels of it may increase OA risk. Previous studies have been conflicting [1–3]. In the VIDEO study [56–58], patients with vitamin D insufficiency and KOA were randomized to receive either vitamin D3 or placebo. Vitamin D3 supplementation neither slowed progression of joint space narrowing nor did it reduce Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) subscale scores [56]. After two years, though, effusion synovitis (measured by MRI) remained stable in the vitamin D group but increased in the placebo group [57]. Those with consistently sufficient 25-hydroxyvitamin D levels also had less loss of tibial cartilage volume, less increase in effusion synovitis, and less decrease in physical functioning compared to those with consistently insufficient levels [58].
Research on the role of specific diets in OA has also been active. Using OAI data, high dietary fiber intake was linked to lower risk of developing moderate-severe knee pain over time [59]. Findings from two prospective cohort studies also showed that higher total fiber intake was related to lower risk of symptomatic KOA, but its relation to radiographic KOA was unclear [60]. Another study found that higher soy milk intake was negatively associated with prevalence of radiographic knee osteophytes [61]. Finally, higher adherence to a Mediterranean diet was associated with lower prevalence of clinical and radiographic KOA [62].
Bone Density and Mass
Previous reviews reported that high bone mineral density (BMD) was a risk factor for incidence [3] and prevalence [2] of lower extremity OA. Supplementing these findings, high resolution peripheral quantitative computed tomography tests showed that men with hip joint osteophytes had higher radial trabecular volumetric BMD, while men with hip sclerosis had higher cortical volumetric BMD at the tibia [63]. New evidence suggests that high systemic BMD predates early structural KOA features; higher spine and total hip BMD were recently linked to progression of tibiofemoral cartilage defects as measured by MRI in adults without clinical symptoms [64]. High bone mass was also recently associated with radiographic hand OA findings [65] but not with OA in the TMJ [66].
RISK FACTORS: JOINT-LEVEL
Current evidence on joint-level risk factors associated with OA disease development and/or progression follows below.
Bone/Joint Shape
Bone shape may contribute to the risk of OA as had been previously described primarily in the hip joint [2,3]. Contributing to the body of evidence, a recent population-based OA cohort study in France used 5 measures to describe hip morphology [67]. Among all measures, acetabular index was most strongly associated with the severity and progression of hip OA. In addition, the Rotterdam Study found that those with cam deformity or acetabular dysplasia had double the risk of developing hip OA compared to those without deformity [68].
Recent studies are also exploring the contribution of bone/joint shape in OA development in other joints. In the OAI, changes in bone area and shape of the knee over 24 months among those with mild-to-moderate OA were associated with radiographic and pain progression over 48 months [69]. In the Tasmanian Older Adult Cohort study, uncommon proximal tibiofibular joint shapes were positively linked to cartilage defects, bone marrow lesions, and osteophytes in the lateral knee compartment [70]. In the Johnston County OA Project, certain ankle morphologies were linked to injury history that could lead to greater predisposition for ankle OA [71].
Muscle Strength
The association between muscle strength and OA may vary depending on the muscles and joints being studied [1–3]. In an examination of anterior cruciate ligament (ACL) injured knees, high thigh muscle cross-sectional area (CSA) and high muscle/fat ratio had a protective effect against KOA prevalence [72]. On the other hand, among OAI subjects without radiographic KOA and with minimal extension strength variability, higher total extensor CSA and vastus medialis CSA were found to increase patellofemoral cartilage loss over time [73]. There was also a strong positive association between extensor-flexor CSA ratio and patellofemoral cartilage deterioration. Similarly, higher knee extensor strength in adolescent men was associated with greater risk of KOA by middle age in a longitudinal study of Swedish registries [74]. However, in a cross-sectional study of hip muscle strength and joints of subjects with hip OA, greater isometric strength of hip and thigh muscle groups was associated with better self-reported physical function [75].
Joint Loads and Alignment
Knee malalignment is a strong predictor of KOA disease progression [1–3]. The association between malalignment and the incidence of KOA is less clear, however [1,2]. More recent studies confirm these assertions [76,77]. In an OAI study, varus thrust (i.e., first appearance/worsening of varus alignment during stance) was associated with KOA progression, but not KOA incidence [77]. In the Multicenter Osteoarthritis Study (MOST), varus thrust increased the odds of worsening medial bone marrow lesions (BMLs) and medial cartilage loss as well as the odds of incident medial BMLs of the knee among those with KOA and those with increased risk of KOA, respectively [78].
Occupation & Sports
Particular repetitive activities inherent in certain occupations (e.g., firefighting, construction work) have long been and continue to be associated with greater risk of OA [1,3,79]. Reports of the associations between sports activities and OA have been conflicting [1,3,80–83] (Table 2). It is also unclear if positive associations are due to sports participation itself or to consequences of injury that occurred with sports participation.
Table 2.
