for application of techniques in OT evaluation and intervention. These include specific interventions, physical agent modalities,
orthoses (splints), adaptive equipment, and joint protection to al- low clients to engage in meaningful daily occupations.
PATHOPHYSIOLOGY OF OSTEOARTHRITIS
Although obesity is understood universally to impact load-bearing joints, metabolic factors associated with obesity can also cause development of OA in the non-load-bearing joints of the hand and wrist (Gabay & Gabay, 2013; Wang & He, 2018). The joints most commonly associated with painful and function-limiting OA are the load-bearing joints of the hip and knee and the small joints of the hand. The distal interphalangeal joints (DIP) and the carpometacarpal (CMC) joints of the thumb are the most symp- tomatic when OA develops (Figure 2). It is difficult for individuals who have OA in the hands to avoid constant trauma to the joints because of the inevitable need to use the hands for most daily functions. For example, if a person with OA of the lower body and the hand requires use of a walker, cane, or crutch due to pain or weakness, forces generated on the arms and hands by use of the assistive device can put excessive stress on the upper extremities and lead to greater degrees of hand and wrist pain and disability (Beasley, 2012). Figure 2: Hand Osteoarthritis
Cartilage is a stiff connective tissue that covers the articular bony surfaces in joints, providing a nearly frictionless, gliding surface. In addition to reducing friction during movement, cartilage func- tions to disperse forces of compression during mechanical load- ing of the joint. Cartilage cells fit snugly within a fibrous matrix made up of collagen fibers and are embedded in a stiff, water- based ground substance. In addition to water, the ground sub- stance contains dissolved salts, proteins, lipids, and interwoven proteoglycan molecules. The collagen fibers, which account for nearly 50% of the cartilaginous matrix, are strengthened and held in place by long proteoglycan molecules (Wang & He, 2018). In adulthood, cartilage cells (i.e., chondrocytes and chondroblasts) become relatively inactive metabolically and have a limited vas- cular supply. As a result, the cartilage cells have difficulty healing, which can lead to arthritic joint changes. OA results when changes within joint cartilage lead to a reduction in both joint lubrication and the cushion that protects bone ends (Figure 1). Risk factors for OA in the hands and wrists are multiple and include overuse, genetic predisposition to collagen break- down, prior fractures, significant disuse of a joint, prior surgical in- tervention, and congenital defects (Dewing et al., 2012). Individu- als who have congenital joint abnormalities or joint hypermobility have increased incidences of OA, as do individuals employed in highly repetitive work, particularly work involving resistance. Sys- temic conditions such as hemochromatosis and Wilson’s disease can contribute to development of OA of the hand or wrist (Dew- ing et al., 2012). Other conditions, including hemophilia and sep- sis, create trauma within the joint, disrupt the collagen matrix, and can lead to development of OA (Dewing et al., 2012). Figure 1: Joint Structure
Note . “Erosive osteoarthritis” by Mikael Häggström, used under Creative Commons License CC0 1.0. Identifying the cause of OA continues to be elusive despite its long diagnostic history and extensive research. There is no known cure, and symptom management—including surgical, pharmaco- logical, and therapy approaches—are the primary means of alle- viating discomfort and preserving occupational participation. The culprit in the development of OA is defective collagen (Heine- gård & Saxne, 2010). When the proteoglycans that give articular cartilage its stiffness are compressed, collagen becomes brittle and more susceptible to injury, especially from forces of mechani- cal loading. According to Heinegård and Saxne (2010), molecu- lar processes elicited in the cartilage might then initiate a cycle in which the quality of the matrix is downgraded by proteolysis, along with removal of matrix components. Although this increases sensitivity to mechanical load, fragments of the released mole- cules might induce or worsen inflammation, furthering cartilage breakdown. Progressive articular cartilage deterioration slowly causes increasing pain, stiffness, disuse, and disability. Due to thinning cartilage, decreased cartilage integrity, and bone erosion, joint space narrows and osteophytes form (i.e., osteo- phytosis). Osteophytes are a pattern of bony outgrowth, usually branched in form. Subchondral bone changes such as osteo- phytes, microfractures, and cyst formation result in abnormal bony contours. These are visible during examination on the outer surface of the hand, and they present as Bouchard’s nodes on the proximal interphalangeal joints (PIP) or Heberden’s nodes on the distal interphalangeal joints (DIP) (Kalichman & Hernández-
Note . “Arthritis” by OlafJanssen, used under Creative Commons License BY-SA 3.0 / Cropped from original. In the literature, OA is known by several names, including os- teoarthrosis, degenerative joint disease (DJD), and hypertrophic OA. Lubahn and colleagues (2011) point out that the term os- teoarthropathy might be most accurate for the condition, since OA does not involve the amount of inflammation typical of other arthritic conditions. OA is thought to be a condition associated exclusively with aging and wear, but research also suggests that breakdown of the articular cartilage in OA results from biochemi- cal and cellular changes in addition to mechanical factors (Sovani & Grogan, 2013). Genetics have also been shown to play a role in the occurrence of OA, with a higher prevalence noted in those who have positive family histories for the condition (Tschon et al., 2021). Women have higher susceptibility and prevalence than men, particularly women older than age 50, due to the onset of menopause and bone density changes (Tschon et al., 2021). Re- sults from recent studies emphasize the association of OA with obesity.
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