1
Knee pain for most days of previous month
2
Osteophytes at joint margins on radiographs
3
Synovial fluid typical of osteoarthritis (laboratory)
4
Age ≥40 years
5
Crepitus on active joint motion
6
Morning stiffness ≤30 min duration
Although radiographic imaging classification has stood the test of time, the most limiting aspect of this classification is that it often does not detect arthritis until a more advanced stage. Plain radiographs are an imperfect indicator for early arthritis, with a more complete picture of intra-articular disease revealed by other methods, including magnetic resonance imaging (MRI) (Table 1.2) and, more recently, serum and urinary markers looking for bone/cartilage/synovial degradation and/or bone/cartilage/synovial synthesis [5, 6].
Table 1.2
Advanced imaging for osteoarthritis of the knee
MRI |
|---|
Standard SPGR |
Cartilage morphology quantitative/time-consuming analyses |
T2 MRI relaxation |
Collagen distribution |
Semiquantitative information on cartilage quality/complex interpretation |
T1ρ proteoglycan distribution |
Semiquantitative information on cartilage quality/complex interpretation |
23Na MRI FCD/proteoglycan content |
Semiquantitative information on cartilage quality/field strength ≥3 T |
dGEMRIC FCD/proteoglycan content |
Semiquantitative information on cartilage quality, early changes/contrast agent needed |
In addition to defining and classifying established arthritis, more difficult to define are the following:
Classification strategies for radiographic imaging have emphasized joint space narrowing, subchondral sclerosis, and osteophyte formation (Tables 1.3 and 1.4). A recent study assessed the validity and sensitivity to change of three radiographic scales of knee OA [7]. The authors found high validity to assess knee OA severity but only moderate sensitivity to change. The authors recommended caution when using ordinal radiographic grading scales to monitor knee OA over time. Joint axis deviation is a much-used clinical tool, although it is not as frequently used in radiographic classifications. By advanced imaging (MRI), the most common features that indicate osteoarthritis are cartilage thinning and subchondral bone edema. Whole-organ body imaging is largely being used as a research tool only (Table 1.5).
1.
(a) How does one define “early arthritis”? If you have radiographic and/or imaging signs only, with no correlation to clinical symptoms or objective physical exam signs, is this arthritis?
(b) Should we define clinical (symptomatic) arthritis separate from radiographic (imaging) arthritis?
2.
If there are focal defects, particularly focal defects on only one side of the joint, is this defined as arthritis?
3.
Is chondrosis and arthrosis the same disease along a continuum?
4.
Should post-traumatic arthrosis and idiopathic arthrosis follow the same disease progression? If these two diseases are separate, then in which category would we place overuse or overload OA?
Kellgren–Lawrence grading system | |
|---|---|
Grade 0 | No feature of osteoarthritis |
Grade 1 | Doubtful narrowing of joint space and possible osteophytic lipping |
Grade 2 | Definite osteophytes and possible narrowing of joint space |
Grade 3 | Moderate multiple osteophytes, definite narrowing of joint space, and some sclerosis and possible deformity of bone ends |
Grade 4 | Large osteophytes, marked narrowing of joint space, severe sclerosis, and definite deformity of bone ends |
Osteoarthritis research society international grading system for medial and lateral tibiofemoral joint space narrowing | |
|---|---|
Grade 0 | Normal |
Grade 1 | Mild (1–33 % narrowed) |
Grade 2 | Moderate (34–66 % narrowed) |
Grade 3 | Severe (67–100 % narrowed) |
Table 1.5
MRI whole-organ scoring for osteoarthritis of the knee
KOSS [19] | Semiquantitative, whole-organ score, time consuming, observer variance |
WORMS [20] | Semiquantitative, whole-organ score, time consuming, observer variance |
BLOKS [21] | Semiquantitative, whole-organ score, time consuming, observer variance |
The struggle to define osteoarthritis is compounded when the clinician (or researcher) tries to define arthritis progression. One could define progression based on the classification strategies, i.e., change in radiographic markers (joint space narrowing, osteophyte formation, and/or axis deviation), change in MRI imaging (increase in cartilage thinning, increase in subchondral bone edema, and/or osteophyte formation), and increase in symptoms of stiffness and swelling best evaluated by a change in patient-reported outcome measure scales. Indeed, thought leaders of the Osteoarthritis Research Society International have called for greater consensus around more sensitive and specific diagnostic criteria for OA to aid in both research and clinical endeavors [8].
This chapter will not answer these questions, but the reader should be apprised that these questions continue to be debated without consensus in our literature. Though clinical knowledge depends on research-directed discoveries, the rigor necessary to answer these questions is different for the clinician and the researcher.
