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Knee Problems: Arthritis

What is Arthritis?

Osteoarthritis (OA), or perhaps more correctly osteoarthrosis, is a complicated disease, involving the articulating cartilage, synovial membrane, and subchondral bone. The causes of osteoarthritis are not well understood. Although ageing is the factor most strongly associated with OA, it is important to understand that OA is not a normal consequence of ageing. However, previous injuries and consequent damage to articulating cartilage will result in "accelerated" wear and tear of articulating surfaces. There may be a genetic tendency in some people that increases chances of developing osteoarthritis.

Osteoarthritis (OA) was found in “Java man”, one of our earliest known ancestors (ca 500,000 years ago). However, from a medical perspective, OA as a clinical entity was not separated from other arthritides such as rheumatoid arthritis until 1859 by Garrod. In addition, OA did not receive its name until 1888 from John Kent Spender, a physician in Bath, England, who also used the same terminology for a variety of rheumatic conditions (Altman et al., Osteoarthritis and Cartilage, Volume 15, Supplement 1, 2007).

The pathophysiology of osteoarthritis (OA) is also incompletely understood. The currently accepted model, with pathologic processes centered primarily at the level of the articular cartilage, does not define many of the findings of OA, such as bone marrow edema in subchondral bone observed on MRI in affected joints. Hyaline articular cartilage loss is a signature event in osteoarthritis. Its loss is a central necessary piece of the disease puzzle but not the only piece. Felson et al. defined a relationship between knee pain and bone marrow lesions observed on MRI (Ann Intern Med. 2001; 134:541), in which bone marrow lesions on MRI were present in 77.5% of patients with painful knee OA compared to only 30% of patients with painless knee OA. Expanding the concept that other aspects of knee OA can be mechanistically modeled at the level of subchondral bone rather than the articular cartilage, Felson et al. seek to show a relationship between bone marrow edema, mechanical malalignment and risk of progression of OA of the knee (Jon Giles, M.D.: Does bone marrow edema predict progression of knee osteoarthritis? Ann Intern Med. 2003; 139:330).

OA is estimated to be the eighth most common cause of disability worldwide, and in the US it is the leading cause. According to the World Health Organization (WHO) worldwide estimates are that 9.6% of men and 18.0% of women over 60 years of age have symptomatic OA. WHO also estimates that 80% of those with OA have limitations in movement and 25% cannot perform the major daily activities of life.

New treatment approaches have been aimed at inhibiting the breakdown of articular cartilage by mechanisms such as matrix metalloproteinases, or at stimulating repair activity with chondrocytes. Although a number of agents are being studied, none have been shown to be disease-modifying osteoarthritis drugs (DMOADs) in humans, and none have been approved. Some physicians go as far as saying drug treatment may not be the best option for OA, as it is both a biochemically and mechanically mediated disease.

Arthritis and Pain

It is not clear where pain in osteoarthritis comes from. Worn out articulating surfaces, which are often blamed for the onset of arthritis, do not hurt as articular cartilage is aneural and avascular (which is not entirely true). However, the supporting subchondral bone is the most likely source of pain, not only on weight bearing but also at rest, possibly because of local intra-osseous hypertension and venous congestion. Swollen joints also hurt because of the distension of the joint lining (synovium).

In athletes and younger adults who do not have osteoarthritis, traumatic knee injuries produce high signal MRI lesions in the medullary space extending to subcortical bone (bone bruising and bone marrow oedema). These lesions are thought to represent contusions within the bone marrow and have been correlated with the occurrence of pain in athletes. Bone marrow lesions that are similar in appearance to those contusions have been noted in patients with knee osteoarthritis, but their association with the occurrence of pain in this disease is unknown. Felson and collaborators have reported that bone marrow lesions on MRI are strongly associated with the presence of pain in knee osteoarthritis.

There are two related but different terms which define pain: nociception and pain. Nociception is a neurophysiological term and describes the activity in a nerve pathway which transmit signals from a potentially noxious stimulus but is not always perceived as painful. The term pain is used to describe the subjective experience that accompanies nociception, but can also arise without a stimulus and includes the cognitive and emotional response. From a research perspective, pain associated with osteoarthritis (OA) presents a number of dilemmas that demand further consideration. First, not all OA causes pain and it is not possible to predict with any degree of precision who will experience pain in the presence of joint degeneration. Secondly, the pain associated with OA has been shown to be reduced using techniques of placebo surgery, implying that not all the benefit seen following operations can be attributed to the technical process alone. Finally, more than one in ten patients who undergo joint replacement continue to experience pain attributed to the affected joint (Gwilym et al.).

