Millican Osteoarthritis

This is an essay discussing osteoarthritis, which involves normal joint functioning before contracting the disease, its’ pathophysiology and associated symptoms regarding the disease.

Osteoarthritis (OA), also known as degenerative joint disease, is the most common joint disorder. It is characterized by a progressive loss of cartilage (, 2004). Just like what the name implies, osteoarthritis is mainly a disease involving the joints.  A joint or place of articulation is formed where 2 or more bones come in close contact in the body and are attached to each other by ligaments or cartilage (, 2002). There are three types of joints; they are classified according to the type of movement they follow. These are the synarthroses or immovable joints, ampiarthroses or slightly-movable joints and diarthroses or synovial joints (, 2002). Synovial joints, also known as, freely-movable joints, are the most common type of joint that is found in our body. As with most other joints in the body, synovial joints achieve movement at the point of contact of the articulating bones. Its main difference with the other type of joints is the presence of a ‘synovial fluid’ (, 2002), a fluid enclose in a capsule that permits an almost friction-free movement of bony ends against each other (, 2005). In studying osteoarthritis, it is important to know the joints involve in this disease. In this case, synovial joints are usually the most affected. An overview regarding the normal function of a synovial joint and the cartilage involve would be helpful in studying this disease.

 

Normal Structure and Function of a Synovial Joint

As stated earlier, a joint or place of articulation is formed where 2 or more bones come in close contact in the body and are attached to each other by ligaments or cartilage (, 2002). Synovial joints are highly-movable joints; they are equipped with special properties that other joints seem to be lacking. Basic structures include: (a) Articular cartilage, a layer of tissue that covers the ends of opposing long bones in our joints (, 2005). This layer permits almost friction-free movement of the bony ends against each other. Cartilage basically consists of two components: water and a framework of structural macromolecules (matrix) that give the tissue its form and function. The matrix is highly organized and composed of collagens, proteoglycans and noncollagenous proteins. The interaction of water and the macromolecular framework give the tissue its mechanical properties and thus its function. Up to 65% - 80% of the wet weight of cartilage consists of water; the rest is matrix, mainly collagens and proteoglycans. In case of elastic cartilage, elastic fibers are present that make the cartilage more flexible. Proteoglycan and noncollagenous proteins bind to the collagenous meshwork and water, attracted by negatively charged glycosaminoglycans, fills the molecular framework. Embedded in this tight matrix are the cells, called chondrocytes that take care of maintenance of the matrix. The volume of cells is rather small; In adult human cartilage for example, cells make up about 1-2% of the tissue volume. Chondrocytes are of mesenchymal origin and are responsible for extracellular matrix production. Cartilage is an avascular, aneural and alymphatic tissue. Nutrition of chondrocytes occurs by diffusion. (, 2005).

(b)  a joint capsule made of a tough membrane encloses the joint and connects one bone to another holding them firmly in place (, 2007).

(c) Synovium, the inner lining of the capsule which secretes synovial fluid to lubricate and nourish the cartilage (, 2007) furthermore, synovial fluid eases friction to prevent bones from rubbing in to each other. (d) Bursae, small, fluid-filled sacs positioned at strategic points to cushion ligaments and tendons, protecting them against friction and wear and tear (, 2007). And the usual properties of a joint like ligaments, tendons and muscles which are responsible for maintaining its structure and facilitate movements. Osteoarthritis can affect any joints in our body, though, it is usually more common to weight-bearing joints such as hips, knees, feet and spine, it is not systemic, it is usually localized to a certain joint. The articular cartilage of the synovial joint is the one usually involved in OA, damage in this area could lead to further joint degeneration. Damage in the cartilage could be of several causes and factors, all of which will be discussed in the review of pathophysiology of OA.

Pathophysiology of Osteoarthritis

Osteoarthritis (OA) has been classified as primary OA, idiopathic or of an unknown cause and secondary OA which is related to risk factors and other causes (, 2004). Secondary OA have a variety of causes that contributes to the development of symptoms. Causes such as (a) Genetic disposition is one of the main predisposing factors, incidence of OA is higher if there is a familial history and also in cases of identical twins. Identical twins are most likely to inherit the disease than that of fraternal twins (, 2004). (b) Another common factor is aging, the wear and tear theory. Physical changes in aging cause the water content of the cartilage increases and the protein makeup of cartilage degenerates, (, 2007). Add to the fact that OA usually peaks between the fifth and sixth decade of life, Over many years the cartilage may become frayed and may even wear away entirely. When this happens, the bone surface on one side of the joint grates against the bone on the other side of the joint, providing a much less elastic joint surface (, 1999). (c) Obesity, in addition to being a risk factor, it also increases pain and discomfort of the disease (, 2004). Moreover, since weight-bearing joints are usually the affected area in OA, joints in knees, hips and feet suffers the most due to mechanical stress to cartilage cause by obesity. (d) Trauma is also a common factor, this can be a result of an injury or stress to that part of a joint, usually in the knees. This could be a common scenario among those in the field of sports such as soccer, basketball, and long distance running where it uses muscles of legs, knees and feet. (e) Endocrine and metabolic factors such as gout and diabetes could also predispose to OA (, 2004). In cases of gout where there is an increase in uric acid production, this uric acids when solidifies could become crystals deposits in the cartilage, thus, it would restrict movement between the joints due to inflammation of the joint membrane and the client would most likely experience pain (,2007). In cases of diabetes, uncontrolled diabetes mellitus can cause multi-organ failure via micro- and macrovascular damage, and may lead to articular cartilage degeneration (, 2007) Moreover, diabetes and OA have a common predisposing factor: obesity.

