In cross-sectional studies, the PAM has been shown to be significantly greater in patients with medial compartment knee OA than in controls14 (and in subjects with more severe OA than in those with less severe disease15). In subjects who had relatively mild radiographic knee OA, medial compartment loads were significantly higher among those who had knee pain than those who were asymptomatic.
A greater degree of toe-out during walking, which reduces the PAM, diminished the risk of radiographic progression in subjects with medial compartment knee OA. Use of lateral wedge orthoses for more than a year resulted in significant and persistent decreases in the PAM compared with use of neutral orthoses. Also, use of lateral wedge orthoses recently was found to slow the progression of medial compartment joint-space narrowing over 3 years relative to that seen with neutral orthoses,16 suggesting that structural damage, and not only symptoms, improves as a result of improved biomechanics.
PROTECTING AGAINST MECHANICAL DAMAGE
When a normal joint is in the unloaded state, the opposing surfaces are incongruent. With loading, the cartilage and bone on both sides of the joint space deform, maximizing the contact area and thereby minimizing stress within the cartilage.17
With aging, the congruity of joints increases, rendering them less flexible under load. Although the prevalence of OA clearly increases with age and age is the major risk factor for OA, nearly one-third of knee joints of human tissue donors who were in their seventh through ninth decade and had no history of arthritis showed no evidence of OA.18 The increased prevalence of OA in older persons most likely reflects a gradual accumulation of microdamage to the joint over a lifetime rather than a direct consequence of the aging of joint tissues.
During normal walking, 3 to 4 times body weight is transmitted through the knee. During a deep knee bend, the patellofemoral joint is subjected to a load as great as 9 to 10 times body weight. Although the bulk properties of articular cartilage would make it an excellent shock absorber, in most joints it is too thin to serve as much of a shock-absorbing structure. Therefore, adaptive mechanisms are needed to protect joints from these physiological loads.
Viscoelasticity is important
Because articular cartilage is viscoelastic (has a fluid/matrix composite that permits movement of interstitial fluid through its matrix), when it is loaded, fluid flows away from the load and weeps from the surface at the periphery of the loaded area. This hydrostatic compression, which is essential to the function of articular cartilage, transmits the load to the underlying subchondral bone, sparing the cartilage matrix and cells from damage.2
If deformation of the articular cartilage with loading is restricted so that the cartilage cannot conform to the load completely, the size of the contact area becomes restricted and high stresses are generated within the cartilage. If the cartilage is thinned, as in OA, the process is exacerbated.
Like articular cartilage, normal subchondral bone is viscoelastic; the fluid phase is bone marrow. Bone deforms less, or becomes stiffer, when the load is applied rapidly than when loading is more gradual. As a consequence, the chondroprotective effect of the shock absorbing of the subchondral bone has limits. This is why joint damage caused by excessive loading is related to the rate of loading as well as to the magnitude of the load. On the basis of the results of the animal studies and observations in humans described herein, and our understanding of the structure, composition, and material properties of articular cartilage, it is likely that rapid RIL does not allow sufficient time for interstitial fluid to flow and absorb the energy transmitted and thereby protect the cartilage matrix and cells.
Articular cartilage viscoelasticity helps protect the cartilage matrix. However, most of the shock absorption is provided by subchondral, metaphyseal, and diaphyseal bone and, as noted below, by the periarticular soft tissues, especially muscle.
1. Brandt KD, Dieppe P, Radin EL. Etiopathogenesis of osteoarthritis. Rheum Dis Clin North Am. 2008;34:531-559.
2. Brandt KD, Dieppe P, Radin EL. Commentary: is it useful to subset “primary” osteoarthritis? A critique based on evidence regarding the etiopathogenesis of osteoarthritis. Semin Arthritis Rheum. 2009;39:81-95.
3. Weinstein SL. Bristol-Myers Squibb/Zimmer award for distinguished achievement in orthopaedic research. Long-term follow-up of pediatric orthopaedic conditions: natural history and outcomes of treatment. J Bone Joint Surg. 2000;82A:980-990.
4. Bergenudd H, Johnell O, Redlund-Johnell I, Lohmander LS. The articular cartilage after osteotomy for medial gonarthrosis: biopsies after 2 years in 19 cases. Acta Orthop Scand. 1992;63:413-416.
5. Radin EL, Burr DB. Hypothesis: joints can heal. Semin Arthritis Rheum. 1984;13:293-302.
6. Hirsch C. The pathogenesis of chondromalacia of the patella: a physical, histologic and chemical study. Acta Chir Scand. 1944;90(suppl 83).
7. Simon SR, Radin EL, Paul IL, Rose RM. The response of joints to impact loading, II: in vivo behavior of subchondral bone. J Biomech. 1972;5:267-272.
8. Radin EL, Boyd RD, Martin RB, et al. Mechanical factors influencing cartilage damage. In: Peyron JG, ed. Osteoarthritis: Current Clinical and Fundamental Problems. 2nd ed. Paris: Geigy; 1985:90-99.
