Knee malalignment that places the joint into a varus position can increase loading on the medial side of the joint. Static alignment alone does not predict incidence of OA. The M add is produced when the foot is in contact with the ground and the line of action of the force vector passes medial to the knee joint.
An increased distance between the force vector and the knee joint will result in a higher M add and greater loading on the medial joint. Varus alignment will cause the knee joint to move laterally relative to the position of the foot on the ground, which increases the M add.
On the contrary, shifting the position of the trunk laterally can move the line of action of the ground reaction force more medial, which can decrease the M add moment. In persons with OA, however, the cartilage is thinnest in persons with the highest M add. Increasing gait speed increases the ground reaction force, and net joint forces and moments experienced at the joint level.
Individuals with OA walk more slowly compared to asymptomatic controls, which presents a confounding factor when interpreting studies where subjects walked at a self-selected speed.
In most studies, 27 , 28 with the exception of Zeni and Higginson, 29 the changes in M add are not completely explained by gait speed and seem to indicate that some fundamental gait adaptation has occurred to attempt to unload the medial compartment of the knee. At least seven assisted gait modifications can reduce the peak M add , including the use of lateral wedge insoles, 30, 31 lateral wedge insoles combined with subtalar strapping, 32 variable stiffness shoes with softer medial sides, 33 or high mobility shoes that act similarly to natural foot flexibility , 34 valgus knee braces that use three point bending, 35 , 36 canes, 37 and hiking poles to offset the M add generated by the opposite knee.
The ultimate goal of reducing the peak knee adduction moment is to reduce peak medial contact force during stance phase. For gait tests performed to date, variable stiffness shoes and valgus knee braces have produced the largest reductions in medial contact force. Though walking with knees medialized and with hiking poles reduced the first and largest peak of medial contact force by only a small amount, these gait modification methods reduced medial contact force significantly over the rest of stance phase Furthermore, elimination of excessive knee flexion during mid stance may make these two methods effective at reducing the first peak as well While these collective data do not show a causative effect of the M add on the development of knee OA, strategies to modify the biomechanical mechanisms involved in symptomatic knee OA were obtained.
While high tibial osteotomy surgery can significantly reduce the peak M add 40, gait modification may be a non-invasive alternative.
The best outcome of gait modification would be to reduce the peak M add similar to that achieved after a high tibial osteotomy surgery. A number of studies have evaluated the ability of these different gait modification methods to reduce the peak M add. Gait modifications that can reduce the peak M add include walking with decreased speed 41 , 42 widening base the base of support at stance, 43 pointing toes outward 12 , 44 , 45 medializing the knees, 39 , 46 , 47 and increasing the magnitude of medial-lateral trunk sway.
There are several important considerations when interpreting data from gait modification research. For example, in a study that explored the effectiveness of walking with knees medializing or hiking poles on peak M add 39 both modifications produced little change in peak medial contact force, despite significant reductions in the peak M add. Second, beneficial changes at the knee could induce detrimental changes at other joints Such changes are most likely to occur at the ankle or the lower back, where load changes are the largest depending on the gait modification.
Because ankle OA induced by lateral heel wedges has not been reported, it is unlikely that gait modifications that alter ankle loads will be detrimental. Third, different M add calculation methods yield different interpretations of the effectiveness of a particular gait modification Many studies do not provide details of how the peak M add was calculated, making it difficult to compare results from different studies.
Furthermore, several studies have suggested that the knee adduction angular impulse, which is the area under the knee adduction moment curve during stance phase, may be a better clinical target than M add 16 , 52 , The concepts relating to OA and altered biomechanical parameters between two articular surfaces might be applied to joint degeneration in other joints or in medical conditions such as the following:.
Among lower extremity rehabilitating populations, those with transtibial amputations demonstrate biomechanical alterations that contribute to OA onset in the intact limb. Some prosthetic foot characteristics significantly affect the M Add of the intact knee during gait. Once this occurs, the contact area and motion increase frictional shear stress that facilitate OA onset. Over time, the repetitive stressors with average weight-bearing activity can exacerbate frictional stress within the hip joint, causing premature cartilage breakdown and OA.
Hip OA onset might be related in part to participation in high performance competitive sport such as javelin and high jump. These sport motions induce high moments with high velocity rotation within the hip. Cross sectional data of these athletes 10 years after retirement from their sport revealed that the odds risk of developing OA was 6. In patients with spinal cord injury, the mechanical loading of upper limb joints is significantly altered compared to pre-injury.