1.2 Etiology
One factor that is consistent in all studies of arthritis is its association with the aging process. The etiology of osteoarthritis has long been thought to be cartilage driven. Imaging definitions of osteoarthritis have as a main factor some inclusion of changes in the subchondral bone. Osteophyte formation, bone remodeling, subchondral sclerosis, and bone attrition are crucial for radiographic diagnosis; several of these bone changes take place not only during the final stages of the disease but sometimes at the onset of the disease, before cartilage degradation is apparent. This adds to the difficulty of using radiographic markers as an indication of the stage of the disease or the stage of potential disease progression. However, findings collectively suggest that the subchondral bone could be the initiator of cartilage damage, and current attention has focused on the role subchondral bone plays in the etiology of osteoarthritis.
Recent evidence shows an additional and integrated role of bone and synovial tissue. Synovial inflammation corresponds to clinical symptoms such as joint swelling and inflammatory pain and is thought to be secondary to cartilage debris and catabolic mediators entering the synovial cavity. Synovial macrophages produce catabolic and pro-inflammatory mediators, leading to inflammation, which starts a negative balance of cartilage matrix degradation and repair. This process, in turn, amplifies synovial inflammation, thus creating a vicious cycle. Inflammation is an important aspect of arthritis, and the degree of inflammation likely varies depending on patient-specific innate factors and local joint factors. This can create a spectrum of clinical presentations for the same imaging picture and varying timelines for disease progression.
1.3 Risk Factors
A review of relevant literature on risk factors is presented in Table 1.6. Pertinent points are discussed below.
Table 1.6
Risk factors for, and etiology of, osteoarthritis of the knee
Study | Topic | Study type | Results |
|---|---|---|---|
Andriacchi (2015) [22] | Risk factors of knee OA – systems view of pathogenesis | Literature review to develop systems model to predict cartilage thinning at 5-year follow-up | The primary risk factors for OA (aging, obesity, and joint trauma) are associated with systemic biological, mechanical, and structural changes; when one risk factor spikes, the interaction among these systems determines the rate of progression to clinical OA |
Evangelou (2015) [23] | Meta-analysis of genome-wide association studies confirms a susceptibility locus for knee osteoarthritis on chromosome 7q22 Etiology: genetics | Meta-analysis of four genome-wide association studies of 2371 cases of knee OA and 35,909 controls in Caucasian populations, with data from ten additional replication data sets | Cumulative sample size of 6709 cases and 44,439 controls. One genome-wide significant locus was identified on chromosome 7q22 for knee OA (rs4730250, p = 9.2 Å ~ 10 − 9), thereby confirming its role as a susceptibility locus for OA |
Kerkhof (2015) [24] | Prognostic model for knee OA incidence | Risk model + validation, prospective study | The cohorts of three prospective studies were used, each with differing patient characteristics (e.g., only age ≥55, only female). Of modest predictive value for OA were genetic score, pain, collagen levels, sex, age, and BMI. The strongest predictive value was minor or doubtful radiographic degenerative features, of a sort that radiologists tend not to report (KL score of 1) |
Lo (2015) [25] | Habitual running is not detrimental and may be protective of symptomatic knee OA | Cross-sectional study of 2439 OAI participants using knee XRs, symptoms assessment, and lifetime activity surveys | 55 % female, mean age of 64.7, 28 % ran at some time in their life. Exposure to nonelite running at any time in one’s lifetime is not associated with higher odds of prevalent knee pain, symptomatic OA, or radiographic OA |
Sanghi (2015) [26] | Risk factors of knee OA – diet | Case (180) + control (180) | Low intake of vitamin D and vitamin C is a possible risk factor for OA, especially in females |
Yucesoy (2015) [15] | Risk factors of knee OA – occupation and genetics | Literature review (not systematic) | Describes OA in all joints. For knees, a clear occupational risk factor was heavy physical workload. Also of note were vibration, repetitive movement, and long hours of kneeling, squatting, or standing |
Apold (2014) [27] | Risk factors for knee replacement – sex as a variable | Prospective 12-year study of 315,495 Norwegians | 1323 individuals received knee replacement for primary OA (0.4 %). Independent risk factors were high BMI and heavy labor at work. Rate of knee replacement was double for women (.55) than men (.28). High BMI risk increase in men = 6× and women = 11×. Combining heavy labor with high BMI was particularly hazardous, with risk increase in men = 12× and women = 16×. Smoking had no association in males and a (strangely) positive effect in females |
Fanelli (2014) [28] | Follow-up on surgically treated knee dislocations – joint injury as a variable | Case review, minimum 5-year follow-up, 44 cases | At a mean of 10 years post-op (range 5–22 years), dislocated knees treated surgically were stable, but incidence of OA was 23 %. (This study notes that Engebretsen 2009 and Richter 2002 saw OA at 85 %) |
Logerstedt (2014) [29] | Moderate and severe knee OA by sex differences – progression and sex | Cross-sectional, 2-year longitudinal, case (226) + control (63) | For moderate OA (only), females had weaker performance scores and higher ADL impairment. No difference in controls or in severe OA |