9. Radin EL, Whittle MW, Yang KH, et al. The heelstrike transient, its relationship with the angular velocity of the shank, and the effects of quadriceps paralysis. In: Lantz SA, King AI, eds. Advances in Bioengineering. New York: American Society of Mechanical Engineering; 1986:121-123.
10. Radin EL, Yang KH, Riegger C, et al. Relationship between lower limb dynamics and knee joint pain [published correction appears in J Orthop Res. 1991;9:776]. J Orthop Res. 1991;9:398-405.
11. Andriacchi TP. Dynamics of knee alignment. Orthop Clin North Am. 1994;25:395-403.
12. Miyazaki T, Wada M, Kawahara H, et al. Dynamic load at baseline can predict radiographic disease progression in medial compartment knee osteoarthritis. Ann Rheum Dis. 2002;61:617-622.
13. Amin S, Luepongsak N, McGibbon CA, et al. Knee adduction moment and development of chronic knee pain in elders. Arthritis Rheum. 2004;51:371-376.
14. Baliunas AJ, Hurwitz DE, Ryals AB, et al. Increased knee joint loads during walking are present in subjects with knee osteoarthritis. Osteoarthritis Cartilage. 2002;10:573-579.
15. Mündermann A, Dyrby CO, Hurwitz DE, et al. Potential strategies to reduce medial compartment loading in patients with knee osteoarthritis of varying severity: reduced walking speed [published correction appears in Arthritis Rheum. 2004;50:4073]. Arthritis Rheum. 2004;50:1172-1178.
16. Gocker B, Demirag MD, Block JA. Lateral wedge orthotics delay progression of joint space narrowing in patients with medial knee osteoarthritis. Arthritis Rheum. 2008;58(suppl):S241.
17. Bullough P, Goodfellow J, O’Connor J. The relationship between degenerative changes and load-bearing in the human hip. J Bone Joint Surg. 1973;55B:746-758.
18. Loeser RF, Shakoor N. Aging or osteoarthritis: which is the problem? Rheum Dis Clin North Am. 2003;29:653-673.
19. Slemenda C, Heilman DK, Brandt KD, et al. Reduced quadriceps strength relative to body weight: a risk factor for knee osteoarthritis in women? Arthritis Rheum. 1998;41:1951-1959.
20. Segal NA, Torner JC, Felson D, et al. Effect of thigh strength on incident radiographic and symptomatic knee osteoarthritis in a longitudinal cohort. Arthritis Rheum. 2009;61:1210-1217.
21. Segal NA, Glass NA, Torner J, et al. Quadriceps weakness predicts risk for knee joint space narrowing in women in the MOST cohort. Osteoarthritis Cartilage. 2010;18:769-775.
22. Arnoldi CC, Linderholm H, Müssbichler H. Venous engorgement and intraosseous hypertension in osteoarthritis of the hip. J Bone Joint Surg. 1972;54B:409-421.
23. Radin EL. Osteoarthrosis—the orthopedic surgeon’s perspective. Acta Orthop Scand Suppl. 1995;266:6-9.
24. Hunter DJ, Niu J, Zhang Y, et al. Altered perfusion and venous hypertension is present in regions of bone affected by BMLs in knee OA. Osteoarthritis Cartilage. 2007;15(suppl C):C171.
25. McAlindon TE, Watt I, McCrae F, et al. Magnetic resonance imaging in osteoarthritis of the knee: correlation with radiographic and scintigraphic findings. Ann Rheum Dis. 1991;50:14-19.
26. Dieppe P, Cushnaghan J, Young P, kirwan J. Prediction of the progression of joint space narrowing in osteoarthritis of the knee by bone scintigraphy. Ann Rheum Dis. 1993;52:557-563.
27. Lo G, Hunter D, Nevitt M, et al. Strong association of meniscal maceration and bone marrow lesions in osteoarthritis. Arthritis Rheum. 2007;56(suppl):S125.
28. Felson DT, McLaughlin S, Goggins J, et al. Bone marrow edema and its relation to progression of knee osteoarthritis. Ann Intern Med. 2003;139(5, pt 1):330-336.
29. Lafeber FP, Intema F, Van Roermund PM, Marijnissen AC. Unloading joints to treat osteoarthritis, including joint distraction. Curr Opin Rheumatol. 2006;18:519-525.
30. Intema F, van Roermund PM, Castelein RM, et al. Joint distraction in the treatment of knee osteoarthritis: the first clinical results. Osteoarthritis Cartilage. 2007;15(suppl C):C234.
31. Mazzuca SA, Brandt KD, Chakr R, Lane KA. Varus malalignment negates the structure-modifying benefits of doxycycline in obese women with knee osteoarthritis. Osteoarthritis Cartilage. 2010;18:1008-1011.