Study | Activity | Effects |
---|---|---|
Alentorn-Geli et al [81] |
|
Decreased risk of knee and hip OA |
Driban et al [82] |
|
Increased knee OA prevalence |
Vigdorchik et al [83] |
|
Increased radiographically-confirmed hip OA |
|
No increased risk of radiographically-confirmed hip OA |
Injury/Surgery
ACL injury, meniscal tear (MT), and direct articular cartilage damage following injury have all been linked to subsequent KOA development [1–3,5]. In a retrospective cohort study, those with ACL tears and lateral MTs had higher risk of developing arthritis and undergoing TKR surgery than those without ACL tears over 10 years [84]. Using a computer simulation model of KOA natural history and management, it was estimated that those with ACL injury and MT were 2.5 times more likely to develop OA and 4 times more likely to undergo TKR surgery than those without injury [85].
Surgical reconstruction may not necessarily protect those who had sustained these injuries from developing KOA [2]. In the computer simulation model, the estimated cumulative lifetime risk of developing KOA minimally differed between those with ACL tears who were surgically treated vs. those who were not [85]. In another study, having a history of partial meniscectomy was associated with greater risk of incident KOA within a year [86].
Pre-Radiographic Lesions
While previous evidence was sparse [2], new studies have begun focusing on the predictive value of pre-radiographic lesions that may be detected only by MRI.
Synovitis
Effusion and Hoffa synovitis (hyperintensity in the infrapatellar fat pad [IPFP]) were previously associated with the development of incident radiographic KOA [87]. Recently, the Tasmanian cohort study found that baseline IPFP signal score predicted increases in KOA symptoms, tibiofemoral cartilage defects and BMLs, and loss of lateral tibial cartilage volume [88,89]. In the MOST study, Hoffa synovitis was associated with structural damage in the patellofemoral and tibiofemoral joints [90]. Moreover, superolateral Hoffa’s fat pad hyperintensity was found to be a local marker of patellofemoral joint structural damage. Change in total synovitis score (from 11 sites) was not found to be related to change in knee pain in a small study of KOA patients, however [91].
In studies of patients with hand OA, synovitis was associated with joint tenderness and self-reported hand pain [92,93]. In the Hand Osteoarthritis in Secondary Care (OSTAS) cohort, synovitis was also associated with hand OA radiographic progression [94]. MRI synovitis did not correlate with clinical findings and biological markers of inflammation in a third hand OA study, though [95].
Bone Marrow, Cartilage, and Meniscal Abnormalities
Several new OAI studies have elucidated the relationship of MRI detected abnormalities with KOA risk. In one study, BMLs, cartilage damage, and menisci extrusion were assessed at baseline and 3 years after [96]. Worsening of these MRI lesions was associated with incident radiographic KOA. In a similar study with 7 years of follow-up data, these MRI lesions improved prediction of mild and moderate radiographic KOA development when added to prediction models that only included sociodemographic and patient-reported clinical variables [97]. In a case-control study, worsening of these lesions was more often detected among those who had radiographic and pain progression due to KOA compared to the control group [98]. Finally, BMLs and meniscal extrusion were recently associated with eventual TKR surgery receipt [99].
Other studies have evaluated the association of these pre-radiographic lesions with the risk of other OA types. In the OSTAS study, BMLs did not associate with hand pain in the absence of synovitis [93]. In a different cohort of erosive hand OA patients, BMLs at the proximal and distal joints correlated with examined joint tenderness [92]. BMLs were also linked to radiographic hand OA progression after 2 years in another study [94]. The Tasmanian cohort study also found that hip cartilage defects were associated with greater pain and radiographic hip OA diagnosis [100].
CONCLUSIONS
OA continues to be a leading cause of morbidity and healthcare cost in the US and around the globe. There may be different OA clinical phenotypes that reflect heterogeneous disease mechanisms. A variety of person-level and joint-level risk factors have been linked to disease development and progression. While many of these risk factors are difficult to change, some may be more amenable to medical and behavioral interventions (e.g., obesity, muscle strength). Recent MRI studies have improved our understanding of MRI-detected damage which precedes radiographic evidence of OA.
KEY POINTS.
Osteoarthritis (OA) continues to impact the lives of a substantial proportion of adults globally.
More recent evidence suggests that there are several OA clinical phenotypes that represent different disease mechanisms.
Person-level risk factors associated with OA include genetic and environmental influences.
Joint-level risk factors associated with OA include structural abnormalities in bone shape, muscle mass and joint alignment.
New magnetic resonance imaging studies have begun to allow prediction of radiographic/symptomatic OA development and progression.
Acknowledgments
None
Funding
Drs. Vina and Kwoh receive funding from the NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), award numbers: K23AR067226 (Vina) and R01AR066601 (Kwoh).
Footnotes
Conflicts of Interest
Neither of the authors declares any potential conflicts of interest in regard to this manuscript. Potential conflicts outside of this work: CKK has received grants from Abbvie and EMD Serono and consulted for Astellas, EMD Serono, Thusane, Express Scripts and Novartis. EV has consulted for Astra Zeneca.