Findings of a new study (Fiorentino et al.) suggest that pain is not merely a symptom of arthritis but rather a cause of the condition! The researchers from the University of Rochester School of Medicine and Dentistry and the University of Torino, Italy, said new treatments may seek to interrupt “crosstalk” between joints and the spinal cord. More specifically, the study, which appears in the October issue of Arthritis & Rheumatism, suggested that pain signals originating in arthritic joints — and the biochemical processing of those signals as they reach the spinal cord — worsen and expand arthritis. Researchers reported that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends, according to the press release. The current study provides strong evidence that two-way, nociceptive crosstalk may first enable joint arthritis to transmit inflammation into the spinal cord and brain and then to spread through the central nervous system from one joint to another. Armed with the results, researchers have identified likely drug targets that could interfere with key inflammatory receptors on sensory nerve cells as a new way to treat osteoarthritis (Source: ORTHO SuperSite, October 2, 2008).

Further information:

Where does OA pain come from?

Again, this is still not clear but we will try to add a few more thoughts from the literature. Experimental and clinical observations suggest that the structural integrity of articular cartilage is dependent on normal subchondral bone turnover, intact chondrocyte function and ordinary biomechanical stresses. An increasing line of evidence suggests that there are strong communication and interaction between the subchondral bone and the articular cartilage. As bone and cartilage are closely interrelated, interventions affecting pain related to bone turnover may, in addition, be related to pain relevant to osteoarthritis. Pain is a central part of the clinical presentation of OA and the main reason for patients to seek consultation. Many and diverse structural features of the joint have been suggested to be involved in OA-associated pain, including, but not limited to, the presence of osteophytes in the patellofemoral compartment, focal or diffuse cartilaginous abnormalities, subchondral cysts, bone marrow oedema, subluxation of the meniscus, meniscal tears and Baker cysts. The literature also suggests an association of capsular distention with knee pain (an association of effusion with knee pain)

In athletes and younger adults who do not have osteoarthritis, traumatic knee injuries produce high-signal lesions in the medullary space extending to subcortical bone. These lesions are thought to represent contusions within the bone marrow and have been correlated with the occurrence of pain in athletes. Bone marrow lesions that are similar in appearance to those contusions have been noted in patients with knee osteoarthritis, but their association with the occurrence of pain in this disease is unknown.

Bone, and especially the subchondral bone plate, is involved in the pathogenesis of osteoarthritis. OA bone tissue is sclerotic yet undermineralized indicating abnormal bone cell metabolism. Studies in both human and animal models of OA support the concept that bone sclerosis could precede cartilage degradation and loss. Thus, subchondral bone sclerosis in OA may be due to abnormal osteoblasts characterized by increased metabolic activities that result in an increase in osteoid matrix that is undermineralized.

The correlation of bone marrow lesions with pain in knee OA has been convincingly established. Here, another compelling association is established between bone marrow (oedema) lesions and risk for progression of knee OA. What remains to be established is the cause-and-effect relationship between the various variables. For instance, whether an initial insult to articular cartilage leads to mechanical malalignment and subsequent subchondral bone destruction or rather subchondral bone damage leads to mechanical malalignment and subsequent articular cartilage destruction is not explained by the current analysis. In addition, the evolution and natural history of the baseline bone marrow lesions on follow-up MRI studies with respect to progression of knee OA has yet to be investigated. It is interesting to note that, histologically, the lesions that appear as bone marrow edema on MRI contain very little edema at all. Rather, they demonstrate fibrosis, osteonecrosis, and extensive bony remodeling and are likely the result of contusions and focal micro-fractures. These data contribute to a new understanding of the natural history of knee OA and suggests new areas of investigation and alternative treatment modalities to the few currently available.

Normal adult human articular cartilage is thought to be avascular and aneural. However, very recently, sympathetic and sensory nerves were both found to be present within vascular channels in articular cartilage in both mild and severe OA. Perivascular and free nerve fibres and nerve trunks have also been observed within the subchondral bone marrow and within the marrow cavities of osteophytes. Nerve endings localised in damaged human articular cartilage suggest that vascularisation and the associated innervation of articular cartilage may contribute to tibiofemoral pain in OA across a wide range of structural disease severity. The implications of these findings are that the musculoskeletal pain associated with osteoarthritis may result from a combination of the hitherto accepted central and bone-derived effects. A mechanism-based understanding of the factors involved in generating OA pain has gained acceptance and will further develop the area.

Arthritis and Weight

Joint pain is strongly associated with body weight. Being only 10 pounds overweight increases the force on the knee by 30-60 pounds with each step. Being overweight is a clear risk factor for developing OA. However, it is unclear exactly how excess weight influences OA. Being overweight increases the load placed on the joints such as the knee, which increases stress and could possibly hasten the breakdown of articular cartilage. Data from the first National Health and Nutrition Examination Survey (HANES I) indicated that obese women had nearly 4 times the risk of knee OA as compared with non-obese women; for obese men, the risk was nearly 5 times greater. Even small amounts of weight loss reduce the risk of developing knee OA. Preliminary studies suggest weight loss decreases pain substantially in those with knee OA. Thus, weight loss potentially offers an important modifiable factor in the behavioral treatment of knee OA.

Christensen and collaborators analysed the effect of rapid diet-induced weight loss on the knee function of 80 obese patients with knee osteoarthritis. They conclude: "We found that an 8-week program with a 10% weight loss gave a highly significant increase in function (28%) in obese patients with knee OA. As the patients show a corresponding reduction in their risk of other health problems as well, weight loss is proposed as a first-choice therapy for knee OA."

