Aug 15, Knee pain — Comprehensive overview covers symptoms, causes, treatment of this common joint condition. Arthritis of the knee is typically a particularly debilitating form of arthritis. The knee may become affected by almost any form of arthritis. The word arthritis refers to inflammation of the joints. Pharmaceutical; Orthostic; Lifestyle. Jan 9, Senior woman consulting with a doctor about her joint pain. Nearly million South Africans suffer from osteoarthritis, according to the way of carrying things : bend your knees instead of your back when lifting heavy stuff.
Knee inflammation 3.2 joint
Knee OA patients showed lower PPTs compared to the matched controls in all 24 muscular, ligamentous, and subcutaneous points tested, both at the knees and at distant sites Table 2. IL-6 and IL levels were significantly elevated in patients Table 3.
Correlation analyses of variables are given in Table 4. Stepwise analysis revealed that a combination of three variables added gain to the equation. OA patients presented spreading sensitization as assessed by pressure pain hyperalgesia from all the structures investigated. As an exploratory study, we have not corrected for multiple analyses, and therefore, for 30 comparisons, two positive results can be by chance.
Cytokines are glycoproteins of light molecular weight, responsible for the communication among cells of the immune system [ 29 ].
Classically, increased levels of proinflammatory cytokines are related to development and progression of OA due to upregulation of metalloproteinase gene expression, stimulation of reactive oxygen species production, alteration of chondrocyte metabolism, and increased osteoclastic bone reabsorption [ 15 , 30 — 33 ]. Several authors have described the association of disability, measured by the WOMAC scores, with higher levels of proinflammatory cytokines [ 14 , 15 , 18 , 34 ].
TNF has been compared to other proinflammatory cytokines and shown to be elevated in elderly patients with knee osteoarthritis [ 6 , 35 , 36 ].
Similar to previous reports [ 6 , 35 , 39 ], we observed that serum levels of IL-6 had a twofold increase in patients when compared to controls, comparable to a study that showed increased IL-6 in patients with more severe disease as measured by radiologic knee OA findings [ 6 ].
On the other hand, serum concentrations of the other cytokines are very heterogeneous to draw any conclusions. We also demonstrated that symptomatic patients presented less resistance to algometer-induced PPT than did the healthy controls in all 24 muscular, ligamentous, and subcutaneous points tested, not only at the knees. In fact, many have investigated the effect of different presentations of OA on the serum or intra-articular levels of cytokines [ 6 , 14 — 16 ].
However, to the best of our knowledge, this is the first report regarding the association between serum proinflammatory cytokines and PPTs that are located further beyond the painful area at the involved joint. This indicates a sclerotome-wide phenomenon that can be explained only neurologically.
Additionally, since cytokine IL was not detectable in the cerebrospinal fluid of patients with knee OA, the concept of central sensitization as an important mechanism in the causal chain of disability would be noteworthy [ 40 ]. Several authors have already demonstrated that proinflammatory mediators as interleukins are increased in fibromyalgia patients [ 41 , 42 ]. It seems that chronic pain, hyperalgesia, and fatigue are associated with increased levels of IL-6 and IL-8 in these patients [ 18 , 41 ].
Similarly, tissue lesion may, in most cases, not be the major issue determining loss of function and quality of life in OA. In subjects with spontaneous pain, areas distant from the site of pain also showed a significant increase of these chemical mediators [ 45 ]. Cytokine production has also been demonstrated in nonimmune tissue under special conditions such as acute inflammation.
However, the influence of hyperalgesia found in muscle tissues of patients with OA on serum cytokines has not been determined, although leaking from local microenvironment could be a possible mechanism. Still, we must remember that the process called inflammaging indicating a regulation of the inflammatory response that occurs with aging can result in the production of inflammatory cytokines, which generates a low level of chronic and systemic proinflammatory state [ 47 , 48 ].
This may occur due to the presence of chronic diseases associated with aging such as OA, as well as other conditions such as obesity and physical inactivity [ 47 ]. A possible source of local cytokine production, different from the inflammatory cells, may be the adipose tissue.