References
- 1.Johnson VL, Hunter DJ. The epidemiology of osteoarthritis. Best Pract Res Clin Rheumatol. 2014;28:5–15. doi: 10.1016/j.berh.2014.01.004. [DOI] [PubMed] [Google Scholar]
- 2.Allen KD, Golightly YM. State of the evidence. Curr Opin Rheumatol. 2015;27:276–283. doi: 10.1097/BOR.0000000000000161. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Neogi T, Zhang Y. Epidemiology of osteoarthritis. Rheum Dis Clin North Am. 2013;39:1–19. doi: 10.1016/j.rdc.2012.10.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Lane NE, Shidara K, Wise BL. Osteoarthritis year in review 2016: clinical. Osteoarthritis Cartilage. 2017;25:209–215. doi: 10.1016/j.joca.2016.09.025. [DOI] [PubMed] [Google Scholar]
- 5.Zhang Y, Jordan JM. Epidemiology of osteoarthritis. Clin Geriatr Med. 2010;26:355–369. doi: 10.1016/j.cger.2010.03.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Deshpande BR, Katz JN, Solomon DH, et al. Number of Persons With Symptomatic Knee Osteoarthritis in the US: Impact of Race and Ethnicity, Age, Sex, and Obesity. Arthritis Care Res (Hoboken) 2016;68:1743–1750. doi: 10.1002/acr.22897. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Quintana R, Silvestre AM, Goni M, et al. Prevalence of musculoskeletal disorders and rheumatic diseases in the indigenous Qom population of Rosario, Argentina. Clin Rheumatol. 2016;35(Suppl 1):5–14. doi: 10.1007/s10067-016-3192-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Del Rio Najera D, Santana N, Pelaez-Ballestas I, et al. Prevalence of rheumatic diseases in Raramuri people in Chihuahua, Mexico: a community-based study. Clin Rheumatol. 2016;35(Suppl 1):43–52. doi: 10.1007/s10067-016-3225-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Lee S, Kim SJ. Prevalence of knee osteoarthritis, risk factors, and quality of life: The Fifth Korean National Health And Nutrition Examination Survey. Int J Rheum Dis. 2017;20:809–817. doi: 10.1111/1756-185X.12795. [DOI] [PubMed] [Google Scholar]
- 10.Pal CP, Singh P, Chaturvedi S, et al. Epidemiology of knee osteoarthritis in India and related factors. Indian J Orthop. 2016;50:518–522. doi: 10.4103/0019-5413.189608. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Kodama R, Muraki S, Oka H, et al. Prevalence of hand osteoarthritis and its relationship to hand pain and grip strength in Japan: The third survey of the ROAD study. Mod Rheumatol. 2016;26:767–773. doi: 10.3109/14397595.2015.1130673. [DOI] [PubMed] [Google Scholar]
- 12.Davatchi F, Sandoughi M, Moghimi N, et al. Epidemiology of rheumatic diseases in Iran from analysis of four COPCORD studies. Int J Rheum Dis. 2016;19:1056–1062. doi: 10.1111/1756-185X.12809. [DOI] [PubMed] [Google Scholar]
- 13.Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the global burden of disease 2010 study. Ann Rheum Dis. 2014;73:1323–1330. doi: 10.1136/annrheumdis-2013-204763. [DOI] [PubMed] [Google Scholar]
- 14.Haan MN, Lee A, Odden MC, et al. Gender Differences in the Combined Effects of Cardiovascular Disease and Osteoarthritis on Progression to Functional Impairment in Older Mexican Americans. J Gerontol A Biol Sci Med Sci. 2016;71:1089–1095. doi: 10.1093/gerona/glw014. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Park JI, Jung HH. Estimation of years lived with disability due to noncommunicable diseases and injuries using a population-representative survey. PLoS One. 2017;12:e0172001. doi: 10.1371/journal.pone.0172001. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Hubertsson J, Turkiewicz A, Petersson IF, et al. Understanding Occupation, Sick Leave, and Disability Pension Due to Knee and Hip Osteoarthritis From a Sex Perspective. Arthritis Care Res (Hoboken) 2017;69:226–233. doi: 10.1002/acr.22909. [DOI] [PubMed] [Google Scholar]
- 17.Veronese N, Stubbs B, Solmi M, et al. Association between lower limb osteoarthritis and incidence of depressive symptoms: data from the osteoarthritis initiative. Age Ageing. 2016 doi: 10.1093/ageing/afw216. [DOI] [PubMed] [Google Scholar]
- 18.Kye SY, Park K. Suicidal ideation and suicidal attempts among adults with chronic diseases: A cross-sectional study. Compr Psychiatry. 2017;73:160–167. doi: 10.1016/j.comppsych.2016.12.001. [DOI] [PubMed] [Google Scholar]
- 19.Innes KE, Sambamoorthi U. The Association of Perceived Memory Loss with Osteoarthritis and Related Joint Pain in a Large Appalachian Population. Pain Med. 2017 doi: 10.1093/pm/pnx107. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20*.Schieir O, Tosevski C, Glazier RH, et al. Incident myocardial infarction associated with major types of arthritis in the general population: a systematic review and meta-analysis. Ann Rheum Dis. 2017;76:1396–1404. doi: 10.1136/annrheumdis-2016-210275. This meta-analysis quantified and compared the risk for incident myocardial infarction across various types of arthritis in population-based studies and found that the risk of myocardial infarction was significantly increased in four types of arthritis, including OA. [DOI] [PubMed] [Google Scholar]
