new bone by osteoblasts is usually balanced and results in no net change in bone. In older adults, an uncoupling of bone resorption and formation occurs. With aging, osteoclasts typically increase their activity, while osteoblasts decrease their work of forming new bone, which results in a net loss of bone in older adults (Schulman et al., 2011). This imbalance results in decreased bone mass and increased risk for fracture. Osteoporosis While aging is associated with decreased bone mass, inactivity accelerates this decline, and a sedentary lifestyle is a risk factor for the development of osteoporosis (Booth et al., 2011). Studies have shown that older adults who have been active throughout their lives and have higher cardiovascular fitness also have higher bone density than inactive adults, thus decreasing their risk for osteoporosis (Booth et al., 2011; DeFina et al., 2016). Increased levels of proinflammatory cytokines, which are often associated with physical inactivity, stimulate osteoclasts and result in increased levels of bone resorption. Increased levels of adiposity, which are frequently attributed to a sedentary lifestyle, are also associated with low total bone mineral density. A study of more than 13,000 older adults demonstrated that the percentage of body fat was positively associated with osteopenia, indicating that older adults with increased body fat were more likely to have bone loss (Cao, 2011). While the exact mechanism behind the association between increased fat mass and bone loss is unknown, it is suspected that increased levels of inflammatory cytokines may be the reason this occurs (Cao, 2011). It is known, however, that increased physical activity can decrease inflammation and increase bone mineral density. A recent meta-analysis of 43 studies reported that physical exercise results in increased bone mineral density and a decreased risk of fracture in postmenopausal women. These findings suggest that exercise is important for both the prevention and treatment of osteoporosis (Howe et al., 2011). Osteoarthritis Women over age 50 in the U.S. have a 9.8% prevalence of arthritis of the femur, 11.6% have arthritis of the lumbar spine, and 16.5% have arthritis of either the femur neck or lumbar spine (Frontera, 2017). In general, these statistics show a higher prevalence of osteoarthritis in women over age 50 than compared to 15 years ago (Frontera 2017). The prevalence of low bone mass ranges from 36% to 53% of women, which is slightly higher than that found with men (Frontera 2017). Intramuscular fat and bone function Intramuscular fat may also impair bone function. Increased rates of intramuscular fat are associated with an increased risk of hip fracture, independent of bone density (Lang et al., 2010). Aging is known to result in a decrease in bone mass by 0.5% after age 40 and by as much as 2% to 3% in women after menopause (Concannon et al., 2012). Although osteoporosis is more common in women, it can also occur in men and is frequently underdiagnosed in this population (Lambert et al., 2011). Men are less likely to have osteoporosis but are more likely to experience complications and even death following a hip fracture. Lambert et al. (2011) found that men are more likely to experience subsequent fractures and are less likely to return to independent function than are women who experience hip fracture. Therefore, while osteoporosis may not occur as often in men, it is still a significant problem. Effects of bedrest on the musculoskeletal system As little as five to seven days of bedrest in healthy older adults results in a decrease of lean mass in the leg by 3% to 4% (Reidy et al., 2017). If healthy older adults suffer such a rapid loss of muscle mass with decreased physical activity, it is reasonable to suspect that in older, frail, or hospitalized patients the loss of muscle mass may actually be much greater than 1% per year. Lack of mechanical stimulation (which is typical of bedrest), immobilization, and sedentary behavior results in thinner and softer articulated cartilage (Reidy et al., 2017). Studies have shown, however, that exercise has the opposite effect.
movements in older adults. Another well-known change with aging is decreased bone density, which explains some other structural changes seen in the musculoskeletal system (Frontera, 2017). Articular cartilage Aging is associated with a higher prevalence of chondrocytes’ (the cells responsible for cartilage formation) ability to divide (Frontera, 2017). This diminished mitotic activity leads to chondrocyte loss and lessened ability to synthesize collagen (Frontera, 2017). The articular cartilage ends up with stiffness within the collagen network of its tissues, which is even more pronounced after bedrest and which explains the stiff joints older adults often mention in the morning. Fat infiltration and muscle One reason for the decrease in muscle quality seen with aging may be the increase in fatty infiltration found in the muscle. As mentioned previously, aging is associated with changed body fat distribution, away from subcutaneous tissue and toward storage in the more harmful ectopic locations, including muscle. It is currently unknown whether increased intramuscular fat is a product of aging, inactivity, or both—but we do know that increased levels of intramuscular fat are associated with decreased muscle strength, muscle quality, and mobility function in older adults (Addison et al., 2014). Even older adults without current mobility limitations are at an increased risk of future limitations if they have high amounts of intramuscular fat within their thigh muscles (Visser et al., 2005). It is also known that older adults with higher amounts of intramuscular fat may have a decreased ability to activate their muscles to produce a full contraction (Yoshida et al., 2012) and that they may experience a decreased ability to improve their muscle quality with exercise (Marcus et al., 2012). This is an important finding because it suggests that increased intramuscular fat may not only impair the muscles’ ability to function, it may also impair the ability to improve muscle function. Bones It is well known that with advanced age, there is a reduction in bone mineral content and density (Frontera, 2017). Over a lifetime, the human skeleton continuously undergoes a regulated process of bone resorption and formation. This continuous process allows for the repair of microdamage in the bone, the removal of unneeded bone, and the release of calcium from the bones for the maintenance of calcium levels in the body (Schulman et al., 2011). Multiple types of cells are found within the bone, where they work together to regulate bone formation and resorption. Bone is composed of three distinct types of cells. Ninety percent of all bone cells are osteocytes—long-lived bone cells that participate in almost all major bone regulation activities (Atkins & Findlay, 2012). Osteocytes act as regulators of bone formation by detecting strain in the bone. To increase bone formation, the osteocytes transmit signals to osteoblasts, which are the cells responsible for laying down the mineral matrix. Osteoblasts account for 4% to 6% of all bone cells (Atkins & Findlay, 2012). Layers of osteoblasts deposit successive layers of new bony matrix. As these layers are mineralized, new bone is formed. Bone density/mass Equally as important as the formation of new bone is the resorption of older bone. Resorption of older or damaged bone allows for constant bone repair to occur, which ensures healthy bone turnover. Bone resorption is also important for the release of calcium stores from the bone in times of need. Calcium is critical for the propagation of nervous signals and for cellular transport. Cells called osteoclasts, working under the direction of osteocytes, are able to destroy the bony matrix, releasing calcium into the body for use by other cells (Schulman et al., 2011). Osteoclasts are large, multinucleated cells found on the surface of the bone; they account for only 1% to 2% of the cells in bone (Atkins & Findlay, 2012). In a younger adult, the resorption of bone by osteoclasts and the formation of
EliteLearning.com/ Physical-Therapy
Book Code: PTNY1024
Page 90
Powered by FlippingBook