 Factors such as congenital disorders, previous bone and joint disorder, bleeding disorders such as hemophilia that cause bleeding to occur in a joint (, 2003) and other inflammatory joint diseases such as a bacterial invasion could also be the caused. This predisposing factors all leads to one thing, irritation of the articular cartilage. In the early stages of the disease, the surface of the cartilage or even the synovium becomes inflamed and swollen. There is a loss of proteoglycan molecules and other tissue components that causes water loss leading to the appearance of fissures. As disease progresses, more tissue is lost and the cartilage losses elasticity making it more prone to damage. This loss of elasticity could eventually lead to large amount of cartilage being destroyed, leaving the ends of the bone within the joint unprotected (, 2003). With the joint now unprotected, rubbing between two bones would be inevitable and various pathogens such as bacteria, virus and fungi could easily infiltrate the now unprotected joint, thus, deterioration of cartilage. Despite the deterioration of cartilage, by virtue of negative feedback mechanism, an attempt of our body regain homeostasis, it would most likely take measures to recover itself from damage, however, more problems arises in the bone as the body tries to repair the damage. Clusters of damaged cells or fluid-filled cysts may form around the bony areas and within the bone marrow itself, causing swelling which will eventually lead to pain. Bone cells may respond to damage by multiplying growing misshapen plates around exposed areas. And, at the margins of the joint, the bone may produce outcroppings, on which new cartilage cells (chondrocytes) proliferate and grow abnormally (, 2003). These changes in the cartilage could bring about different signs and symptoms commonly found in a person with osteoarthritis.

Clinical Manifestations/ Symptoms of Osteoarthritis

Osteoarthritis have a variety of symptoms, it can range from mild to severe, depending on the severity of the course of the disease. Primary clinical manifestations are pain, stiffness and functional impairment (, 2004). Pain itself is the presenting symptom. Pain usually worsens during periods of activity but can be relieved with proper rest. However, pain could still be present even in periods of rest as the disease advances and can keep the person awake at night. OA in the knee may cause a crackling like noise (called crepitus) when moved, pain also seems to increase in a humid weather and some people experience muscle spasm and contractions in the tendons (, 2003). Stiffness is most common in the morning after awakening. It usually lasts less than 30 minutes and decreases with movement; it also tends to follow periods of inactivity, such as sleeping or sitting which can last for more than an hour. Functional impairment is due to pain on movement and limited to joint motion when structural changes develop (, 2004).

Symptoms of osteoarthritis could also be classified according to location. Examples are in: (a) Fingers, this is the mildest form of OA. It causes knobby enlargement of the finger joints. The end joints of the fingers become bony and the hands begin to assume the appearance we associate with old age (, 1999). Most common form of OA occurs in the first joint below the tips, known as Heberden’s nodes and less commonly in the next joint down, Bouchard’s nodes (, 2003). Furthermore, this changes could bring about stiffness, making it harder for the person to use the fingers in performing activities of daily living such as eating using spoon and fork, picking a glass, carrying bags etc. (b) Spine, OA may affect the disk that form cushions between the bones of the spine. Though this case is relatively seldom, it is troublesome when it occurs in the lower back or in the neck where it can cause difficulty in swallowing (, 2003) which might lead to choking. Also, OA of the spine doesn’t cause symptoms unless there is pressure on one of the nerves or irritation of some of the other structures of the back (, 1999).  (c) Hips and Knees. OA most commonly occur in these areas and problems could be quite severe. Joint in the knee is usually stable until the disease progresses, when the knee becomes enlarge and swollen (, 2003). This may result in the leg becoming bowed or splayed outward (, 1999). OA in knee is common among the aged (old) due to wear and tear and also to athletes particularly to long distance runners which puts a lot of stress to their knees making it susceptible to damage as years goes by, however, intensive activity does not always predispose a person to osteoarthritis. There is also a difficulty in walking and standing due to loss of synovial fluid within the joint capsule, the sufferer might restrict his/her movements which might lead to larger problems such as atrophy of the muscle due to immobility. In the hips, pain develops slowly, usually in the groin and on the outside of the hips or sometimes in the buttocks. The pain may radiate to the knee (, 2003). Osteoarthritis of the hip often results with the client restricting her movement to avoid experiencing pain. (d) Shoulder. OA is less common in the shoulder area than in any other joints. It may develop in the shoulder joint itself. In such cases, it is most often associated with a previous injury and patients gradually develop pain and stiffness in the back of the shoulder.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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