- 21.Chung WS, Lin HH, Ho FM, et al. Risks of acute coronary syndrome in patients with osteoarthritis: a nationwide population-based cohort study. Clin Rheumatol. 2016;35:2807–2813. doi: 10.1007/s10067-016-3391-x. [DOI] [PubMed] [Google Scholar]
- 22.Courties A, Sellam J, Maheu E, et al. Coronary heart disease is associated with a worse clinical outcome of hand osteoarthritis: a cross-sectional and longitudinal study. RMD Open. 2017;3:e000344. doi: 10.1136/rmdopen-2016-000344. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Kluzek S, Sanchez-Santos MT, Leyland KM, et al. Painful knee but not hand osteoarthritis is an independent predictor of mortality over 23 years follow-up of a population-based cohort of middle-aged women. Ann Rheum Dis. 2016;75:1749–1756. doi: 10.1136/annrheumdis-2015-208056. [DOI] [PubMed] [Google Scholar]
- 24.Turkiewicz A, Neogi T, Bjork J, et al. All-cause Mortality in Knee and Hip Osteoarthritis and Rheumatoid Arthritis. Epidemiology. 2016;27:479–485. doi: 10.1097/EDE.0000000000000477. [DOI] [PubMed] [Google Scholar]
- 25.Singh JA, Yu S. Septic arthritis in the Emergency Departments in the U.S.: A National Study of healthcare utilization and time-trends. Arthritis Care Res (Hoboken) 2017 doi: 10.1002/acr.23270. [DOI] [PubMed] [Google Scholar]
- 26.Singh JA, Yu S. Time Trends, Predictors, and Outcome of Emergency Department Use for Gout: A Nationwide US Study. J Rheumatol. 2016;43:1581–1588. doi: 10.3899/jrheum.151419. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Sharif B, Kopec JA, Wong H, et al. Distribution and Drivers of Average Direct Cost of Osteoarthritis in Canada From 2003 to 2010. Arthritis Care Res (Hoboken) 2017;69:243–251. doi: 10.1002/acr.22933. [DOI] [PubMed] [Google Scholar]
- 28.Xie F, Kovic B, Jin X, et al. Economic and Humanistic Burden of Osteoarthritis: A Systematic Review of Large Sample Studies. Pharmacoeconomics. 2016;34:1087–1100. doi: 10.1007/s40273-016-0424-x. [DOI] [PubMed] [Google Scholar]
- 29.Pinto LM, Alghamdi M, Benedetti A, et al. Derivation and validation of clinical phenotypes for COPD: a systematic review. Respir Res. 2015;16:50. doi: 10.1186/s12931-015-0208-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Bierma-Zeinstra SM, Verhagen AP. Osteoarthritis subpopulations and implications for clinical trial design. Arthritis Res Ther. 2011;13:213. doi: 10.1186/ar3299. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.Dell’Isola A, Allan R, Smith SL, et al. Identification of clinical phenotypes in knee osteoarthritis: a systematic review of the literature. BMC Musculoskelet Disord. 2016;17:425. doi: 10.1186/s12891-016-1286-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32**.Deveza LA, Melo L, Yamato TP. Knee osteoarthritis phenotypes and their relevance for outcomes: a systematic review. Osteoarthritis Cartilage. 2017 doi: 10.1016/j.joca.2017.08.009. This systematic review determined which characteristics are most relevant for phenotyping knee OA. It found that clinical phenotypes were most frequently investigated. It concluded that pain sensitization, psychological distress, radiographic severity, body mass index (BMI), muscle strength, inflammation, and comorbidities (especially metabolic syndrome) play significant parts in distinguishing clinically distinct phenotypes. [DOI] [PubMed] [Google Scholar]
- 33.Health topics: risk factors. World Health Organization; website http://www.who.int/topics/risk_factors/en/. Accessed November 29, 2017. [Google Scholar]
- 34.Williams VF, Clark LL, Oh GT. Update: Osteoarthritis and spondylosis, active component, U.S. Armed Forces, 2010-2015. Msmr. 2016;23:14–22. [PubMed] [Google Scholar]
- 35.Jin X, Wang BH, Wang X, et al. Associations between endogenous sex hormones and MRI structural changes in patients with symptomatic knee osteoarthritis. Osteoarthritis Cartilage. 2017;25:1100–1106. doi: 10.1016/j.joca.2017.01.015. [DOI] [PubMed] [Google Scholar]
- 36.Vina ER, Ran D, Ashbeck EL, et al. Race, sex, and risk factors in radiographic worsening of knee osteoarthritis. Semin Arthritis Rheum. 2017 doi: 10.1016/j.semarthrit.2017.08.008. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37**.Warner SC, Valdes AM. Genetic association studies in osteoarthritis: is it fairytale? Curr Opin Rheumatol. 2017;29:103–109. doi: 10.1097/BOR.0000000000000352. This recently published review highlighted the main findings from genetic association studies on OA to date. It reported that GWAS studies have so far identified 21 independent susceptibility loci for OA. [DOI] [PubMed] [Google Scholar]