Signs and symptoms of mechanical overuse appear over time and can manifest as secondary arthritis. While prospective data are sparse for elbow OA, the prevalence of the condition is heaviest in heavy manual laborers, weight lifters and throwing athletes.
Biomechanical alterations to joint motion and force are also evident in the ankle and foot in dancers. The foot and ankle are vulnerable to repetitive microtrauma during dance. The prevalence of joint degeneration was found to be higher in a group of retired professional ballet dancers compared with controls. Furthermore, these joints are rotated into positions in the extreme ranges of motion and this causes a valgus deformity. Knee kinematics play an important role in the development and degradation of articular cartilage.
Healthy cartilage responds to loading by adapting its morphology and mechanical characteristics in the areas of greatest stress. However, once normal joint kinematics are altered, loading shifts to areas which are not well suited to accommodate the increased stress. Once the OA cycle has been initiated, the loading that once facilitated cartilage adaption, now serves to facilitate the progression of cartilage degradation.
By changing pathological joint mechanics, gait modification may have disease modifying potential for medial compartment knee OA, at least in terms of slowing progression of the disease.
Summary of the knee adduction moment M add and internal tibiofemoral rotation about the knee during loading in ambulation in healthy knees and knees with medial OA frontal view. Forces and rotation are shown relative to the X,Y,Z coordinate system. The thicker the arrows, the greater the forces or rotation.
Higher M add and internal rotation increase medial contact force; over time, the cartilage degenerates and OA develops and progresses. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication.
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See other articles in PMC that cite the published article. Abstract Osteoarthritis OA is the most frequent cause of disability in the United States, with the medial compartment of the knee being the most commonly affected. Keywords: kinematics, knee, osteoarthritis, gait.
Introduction Osteoarthritis OA is condition with a multifaceted etiology and afflicts both load bearing and non-weight bearing joints. Setting the Stage With normal aging, cartilage breakdown begins in joint areas with little or no contact. Tibiofemoral Rotation The knee joint is commonly thought of as a hinge joint with pure hinge-like motion.
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Received Jun 26; Accepted Jul This article has been cited by other articles in PMC. Abstract As the most common chronic degenerative joint disease, osteoarthritis OA is the leading cause of pain and physical disability, affecting millions of people worldwide. Keywords: osteoarthritis, pathogenesis, experimental model, disease modifying osteoarthritis drugs, microphysiological systems.
Introduction Existing since ancient times and officially named and defined in the 19th century [ 1 ], osteoarthritis OA has been the most common degenerative joint disease. Risk Factors The known risk factors of OA include aging, obesity, genetic predisposition, acute trauma and chronic overload, gender and hormone profile, and metabolic syndrome [ 22 , 23 ] Figure 1. Open in a separate window. Figure 1. Aging Aging, characterized by the progressive loss of tissue and organ function over time, represents the single greatest risk factor for OA [ 25 ].
Trauma Traumatic injury often causes joint instability or intraarticular fractures, causing post-traumatic osteoarthritis PTOA. Genetics OA is considered a multifactorial polygenic disease that is influenced by multiple genetic and environmental factors [ 76 ]. Figure 2. Table 1 Regulatory pathways mediating chondrocyte functions. Pathway Cells Studied Effects Ref. Notch Signaling Pathway Notch receptors are large single-pass transmembrane proteins that regulate differentiation and apoptosis during embryogenesis and postnatal development through binding to transmembrane ligands expressed on adjacent cells [ , ].
Experimental Models Experimental models are critical for the study of human diseases. In Vivo Models The OA risk factors discussed above have been recapitulated in different types of animal models Table 2. Table 2 Advantages and limitations of current animal models for studying OA.
Trauma-Induced OA Models In trauma-induced models, an injurious event, typically instability caused by disrupted joint mechanics, precedes joint arthritis pathogenesis. Obesity-Induced OA Models Higher OA incidence in obese people is attributed to not only excessive joint loading caused by increased body weight, but also the associated systemic inflammation, dysregulated lipid metabolism, and altered adipokine profile [ , ].
Chemically Induced OA Models Several chemicals, including monosodium iodoacetate MIA , papain, collagenase, and quinolone, have been proposed to induce OA in animal models, with MIA being the most commonly used chemical agent to induce OA in mouse and rat models [ , , , ].