Yet increased production and secretion of proinflammatory cytokines biomarkers by adipose cells have been hypothesized as the role played by obesity as a risk factor for OA [ 50 ]. According to Livshits et al. In fact, we have recently demonstrated that aging may play a role in cytokine profile, a finding not so extensively addressed in the literature and that should be further investigated [ 51 ].
Francis Hospital in Mooresville, Ind. The findings were presented last month at the annual convention of the AAOS. I find that patients tend to be very good at deciding when they've reached that point.
Most orthopedic surgeons recommend knee replacements only after all other options have been explored. These options include rest, pain medication, cortisone shots, physical therapy, weight loss and arthroscopic surgery.
And some, mostly younger patients, may see good results with an osteotomy, surgery that shifts the alignment of the knees so that the weight-bearing part of the knee is moved away from diseased cartilage and onto healthier tissue. Lloyd Emanuel knew he had reached the point where he needed a replacement when even standing became painful. He's glad he finally had the surgery. There is no throbbing pain, I can sleep and I can play and teach tennis.
And I am getting better every day. Surgery to replace weight-bearing surfaces of a knee joint. The surgeon cuts away damaged bone, cartilage and one ligament, and replaces them with an artificial joint made of an alloy of cobalt, chrome or titanium, and a plastic compound called polyethylene. A total knee replacement replaces the entire joint; a partial knee replacement replaces only the damaged area. While a partial replacement can be done with minimally invasive surgery and has a speedier recovery time, only about 6 to 10 percent of patients are suitable candidates for this operation.
Partial knee replacements work best where damage to the knees is only in a small area [see "What to Expect After Surgery" ]. To improve mobility and decrease pain caused by degenerative arthritis or injury to the knee joint. Knee replacements are covered by Medicare and most private insurance. Hospital and surgeon costs vary widely, depending on the area of the country and the facility.
But experts say few hospitals actually get that much. Partial knee replacement surgery costs about half that of total knee replacement. Choose your surgeon and hospital wisely.
A study reported in the Journal of Bone and Joint Surgery found that patients operated on by surgeons who performed 50 or more knee replacements a year had a lower risk of complications than those whose surgeons performed 12 or fewer a year.
Patients who went to hospitals where more than procedures were performed a year also fared better than those who went to hospitals that did 25 or fewer a year. In , 63 percent of all knee replacement operations were performed on women. That may be because women over the age of 50 are more likely to develop osteoarthritis of the knee than men, experts say.
Capitalizing on this, some manufacturers are promoting "gender specific" knee replacement devices they claim are tailored to a woman's unique physiology. However, Sierra of the Mayo Clinic says that while there are some subtle differences in structure between men and women, "it really is size-specific, not gender-specific. Your surgeon," he says, "will measure you to get the right size" device. The hospital stay is usually about three days after a total knee replacement operation; one day with a partial replacement.
There is no cast, just a dressing covering the incision. After a total replacement you may need a short stay in a rehabilitation facility. Further, overweight young persons have only a modest risk of OA but older, overweight persons have a very high risk of knee OA. And the proportion of those with knee OA increases further when the person is not only obese and older but also female.
In considering causes of OA, I will contend that mechanical forces play a role in almost all OA but that they do not necessarily act by themselves in causing disease.
Causation is difficult to prove for complex noninfectious human diseases. Generally, proving causation requires an intervention in which a putative causal agent is added or removed and the organism followed to see if they develop disease. Ideally, animal models provide this opportunity, but in osteoarthritis, animal models test causal agents by inducing injury in a normal non-diseased joint and evaluate whether a causal or preventive agent prevents joint damage in the face of this injury.
This is not a model for most human osteoarthritis in which symptoms occur and patients present for treatment only after considerable joint pathology exists.