- 38.Chu M, Zhu X, Wang C, et al. The rs4238326 polymorphism in ALDH1A2 gene potentially associated with non-post traumatic knee osteoarthritis susceptibility: a two-stage population-based study. Osteoarthritis Cartilage. 2017;25:1062–1067. doi: 10.1016/j.joca.2017.01.003. [DOI] [PubMed] [Google Scholar]
- 39.Warner SC, Walsh DA, Laslett LL, et al. Pain in knee osteoarthritis is associated with variation in the neurokinin 1/substance P receptor (TACR1) gene. Eur J Pain. 2017;21:1277–1284. doi: 10.1002/ejp.1027. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40*.Panoutsopoulou K, Thiagarajah S, Zengini E, et al. Radiographic endophenotyping in hip osteoarthritis improves the precision of genetic association analysis. Ann Rheum Dis. 2017;76:1199–1206. doi: 10.1136/annrheumdis-2016-210373. This meta-analysis additionally examined the effects of clinically relevant endophenotyping according to sight of maximal joint space narrowing and bone remodeling response on GWAS signal detection in OA. It determined that stratification of OA cases into more homogenous endophenotypes could assist in identifying genes of importance otherwise obscured by disease heterogeneity. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Castano-Betancourt MC, Evans DS, Ramos YF, et al. Novel Genetic Variants for Cartilage Thickness and Hip Osteoarthritis. PLoS Genet. 2016;12:e1006260. doi: 10.1371/journal.pgen.1006260. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 42.Jiang L, Xie X, Wang Y, et al. Body mass index and hand osteoarthritis susceptibility: an updated meta-analysis. Int J Rheum Dis. 2016;19:1244–1254. doi: 10.1111/1756-185X.12895. [DOI] [PubMed] [Google Scholar]
- 43.Ohfuji S, Jingushi S, Kondo K, et al. Factors associated with diagnostic stage of hip osteoarthritis due to acetabular dysplasia among Japanese female patients: a cross-sectional study. BMC Musculoskelet Disord. 2016;17:320. doi: 10.1186/s12891-016-1179-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 44*.Reyes C, Leyland KM, Peat G, et al. Association Between Overweight and Obesity and Risk of Clinically Diagnosed Knee, Hip, and Hand Osteoarthritis: A Population-Based Cohort Study. Arthritis Rheumatol. 2016;68:1869–1875. doi: 10.1002/art.39707. This large prospective cohort study from Spain found an independent association between weight gain and hip OA. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Gersing AS, Schwaiger BJ, Nevitt MC, et al. Is Weight Loss Associated with Less Progression of Changes in Knee Articular Cartilage among Obese and Overweight Patients as Assessed with MR Imaging over 48 Months? Data from the Osteoarthritis Initiative. Radiology. 2017;284:508–520. doi: 10.1148/radiol.2017161005. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 46.Atukorala I, Makovey J, Lawler L, et al. Is There a Dose-Response Relationship Between Weight Loss and Symptom Improvement in Persons With Knee Osteoarthritis? Arthritis Care Res (Hoboken) 2016;68:1106–1114. doi: 10.1002/acr.22805. [DOI] [PubMed] [Google Scholar]
- 47.Frey N, Hugle T, Jick SS, et al. Hyperlipidaemia and incident osteoarthritis of the hand: a population-based case-control study. Osteoarthritis Cartilage. 2017;25:1040–1045. doi: 10.1016/j.joca.2017.01.014. [DOI] [PubMed] [Google Scholar]
- 48.Garcia-Gil M, Reyes C, Ramos R, et al. Serum Lipid Levels and Risk Of Hand Osteoarthritis: The Chingford Prospective Cohort Study. Sci Rep. 2017;7:3147. doi: 10.1038/s41598-017-03317-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 49.Driban JB, Lo GH, Eaton CB, et al. Exploratory analysis of osteoarthritis progression among medication users: data from the Osteoarthritis Initiative. Ther Adv Musculoskelet Dis. 2016;8:207–219. doi: 10.1177/1759720X16664323. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 50.Michaelsson K, Lohmander LS, Turkiewicz A, et al. Association between statin use and consultation or surgery for osteoarthritis of the hip or knee: a pooled analysis of four cohort studies. Osteoarthritis Cartilage. 2017 doi: 10.1016/j.joca.2017.07.013. [DOI] [PubMed] [Google Scholar]
- 51.Lo GH, McAlindon TE, Katz JN, et al. Systolic and pulse pressure associate with incident knee osteoarthritis: data from the Osteoarthritis Initiative. Clin Rheumatol. 2017 doi: 10.1007/s10067-017-3656-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 52.Magnusson K, Bech Holte K, Juel NG, et al. Long term type 1 diabetes is associated with hand pain, disability and stiffness but not with structural hand osteoarthritis features - The Dialong hand study. PLoS One. 2017;12:e0177118. doi: 10.1371/journal.pone.0177118. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 53.Frey N, Hugle T, Jick SS, et al. Type II diabetes mellitus and incident osteoarthritis of the hand: a population-based case-control analysis. Osteoarthritis Cartilage. 2016;24:1535–1540. doi: 10.1016/j.joca.2016.04.005. [DOI] [PubMed] [Google Scholar]