OA Models Involving Genetic Manipulations Genetically modified models for OA research are predominantly established in mice because of their short life cycle, high fecundity, breeding efficiency, and being amenable to genetic manipulations [ ].
In Vitro Models While biomedical research has been greatly enhanced over the past decades with the use of mammalian animals as a replacement for human subjects, there are also significant limitations and disadvantages, including high costs and social and ethical issues, including the intrinsic genetic differences between human and animals. Table 3 Advantages and disadvantages of current in vitro models for OA research.
Monolayer Culture OA studies involving monolayer culture mostly employ chondrocytes, because degradation of cartilage, in which chondrocyte is the sole cellular component, remains a predominant OA symptom.
Tissue Explant Models Although the exact pathogenesis and etiology of OA are not completely understood, the metabolic state of articular cartilage and its crosstalk with other tissues are believed to play crucial roles in various proposed mechanisms. Microphysiological Systems A microphysiological system MPS , sometimes referred to as an organotypic culture model OCM , describes an in vitro platform that models human tissues by providing living cells, usually heterogenous in nature, with a microenvironment supporting specific structure and responses that define an organ or tissue.
Figure 3. Figure 4. Summary and Future Prospects The significant disease burden of OA and the accompanying compromise to the quality of life of OA patients notwithstanding, development of effective OA prevention and treatment methods have been largely unsuccessful.
Author Contributions Wrote the manuscript, Y. Conflicts of Interest The authors declare no conflicts of interest.
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Liu-Bryan R. Angiogenesis in the synovium is closely associated with chronic synovitis and may occur at all stages of osteoarthritis [ 51 ]. Meniscal degeneration is commonly seen in osteoarthritis, where menisci appear torn, fissured, fragmented, macerated or completely destroyed [ 52 ]. Degeneration of menisci initiates within the substance of the tissue rather than surface.
Tissue fibrillation and disruption is first seen at the inner rim, which spreads to the articular surfaces of the meniscus over time, and progresses to total disruption or loss of meniscus tissue mainly in the avascular zone [ 53 ]. Type I collagen content decrease gradually from the surface zone to the middle and the deep zone of osteoarthritic meniscus [ 54 ].
Different from type I collagen, the decrease of type II collagen content is severe in the surface zone, and also prominent in the middle and deep zones of osteoarthritic meniscus [ 54 ]. In turn, proteoglycan content increase in osteoarthritic menisci when compare to normal menisci [ 54 ].
All these intrameniscal changes correlated with peri-meniscal synovitis, calcification not limited to the outer, peripheral portion of the menisci [ 55 , 56 ] contribute to meniscal degeneration and reduced meniscal tensile strength. The meniscus is less able to withstand loading and force transmission during normal movements of the joint, further leading to degenerative tears [ 57 ].
Meniscal tears are often accompanied by varying degrees of meniscal extrusion [ 58 ]. The tear might be a preceding feature of incipient osteoarthritis, and meniscus damage and extrusion often have a key role in the structural progression of the disease [ 59 ].
In conclusion, osteoarthritis is a multifactorial disease of whole joint, with a complex pathomechanism involving interaction between the multiple joint tissue. Knowing of this complex process of producing osteoarthritis is essential for development of new methods of diagnostic and treatment. National Center for Biotechnology Information , U. Journal List J Med Life v.
J Med Life. Author information Article notes Copyright and License information Disclaimer. Received Sep 25; Accepted Jan 8. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been cited by other articles in PMC. Abstract Abstract Osteoarthritis is the most common joint disorder and a major cause of disability with a major socio-economic impact.
Keywords: osteoarthritis, cartilage, subchondral bone, synovium, menisci. Articular cartilage Normal adult articular cartilage is made up of extracellular matrix water, collagen, proteoglycans and a very small component of calcium salt and chondrocytes [ 12 ].
Subchondral bone It is not yet clear whether changes within subchondral bone precede changes in the articular cartilage or whether they occur in the disease progression, secondary to adaptation processes after changes in the biomechanical properties of the overlying articular cartilage.
Synovial membrane It remains unclear whether the morphological changes that occur in the osteoarthritic synovial membrane are primary or whether they are the result of joint inflammation, cartilage degradation and lesions of the subchondral bone [ 40 ]. Menisci Meniscal degeneration is commonly seen in osteoarthritis, where menisci appear torn, fissured, fragmented, macerated or completely destroyed [ 52 ].
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