  • R. Christensen, et al. Weight loss: the treatment of choice for knee osteoarthritis? A randomized trial. OsteoArthritis and Cartilage (2005) 13, 20-27

Arthritis and Exercise

Evidence clearly shows that patients with osteoarthritis benefit from physical activity. Maintenance of existing function is paramount in caring for patients with osteoarthritis. Increasing physical activity of patients with knee osteoarthritis, in addition to pain reduction, may afford cardiovascular and other health benefits.

Further information:

Arthritis and Unloading (Valgus) Bracing

Osteoarthritis typically involves destruction of articular cartilage and subchondral bone with consequent loss of joint height and repetitive mechanical friction. The medial compartment is the most frequently affected side of the knee. Increased loading of the medial compartment is easily recognized by the bow-legged or varus knee deformity. Wearing an unloading brace may improve gait symmetry, decrease symptomatic pain, and increase activity for patients who have osteoarthritis of the knee or other varus knee deformities. Brace use may contribute to improved knee proprioception, gait parameters, and pain scores.

Further information:

APOS Treatment for Knee Pain

APOS non-surgical medical treatment can reduce your pain and restore your function, simply by walking. The personalised, patented, APOS Walkright system does the work, with minimal impact on your daily routine and a very high rate of success. Read more. APOS is now available for the first time in the UK exclusively at the Bupa Wellness Centres in Reading and Solihull. Further information:

Arthroscopic Surgery for Arthritis

A new study published in The New England Journal of Medicine finds that arthroscopic surgery provides no additional benefit to physical therapy and medication for the treatment of knee osteoarthritis. The take-home message of this study is that for patients with X-ray evidence of moderate to severe arthritis of the knee, arthroscopy added no clinical benefit over and above best medical and physical therapy management. However, in response to the NEJM article, Jack M. Bert, MD, president of the Arthroscopy Association of North America (AANA), said: " Therefore, in joints with mechanical symptoms, including locking, catching or giving way, arthroscopic removal of loose bodies, chondral flaps and/or unstable meniscal tissue, debridement of the arthritic joint improves symptoms, prolongs the need for TKA and clearly is indicated."

The New England Journal of Medicine has previously reported a trial in which patients were randomised to debridement, lavage, or placebo surgery (in which a small incision was made but no instruments inserted). During two years' follow up there was no difference in the three groups. The randomised, placebo controlled trial to evaluate the efficacy of arthroscopy for osteoarthritis was conducted with 180 patients by researchers from the US Department of Veterans Affairs, Baylor College of Medicine and International Survey Research, both in Houston, and Laguna Honda Hospital, San Francisco. Both real and placebo surgeries were performed by Dr Bruce Moseley, a clinical associate professor of orthopaedics at Baylor College. Ethical issues were critically assessed by Dr Baruch Brody, director of the Center for Medical Ethics and Health Policy at Baylor College. The trial also raises the question of whether all surgical procedures should be tested against placebo.

Further information

  • American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Recommendations for the Medical Management of Osteoarthritis of the Hip and Knee. Arthritis & Rheumatism, September 2000.
  • All About Arthritis. The All About Arthritis website is sponsored by DePuy Orthopaedics, a Johnson & Johnson company, to provide arthritis patients, their families and their caregivers with a trusted source of arthritis information.
  • As surgery is not an answer to all arthritis problems we recommend this book for guidance on alternative therapies: Judith Horstman. The Arthritis Foundation's guide to Alternative Therapies. An official publication of the Arthritis Foundation. Buy this book from

Page last updated on: 13 May 2018

Site last updated on: 28 March 2014

Disclaimer: This website is a source of information and education resource for health professionals and individuals with knee problems. Neither Chester Knee Clinic nor Vladimir Bobic make any warranties or guarantees that the information contained herein is accurate or complete, and are not responsible for any errors or omissions therein, or for the results obtained from the use of such information. Users of this information are encouraged to confirm the accuracy and applicability thereof with other sources. Not all knee conditions and treatment modalities are described on this website. The opinions and methods of diagnosis and treatment change inevitably and rapidly as new information becomes available, and therefore the information in this website does not necessarily represent the most current thoughts or methods. The content of this website is provided for information only and is not intended to be used for diagnosis or treatment or as a substitute for consultation with your own doctor or a specialist. Email addresses supplied are provided for basic enquiries and should not be used for urgent or emergency requests, treatment of any knee injuries or conditions or to transmit confidential or medical information. If you have sustained a knee injury or have a medical condition, you should promptly seek appropriate medical advice from your local doctor. Any opinions or information, unless otherwise stated, are those of Vladimir Bobic, and in no way claim to represent the views of any other medical professionals or institutions, including Nuffield Health and Spire Hospitals. Chester Knee Clinic will not be liable for any direct, indirect, consequential, special, exemplary, or other damages, loss or injury to persons which may occur by the user's reliance on any statements, information or advice contained in this website. Chester Knee Clinic is not responsible for the content of external websites.

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