- 54.Garessus ED, de Mutsert R, Visser AW, et al. No association between impaired glucose metabolism and osteoarthritis. Osteoarthritis Cartilage. 2016;24:1541–1547. doi: 10.1016/j.joca.2016.04.007. [DOI] [PubMed] [Google Scholar]
- 55.Strand MP, Neogi T, Niu J, et al. No association between metabolic syndrome and radiographic hand osteoarthritis: Data from the Framingham study. Arthritis Care Res (Hoboken) 2017 doi: 10.1002/acr.23288. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 56.Arden NK, Cro S, Sheard S, et al. The effect of vitamin D supplementation on knee osteoarthritis, the VIDEO study: a randomised controlled trial. Osteoarthritis Cartilage. 2016;24:1858–1866. doi: 10.1016/j.joca.2016.05.020. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 57.Wang X, Cicuttini F, Jin X, et al. Knee effusion-synovitis volume measurement and effects of vitamin D supplementation in patients with knee osteoarthritis. Osteoarthritis Cartilage. 2017;25:1304–1312. doi: 10.1016/j.joca.2017.02.804. [DOI] [PubMed] [Google Scholar]
- 58**.Zheng S, Jin X, Cicuttini F, et al. Maintaining Vitamin D Sufficiency Is Associated with Improved Structural and Symptomatic Outcomes in Knee Osteoarthritis. Am J Med. 2017 doi: 10.1016/j.amjmed.2017.04.038. This study found that those with consistently sufficient Vitamin D levels had significantly less loss of tibial cartilage volume, less increase in effusion-synovitis volume, and less loss of WOMAC physical function. [DOI] [PubMed] [Google Scholar]
- 59.Dai Z, Lu N, Niu J, et al. Dietary Fiber Intake in Relation to Knee Pain Trajectory. Arthritis Care Res (Hoboken) 2016 doi: 10.1002/acr.23158. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 60.Dai Z, Niu J, Zhang Y, et al. Dietary intake of fibre and risk of knee osteoarthritis in two US prospective cohorts. Ann Rheum Dis. 2017;76:1411–1419. doi: 10.1136/annrheumdis-2016-210810. [DOI] [PubMed] [Google Scholar]
- 61.Li H, Zeng C, Wei J, et al. Relationship between soy milk intake and radiographic knee joint space narrowing and osteophytes. Rheumatol Int. 2016;36:1215–1222. doi: 10.1007/s00296-016-3491-6. [DOI] [PubMed] [Google Scholar]
- 62.Veronese N, Stubbs B, Noale M, et al. Adherence to a Mediterranean diet is associated with lower prevalence of osteoarthritis: Data from the osteoarthritis initiative. Clin Nutr. 2016 doi: 10.1016/j.clnu.2016.09.035. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 63.Edwards MH, Paccou J, Ward KA, et al. The relationship of bone properties using high resolution peripheral quantitative computed tomography to radiographic components of hip osteoarthritis. Osteoarthritis Cartilage. 2017 doi: 10.1016/j.joca.2017.03.011. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 64.Teichtahl AJ, Wang Y, Wluka AE, et al. Associations between systemic bone mineral density and early knee cartilage changes in middle-aged adults without clinical knee disease: a prospective cohort study. Arthritis Res Ther. 2017;19:98. doi: 10.1186/s13075-017-1314-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 65.Gregson CL, Hardcastle SA, Murphy A, et al. High Bone Mass is associated with bone-forming features of osteoarthritis in non-weight bearing joints independent of body mass index. Bone. 2017;97:306–313. doi: 10.1016/j.bone.2017.01.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 66.Back K, Ahlqwist M, Hakeberg M, et al. Relation between osteoporosis and radiographic and clinical signs of osteoarthritis/arthrosis in the temporomandibular joint: a population-based, cross-sectional study in an older Swedish population. Gerodontology. 2017;34:187–194. doi: 10.1111/ger.12245. [DOI] [PubMed] [Google Scholar]
- 67*.Bouyer B, Mazieres B, Guillemin F, et al. Association between hip morphology and prevalence, clinical severity and progression of hip osteoarthritis over 3 years: The knee and hip osteoarthritis long-term assessment cohort results. Joint Bone Spine. 2016;83:432–438. doi: 10.1016/j.jbspin.2015.09.005. This population-based OA cohort study in France used 5 measures to describe hip morphology (center edge angle, acetabular index, vertical center anterior angle, acetabular depth and neck-shaft angle). Acetabular index was most strongly associated with hip OA progression and severity. [DOI] [PubMed] [Google Scholar]
- 68.Saberi Hosnijeh F, Zuiderwijk ME, Versteeg M, et al. Cam Deformity and Acetabular Dysplasia as Risk Factors for Hip Osteoarthritis. Arthritis Rheumatol. 2017;69:86–93. doi: 10.1002/art.39929. [DOI] [PubMed] [Google Scholar]