It is ethically impossible to test many causal agents in human osteoarthritis, so this review will infer causation when there has been a consistently found and temporally appropriate relationship between a risk factor e. To demonstrate the pivotal role of abnormal mechanics in causing OA, I shall make three arguments. First, abnormal mechanics cause OA both in animals and humans. Second, once OA has developed, abnormal mechanics overwhelms all other factors in terms of leading to disease worsening.
And third, inflammation in OA is mostly a consequence of abnormal mechanics and is almost never primary. This is not a systematic review but rather draws from selected research findings to make certain points. Further, except when specified, it focuses on structural disease as opposed to pain. Pain is often affected by psychosocial and other factors, making it harder to determine its causes. Among the best examples that abnormal mechanics can cause OA is the widespread use of surgically induced injuries that cause OA in animal models of disease.
These include ACL transection and meniscal injury models in numerous strains of animals. These knees were then compared to the contralateral unoperated knee and for each of the rabbits, histologic changes of cartilage degradation were far greater in the operated than in the unoperated limbs, suggesting that abnormal loading caused disease.
In humans there are many examples of major joint injuries or abnormally shaped joints producing high levels of focal stress across the joint causing OA. First it has been known for at least 60 years 1 that meniscal tears and meniscal removal lead to increased focal stress across the joint and subsequently high rates of OA. Menisci serve as washers to increase stability within the joint and to distribute load so that when the meniscus is intact, focal stress is kept at low levels 5.
When menisci are removed or even partially removed , injury to areas of the joint where the meniscus was removed is far more likely with one large follow-up study estimating that half the knees that underwent meniscectomy during young adulthood had evidence of radiographic osteoarthritis 21 years later vs.
In fact, in joints where the meniscus has been removed and most of it is gone, the only preserved area of cartilage is the small area of the joint where the meniscus remains 7. Tears of the anterior cruciate ligament are also associated with high rates of OA for reasons that are likely to do with increased compressive stress across the medial compartment of the knee where most of the disease in ACL tear patients occurs 8 , 9.
ACL tears are especially likely to lead to OA when accompanied by meniscal tears 8. While it has long been known that traumatic major tears of the meniscus in young athletes lead to high rates of later knee OA, recent evidence suggests that meniscal tears occurring in middle aged and older persons may be a common precipitant of disease.
Many of these persons did not recall any injury to their knees. Following those with incidental meniscal tears in a later cohort study, Englund et al then demonstrated that persons with tears and no other cartilage damage were at marked increased risk of developing cartilage damage and subsequent radiographic OA In fact, among knees with only incidental meniscal tears, the risk of developing OA within 30 months was increased fold compared to those without such tears A posterior medial meniscal tear increased the risk of only posterior cartilage loss, and a tear in the body of the medial meniscus increased the risk of only adjacent cartilage loss, suggesting that meniscal tear per se increased focal stress on the underlying cartilage in that small limited region.
Meniscal tears therefore appear to be a consequence of major trauma at a young age often as an injury during sports participation but occur with minor trauma in older years. Regardless of when those tears occur, they appear to markedly increase the risk of OA by increasing focal loading or stress across adjacent areas of cartilage, leading to cartilage breakdown and subsequent changes of OA.
These tears are common and confer an extremely high risk of later OA. Meniscal tears serve as one of the major pieces of evidence that abnormal mechanics causes OA. Meniscal tears are not the only common risk factor of mechanical basis that leads to high rates of knee OA. In recent work, Sharma et al. After adjusting for age, gender, body mass index and lateral laxity, varus knees had 3. This suggests, like the rabbit studies from Wu and colleagues, that malalignment causes increased stress across a focal area of the joint leading to damage there and subsequent disease.
Indeed, some incidence studies looking at malalignment have shown that varus malalignment is associated not just with cartilage loss but with high rates of radiographic OA and even symptomatic disease later 15 , If mechanical causes of knee OA are common, hip OA may serve as the best example whereby mechanical load or abnormal stresses cause almost all disease. There are at least two anatomic abnormalities that occur often in childhood that predispose to high rates of OA. On the one hand, dysplasia which can occur congenitally puts increased focal stress on a small area of the acetabulum which provides insufficient coverage for the femur.
