Prevention of chronic pain, a human systems approach, coming to you from the University of Minnesota. We're continuing part B, tracing the mechanisms of chronic pain. This is module six. Arthritis, pathophysiology, and risk. There can be many causes of joint pain. From injuring joint structures, such as a meniscus or an ankle ligament, to an infection or a disease process. Here, we have chosen to use, to describe osteoarthritis as a mechanism of joint pain. A very common condition with no immediate remedy. I am Kathy Anderson, a physical therapist and faculty member in the program of physical therapy. The department of Physical Medicine and Rehabilitation in the medical school here at the University of Minnesota. My teaching, clinical, and research interests are in musculoskeletal rehabilitation. Let's review the expectations and understandings for this model. Within the context of this course on chronic pain, some of the overall objectives are to be able to recognize the clinical manifestations, the prevalence, and the impact of common pain conditions and to be aware of ways to enhance wellness. This module has four parts: the clinical characteristics of arthritis pain, risk and protective factors, strategies to manage arthritis pain, and screening for functional mobility. By the end of this module, you'll be able to describe the presentation and clinical findings in osteoarthritis, recognize risk and protective factors for arthritis, discuss strategies to manage arthritis pain, and asses your own functional mobility. Part 1: Clinical Characteristics of Arthritis Pain. Again, recall that this content relates to osteoarthritis. A basic understanding of this process will aid in understanding risk and protective factors for this cause of joint pain. Joints allow us to move our body from place to place. Position our eyes to scan the horizon, and position our hands to manipulate objects. They experience forces from the ground, our body weight and any objects we lift or carry. And they experience these forces while they are moving. Each joint has common parts and tissues. Here, we will use the knee as an example to review. We see the bone as the body framework, although we know it's active in other physiologic processes as well. Here we have the femur and the thigh, the tibia in the leg. Muscles and tendons, here the quadracepts act to move the body through the joint. The joint itself has a capsule, which contains the joint space. A synovial membrane lining the joint cavity which regulates the fluid for nutrition and lubrication of the joint surfaces, and variable internal structures for stability and motion regulation, such as the menisci here in peach, in the knee. And the covering of the bone, the cream color here, the cartilage. This covering is present on all healthy weight-bearing surfaces. Here, we have a slide of the normal articular cartilage stained for better visualization. Note, the smooth surface along the joint lubricated with synovial fluid. Allowing smooth movement between the joint surfaces. This tissue is designed to withstand high compressive loads. It has a few cells, 2 to 5% of the volume, called chondrocytes. Which excrete and manage the extra cellular matrix. Responsible for the cartilage tissue characteristics. The cells respond to intermittent dynamic loading to maintain adequate thickness and the health of the matrix. The matrix is a gel substance of fluid with macromolecules of collagen and proteoglycans. The proteoglycans are hydrophilic attracting and keeping water, and the collagen is a structural protein that provides tensile strength. This tissue has no blood supply, so it relies on diffusion of nutrients from the synovial fluid. It also has no nerve supply. Osteoarthritis is characterized by the gradual failure of the cartilage in the joints with resulting pain and deformity. As the cartilage fails, the bone beneath the joint experiences more compression. The capsule and other joint structures also increase, experiencing increased stress. Joints commonly affected are hips, knees and the spinal joints, but other joints, such as the fingers, can develop arthritis as well. Reported revelence, prevalence rates vary based on the criteria of the study. The Arthritis Foundation reports that 27 million Americans have this condition. Other sources report a rate of 11% of the adult population with hip and 24% with knee osteoarthritis. 6% of adults over 30 are reported to have symptomatic OA. The condition is age related. With osteoarthritis being the most common cause of disability in the elderly population. Normal healthy cartilage is maintained by the chondrocytes in response to dynamic loading. There's a normal balance between the breakdown of old components, and lay down of new matrix, as there are in most tissues of the body. However, during one's lifetime, the stress, and the stiffness and strength of the cartilage decreases. Other factors such as direct injury contribute further to a loss of balance between the breakdown of the old and repair and replacement. As the tissue has no direct blood supply, repair of large lesions is not observed. As we mentioned previously, the cartilage experiences ground reaction forces, gravitational forces and muscle forces. How the cartilage responds to these forces varies by the health of the tissue, the body mass, the rate of loading, and the joint position and congruity of the surfaces. Or how the forces are distributed over the cartilage. Detrimental factors can be excessive static loads. Too rapid of cycling over too long a period of time, with repetitive loading. A sudden rate of loading that exceeds the ability of the tissue to deform. And asymmetric loading with poor force distribution. Major emphasis has been placed on the biomechanical factors linked to cartilage degeneration and understanding osteoarthritis. As opposed to the biochemical factors of other arthritic conditions, such as rheumatoid arthritis. However, we are becoming increasingly aware that multiple factors are contributing to the clinical manifestations of osteoarthritis. Pro-inflammatory cytokines and mediators, such as tissue necrosis factor alpha, interleukins 1 and 6, have been implicated in the breakdown of the cartilage, and in sensitizing pain receptors in the joint tissues in OA. Not only is tissue level injury, the biomechanical factor, related to osteoarthritis, but also biochemical plack, factors play a role. It appears there are variations in the relative contributions of these complex factors across individuals, and work continues to further understand these relationships and target therapies more specifically. Now that we have a better understanding of the etymology of osteoarthritis, let us turn to the clinical presentation. What do we and our patients experience with osteoarthritis? Two basic complaints are characteristic, the first is pain. In the earlier stages, pain may be experienced only with the particular aggravating activities that stress the involved joint. In the hands that can be gripping activities. In the legs it might be climbing stairs or prolonged standing. Often, the pain is relieved with rest. As the condition progresses, however, pain may be present at rest, after use, or with lying on the limb at night. Stiffness is the second common complaint. Present after periods of rest or disuse, such as first getting up in the morning or after sitting a while, this is usually relieved with activity within 30 to 60 minutes. [BLANK_AUDIO] Those with OA also experience limitations in activities due to a combination of pain, stiffness, actual loss of motion and related weakness and deconditioning. Common complaints with hip and knee osteoarthritis are difficulty climbing stairs. Getting in and out of a car, housekeeping tasks, dressing, and walking. Observable clinical signs in the condition as the condition progresses, includes joint deformity and enlargement. Initially, as cartilage degenerates, the joints experience increased motion or laxity, and in response, the body lays down more bone. Here, we can see the bony flare at the finger joints. [BLANK_AUDIO]. At the knees, when the the medial compartment is affected, varum can be noted or curving in towards the midline. Eventually, the extra bone as well as cartilage and capsular changes lead to a loss of motion. This increases the functional limitation, such as one that can knee cannot bend enough to get into the car comfortably. There are characteristic changes noted on medical images. On the left is a radiograph of a healthy knee. Note the apparent space between the fibia, the femur and the tibia. These spaces are actually filled by joint cartilage which is not visible on this type of image. However, on the right we can see the absence of space indicating a loss of cartilage on the medial side. You can imagine that now the knee shows a varus alignment, or a curving in towards the midline. Other findings such as osteophytes, or extra bone at the joint margins, and a hardening of the bone under the degenerative cartilage, or sclerosis, occurs due to increased forces that the subchondral bone experiences. This stress is probably one of the pain generators in osteoarthritis, as we know the bone is innervated. Here, we see the degenerative changes in cartilage in osteoarthritis. At the edge of the joint, the edge of the joint surface is no longer smooth, but fraying and fibrillating. There's a large cleft in the tissue and the chondrocytes are clumped, not dispersed within the matrix. [BLANK_AUDIO]