- 69.Hunter D, Nevitt M, Lynch J, et al. Longitudinal validation of periarticular bone area and 3D shape as biomarkers for knee OA progression? Data from the FNIH OA Biomarkers Consortium. Ann Rheum Dis. 2016;75:1607–1614. doi: 10.1136/annrheumdis-2015-207602. [DOI] [PubMed] [Google Scholar]
- 70*.Lu M, Han W, Wang K, et al. Associations between proximal tibiofibular joint (PTFJ) types and knee osteoarthritic changes in older adults. Osteoarthritis Cartilage. 2017 doi: 10.1016/j.joca.2017.05.013. [DOI] [PubMed] [Google Scholar]
- 71.Nelson AE, Golightly YM, Lateef S, et al. Cross-sectional associations between variations in ankle shape by statistical shape modeling, injury history, and race: the Johnston County Osteoarthritis Project. J Foot Ankle Res. 2017;10:34. doi: 10.1186/s13047-017-0216-3. This unique study found that certain ankle morphologies were linked to injury history that could lead to greater predisposition for ankle OA. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 72.Jungmann PM, Baum T, Nevitt MC, et al. Degeneration in ACL Injured Knees with and without Reconstruction in Relation to Muscle Size and Fat Content-Data from the Osteoarthritis Initiative. PLoS One. 2016;11:e0166865. doi: 10.1371/journal.pone.0166865. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 73.Goldman LH, Tang K, Facchetti L, et al. Role of thigh muscle cross-sectional area and strength in progression of knee cartilage degeneration over 48 months - data from the Osteoarthritis Initiative. Osteoarthritis Cartilage. 2016;24:2082–2091. doi: 10.1016/j.joca.2016.07.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 74.Turkiewicz A, Timpka S, Thorlund JB, et al. Knee extensor strength and body weight in adolescent men and the risk of knee osteoarthritis by middle age. Ann Rheum Dis. 2017 doi: 10.1136/annrheumdis-2016-210888. [DOI] [PubMed] [Google Scholar]
- 75.Hall M, Wrigley TV, Kasza J, et al. Cross-sectional association between muscle strength and self-reported physical function in 195 hip osteoarthritis patients. Semin Arthritis Rheum. 2017;46:387–394. doi: 10.1016/j.semarthrit.2016.08.004. [DOI] [PubMed] [Google Scholar]
- 76.Wang B, Liu Q, Wise BL, et al. Valgus malalignment and prevalence of lateral compartmental radiographic knee osteoarthritis (OA): The Wuchuan OA study. Int J Rheum Dis. 2017 doi: 10.1111/1756-185X.13079. [DOI] [PubMed] [Google Scholar]
- 77.Sharma L, Chang AH, Jackson RD, et al. Varus Thrust and Incident and Progressive Knee Osteoarthritis. Arthritis Rheumatol. 2017 doi: 10.1002/art.40224. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 78.Wink AE, Gross KD, Brown CA, et al. Varus thrust during walking and the risk of incident and worsening medial tibiofemoral MRI lesions: the Multicenter Osteoarthritis Study. Osteoarthritis Cartilage. 2017;25:839–845. doi: 10.1016/j.joca.2017.01.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 79.Cameron KL, Driban JB, Svoboda SJ. Osteoarthritis and the Tactical Athlete: A Systematic Review. J Athl Train. 2016;51:952–961. doi: 10.4085/1062-6050-51.5.03. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 80.Lo GH, Driban JB, Kriska AM, et al. Is There an Association Between a History of Running and Symptomatic Knee Osteoarthritis? A Cross-Sectional Study From the Osteoarthritis Initiative. Arthritis Care Res (Hoboken) 2017;69:183–191. doi: 10.1002/acr.22939. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 81.Alentorn-Geli E, Samuelsson K, Musahl V, et al. The Association of Recreational and Competitive Running With Hip and Knee Osteoarthritis: A Systematic Review and Meta-analysis. J Orthop Sports Phys Ther. 2017;47:373–390. doi: 10.2519/jospt.2017.7137. [DOI] [PubMed] [Google Scholar]
- 82.Driban JB, Hootman JM, Sitler MR, et al. Is Participation in Certain Sports Associated With Knee Osteoarthritis? A Systematic Review. J Athl Train. 2017;52:497–506. doi: 10.4085/1062-6050-50.2.08. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 83.Vigdorchik JM, Nepple JJ, Eftekhary N, et al. What Is the Association of Elite Sporting Activities With the Development of Hip Osteoarthritis? Am J Sports Med. 2017;45:961–964. doi: 10.1177/0363546516656359. [DOI] [PubMed] [Google Scholar]
- 84.Sanders TL, Pareek A, Kremers HM, et al. Long-term follow-up of isolated ACL tears treated without ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2017;25:493–500. doi: 10.1007/s00167-016-4172-4. [DOI] [PubMed] [Google Scholar]