Silverwood (2014) [30] | Risk factors of knee OA – age ≥50 | Systematic review + meta-analysis, 46 studies | Risks = overweight/obese, female, previous trauma; n/a smoking, n/a hand OA |
Bennell (2013) [10] | Genesis and management of knee OA – role of LE muscle | Extensive literature review from PT perspective | This paper is 32 pages long with 181 references, covering the influence of LE muscle activity on knee joint loading, deficits in muscle function in knee OA, and evidence on the role of muscle in the development and progression of knee OA. Covers muscle activation, proprioception, OA onset and progression, and muscle function deficit intervention and modification. Ample evidence for muscle (particularly quadriceps) strengthening exercises resulting in improvements in pain, physical function, and QOL. Pages 17–22 cover exercise Rx for knee OA |
Chundru (2013) [31] | Focal knee lesions in knee pairs for asymptomatic and symptomatic patients | Case + control, radiographic study, 3 T MRI of both knees to assess focal knee lesions | Control = 60 subjects, aged 45–55, with OA risk factors, no radiographic OA, without knee pain; cases = 30. Same demographics with right knee pain; + 30 with bilateral knee pain. Findings: Radiographic focal knee lesions in the right and left knee of subjects with OA risk factors were positively associated with each other. Knee pain is independent of focal lesions |
Felson (2013) [9] | OA as a disease of abnormal mechanics Etiology = progression? | Epidemiological literature review, not systematic | Author picks through OA literature to construct three points regarding abnormal mechanics: increased physical forces cause OA; above all other factors, pathomechanics prompt disease progression; and inflammation in OA is a consequence of abnormal mechanics and is almost never primary |
Jungmann (2013) [32] | Risk of cartilage degradation – metabolic factors (e.g., high abdominal circumference, hypertension, high fat consumption, and diabetes mellitus) | NIH multicenter, longitudinal, observational cohort | Subjects: no symptomatic radiographic knee OA at baseline but ≥1 risk factor for developing knee OA, with full MRI scans (n = 403, aged 45–60). Follow-up MRIs with T2 relaxation data (n = 381). Metabolic risk factors of high abdominal circumference, hypertension, high fat consumption, and diabetes mellitus had significant association with higher baseline T2 relaxation times. The cumulative number of metabolic risk factors present in an individual was associated with higher baseline T2 values, independent of BMI |
Martin (2013) [33] | Risk factors of knee OA – BMI, occupation, activity level | British 1946 birth cohort; snapshots at age 36, 43, and 53; n = 2597 | OA association with BMI, strong and manual labor occupation, moderate. High BMI levels more risky for active than sedentary participants. In low BMI women, high activity levels had a protective effect for OA |
Prieto-Alhambra (2013) [34] | Incidence and risk factors of OA – age, gender, and crossover sites (knee-hip-hand) | Spain cohort, retrospective, 2006–2010, age ≥40, n = 3,266,826 | Diagnosis based on ICD-10 code. OA incidence in only the knee = 96,222 (2.95 %), knee + hand = 14,171 (.43 %), knee + hip = 14,585 (.45 %), and all three = 1391 (.04 %). Total knee incidence 3.87 %. Knee-only were highly female (64.4 %), BMI 25–30 (37.86 %)/BMI ≥30 (51.59 %), and comorbid for hypertension (55.47 %). Mean age at diagnosis 67 years; excellent and detailed figures on incidence by age. Crossover of knee ± hip ± hand attenuate when adjusted for BMI |
Boyan (2012) [13] | Sex differences in knee OA | 2-page editorial | Letter calling for knee OA studies to factor sex in all research done, because women have increased prevalence of knee OA, greater pain, and more substantial reduction in function and quality of life when disease is present |
Hansen (2012) [35] | Running does not cause OA of the hip or knee | Literature review | Low- and moderate-distance running is not associated with OA. Long-distance running is inconclusive. Barefoot and minimalist shoes are inconclusive. Increased risk of developing OA = increasing age, previous joint injury, and greater BMI |
Huffman (2012) [14] | OA and the metabolic syndrome: more evidence that the etiology of OA is different in men and women – sex as a variable | Editorial with literature review | 3-page article listing 15 studies chosen to illustrate the topic. Independent of the effects of obesity, altered metabolism is related to knee OA, and these relations differ for men and women. Example studies are cited: crossover with hand OA, glucose, hormones, growth factors, transcription factors, nitric oxide-reactive oxygen species, systemic inflammatory markers and mediators, leptin, cholesterol, insulin resistance, and sex differences in fat deposition patterns. Sex differences are noted at epidemiologic, radiographic, circulating biomarker, hormonal, and cellular levels |
Palmer (2012) [36] | Risk factors of knee OA – occupational activities | Systematic literature review | 43 papers 1948–2011. Table 3 is a huge synopsis of risk sorted by physical activity and study. High-risk occupational activities were squatting/kneeling, lifting, climbing, and heavy work. Particularly deleterious interactions of high BMI with kneeling/squatting and heavy lifting |
Sridhar (2012) [37] | Obesity and symptomatic osteoarthritis of the knee
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