Congenital dysplasia when severe is recognized often in infancy and corrected. When modest, it is uncorrected and increases markedly the risk of hip OA occurring at a young adult age. Further, Lane and colleagues 17 have shown that mild dysplasia even present in adulthood increases the risk of later life hip OA, a finding corroborated by other longitudinal studies.
A potentially more prevalent cause of increased focal stress across the hip is femoroacetabular impingement FAI. FAI consists of a variety of anatomic abnormalities, but the most common are cam and pincer deformities, which appear to be highly prevalent in young adults At work presented at the OARSI meetings, groups in the Netherlands 19 and investigators from the Chingford Study 20 , 21 convincingly showed that femoroacetabular impingement seen on x-ray in these studies markedly increases the risk of later clinical hip OA, of radiographic disease, and even of the likelihood of hip replacement.
Thus, evidence is quickly accumulating that anatomic abnormalities associated with femoroacetabular impingement are major risk factors predisposing to later-life hip OA, suggesting once again that mechanical abnormalities overwhelm others as causes of this disease.
If there is remaining doubt, one excellent example pointing to the importance of hip shape abnormalities is our understanding of why Chinese populations are only rarely affected by hip OA. In the Beijing OA Study, a population-based study of older adults from Beijing 22 , only one case of symptomatic hip OA was found among older subjects drawn from the city of Beijing. Over 25 such cases would be expected if rates in Beijing were similar to rates in Western populations.
In a study of non-diseased hips drawn from Beijing and from Western populations in which morphometry was assessed, Dudda et al. Surprisingly, evidence of mild dysplasia was, if anything, more common among Chinese.
Further, Chinese populations actually had higher rates of knee OA than did Western populations, suggesting that the low rate of OA in the hips was not a function of low generalized OA rates. Knee and hip OA are not unique in being strongly related to injury and mechanics. In joints rarely affected by OA such as the ankle, major injury accounts for almost all cases of disease While it is obvious that some mechanical abnormalities such as ACL and meniscal tears cause a subset of knee OA, the bigger question is whether mechanical factors account for almost all knee OA as they appear to do for hip OA.
Major risk factors for knee OA according to recent reviews include: Other than older age and female gender which increase the vulnerability of structures within the knee to injury, all of the factors that have been identified consistently represent types for mechanical overload. For knees, obesity represents chronic excess loading, whereas knee injury produces focal increased stress.
The risk of OA in joints in which there has been stereotyped repetitive use patterns typical of occupations has been well documented and represents another type of chronic excess load.
For example, cotton workers have a high rate of OA in their finger joints Miners have a high rate in their knees and spines, jackhammer operators experience excess rates of OA in joints that are very rarely affected by disease such as elbows, wrists and metacarpalphalangeal joints.
Farmers get high rates of OA in their hips and knees. One factor that is not on the list of causes of knee or other OA is inflammation. Even though isolated studies have reported that elevated C-Reactive Protein CRP levels are associated with certain phenotypes of OA, large-scale studies evaluating this question have been consistently negative.
Another piece of evidence that mechanical forces induce all or almost all human OA consists of data from genetic studies. While the heritability of OA is moderate, much of it is joint-specific. As documented by MacGregor and colleagues 29 , the genetic influence on radiographic OA is site-specific at hand, hip and knee, a finding that has been confirmed also in the Framingham Study Specifically, MacGregor et al.
Oct 4, Animal models of OA almost all rely on joint injury to induce disease. showed in a population-based sample recruited without reference to knee pain . for Special Surgery rating scale over an average of years follow-up. Chronic knee pain is long-term pain, swelling, or sensitivity in one or both knees. The cause of your knee pain can determine the symptoms you experience. Sep 27, OA is a chronic arthritic disease characterized by pain, local tissue damage abnormalities and painful knee OA with an odds ratio of .