- 85**.Suter LG, Smith SR, Katz JN, et al. Projecting Lifetime Risk of Symptomatic Knee Osteoarthritis and Total Knee Replacement in Individuals Sustaining a Complete Anterior Cruciate Ligament Tear in Early Adulthood. Arthritis Care Res (Hoboken) 2017;69:201–208. doi: 10.1002/acr.22940. Using a computer simulation model of knee OA natural history and management, this study concluded that those with ACL injury and MT by age 25 were more likely to develop OA and to eventually require TKR surgery than those without injury. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 86.Roemer FW, Kwoh CK, Hannon MJ, et al. Partial meniscectomy is associated with increased risk of incident radiographic osteoarthritis and worsening cartilage damage in the following year. Eur Radiol. 2017;27:404–413. doi: 10.1007/s00330-016-4361-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 87.Atukorala I, Kwoh CK, Guermazi A, et al. Synovitis in knee osteoarthritis: a precursor of disease? Ann Rheum Dis. 2016;75:390–395. doi: 10.1136/annrheumdis-2014-205894. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 88.Han W, Aitken D, Zhu Z, et al. Signal intensity alteration in the infrapatellar fat pad at baseline for the prediction of knee symptoms and structure in older adults: a cohort study. Ann Rheum Dis. 2016;75:1783–1788. doi: 10.1136/annrheumdis-2015-208360. [DOI] [PubMed] [Google Scholar]
- 89.Han W, Aitken D, Zhu Z, et al. Hypointense signals in the infrapatellar fat pad assessed by magnetic resonance imaging are associated with knee symptoms and structure in older adults: a cohort study. Arthritis Res Ther. 2016;18:234. doi: 10.1186/s13075-016-1130-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 90.Jarraya M, Guermazi A, Felson DT. Is superolateral Hoffa’s fat pad hyperintensity a marker of local patellofemoral joint disease? - The MOST study. Osteoarthritis Cartilage. 2017 doi: 10.1016/j.joca.2017.05.020. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 91.de Lange-Brokaar BJ, Ioan-Facsinay A, Yusuf E, et al. Evolution of synovitis in osteoarthritic knees and its association with clinical features. Osteoarthritis Cartilage. 2016;24:1867–1874. doi: 10.1016/j.joca.2016.05.021. [DOI] [PubMed] [Google Scholar]
- 92.Ramonda R, Favero M, Vio S, et al. A recently developed MRI scoring system for hand osteoarthritis: its application in a clinical setting. Clin Rheumatol. 2016;35:2079–2086. doi: 10.1007/s10067-016-3303-0. [DOI] [PubMed] [Google Scholar]
- 93.Liu R, Damman W, Reijnierse M, et al. Bone marrow lesions on magnetic resonance imaging in hand osteoarthritis are associated with pain and interact with synovitis. Osteoarthritis Cartilage. 2017;25:1093–1099. doi: 10.1016/j.joca.2017.02.790. [DOI] [PubMed] [Google Scholar]
- 94**.Damman W, Liu R, Bloem JL, et al. Bone marrow lesions and synovitis on MRI associate with radiographic progression after 2 years in hand osteoarthritis. Ann Rheum Dis. 2017;76:214–217. doi: 10.1136/annrheumdis-2015-209036. In this study, the association of magnetic resonance features with radiographic progression of hand OA over 2 year synovitis was evaluated. BMLs and synovitis associated with hand OA radiographic progression. [DOI] [PubMed] [Google Scholar]
- 95.Roux CH, Foltz V, Maheu E, et al. MRI and serum biomarkers correlate with radiographic features in painful hand osteoarthritis. Clin Exp Rheumatol. 2016;34:991–998. [PubMed] [Google Scholar]
- 96.Sharma L, Nevitt M, Hochberg M, et al. Clinical significance of worsening versus stable preradiographic MRI lesions in a cohort study of persons at higher risk for knee osteoarthritis. Ann Rheum Dis. 2016;75:1630–1636. doi: 10.1136/annrheumdis-2015-208129. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 97**.Sharma L, Hochberg M, Nevitt M, et al. Knee tissue lesions and prediction of incident knee osteoarthritis over 7 years in a cohort of persons at higher risk. Osteoarthritis Cartilage. 2017;25:1068–1075. doi: 10.1016/j.joca.2017.02.788. In this study with 7 years of follow-up data, MRI lesions (BMLs, cartilage damage, and menisci extrusion) improved prediction of mild and moderate radiographic knee OA development when added to prediction models that only included sociodemographic and patient-reported clinical variables. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 98.Roemer FW, Guermazi A, Collins JE, et al. Semi-quantitative MRI biomarkers of knee osteoarthritis progression in the FNIH biomarkers consortium cohort - Methodologic aspects and definition of change. BMC Musculoskelet Disord. 2016;17:466. doi: 10.1186/s12891-016-1310-6. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 99.Teichtahl AJ, Cicuttini FM, Abram F, et al. Meniscal extrusion and bone marrow lesions are associated with incident and progressive knee osteoarthritis. Osteoarthritis Cartilage. 2017;25:1076–1083. doi: 10.1016/j.joca.2017.02.792. [DOI] [PubMed] [Google Scholar]
- 100.Ahedi HG, Aitken DA, Blizzard LC, et al. Correlates of Hip Cartilage Defects: A Cross-sectional Study in Older Adults. J Rheumatol. 2016;43:1406–1412. doi: 10.3899/jrheum.151001. [DOI] [PubMed] [Google Scholar]