Bone Disorders and Physical Activity - Essay Example

Bone Disorders In the human body, bone is the most important supportive tissue. Bones give the body its structure and help it carry weight and move.Bones are made up of living tissues. These living tissues constantly keep rebuilding throughout the life. The process of addition of new bones in the body is faster than the removal of old bones during childhood and teenage. However, after an individual crosses 20 years of age, their tendency to lose bone faster gets greater than their tendency to make bone. Adequate intake of vitamin D, calcium, and exercise is vital to have strong bones and prevent bone loss in the old age. Bone problems are of different kinds. They may include osteoporosis caused by low density of bone and which makes bones weak and susceptible to breakage, osteogenesis imperfect which increases the brittleness of bones, and Paget’s bones disease which makes bones weaker. In addition to these bone disorders, bones may also develop a range of infections and cancers. There can be many reasons for the development of bone disorders. Some major causes of bone disorders include genetic factors, poor nutrition, and poor rate of rebuilding and growth of bones. The most important modulators of the process by which bones form are hormones. Optimal development and maintenance of bones depends upon parathyroid hormone, estrogen, and testosterone. Of these, the most direct impact on the cells of bone is made by estrogen which interacts with specific receptors or proteins on the surface of osteoclasts and osteoblasts (Zallone, 2006). Bones maintain their strength and integrity through a process of continuous renewal known as remodeling. Accelerated bone remodeling may cause a range of bone disorders that include but are not limited to familial expansile osteolysis (FEO), juvenile Pagets disease (JPD), Pagets disease of bone (PDB), early-onset Pagets disease of bone (EOPDB), and expansile skeletal hyperphosphatasia (ESH) (Beyens and Van Hul, 2007). Many studies have concluded that the main cells responsible for causing disease in these bone disorders are bone-resorbing osteoclasts. Connective tissues are unlike the parenchymal organs in that their form and function reflects the extracellular matrices of the matter they are made up of. These different compositions of matrices lend unique appearance and mechanical properties to cartilage, bone, and dense fibrous connective tissue (Teitelbaum and Bullough, 1979). Dense fibrous connective tissue is made up of collagen in the form of well-oriented collagen bundles whose main purpose is to resist tension. Cartilage and bone have to be strong enough to resist all sorts of forces including tension, compression, and shear, and to this end comprise combinations of different materials including mineral, proteoglycans, and collagen. There is a structural inhomogeneity in bone. Ends of the vertebral bodies and long bones are mainly made up of an open network of delicate rods and plates that develop spongy or cancellous bone. This trabecular bone’s surface-to-volume ratio is high and is thus prone to quick turnover. The trabecular bone exhibits changes in the mineral homeostasis. The long bone’s shafts are made up of dense cortical bone whose thickness is generally a quarter of an inch by minimum. Long bones have a tubular shape and their outer shell is strong. The cortical layer surrounds the trabecular bone which is spongier core (Parfitt, 2001). The skeleton gains stability because of trabecular bone as it transmits the compressive forces across the different joints, the role of diaphyseal cortex in resisting the torsional and bending forces is equally important. When the amount of protein-polysaccharide in the cartilage decreases, the physical properties of cartilage change. While the tissue loses turgidity, lack of the support otherwise provided by the protein-polysaccharide gel causes the collagen to distort. Lack of the molecular sieve increases the vulnerability of the cartilage to degradative enzymes, that may enter the damaged tissue rapidly. Osteoclasts cause calcification of cartilage and bone’s morphologically apparent resorption for the most part. Osteoclasts are large cells that are generally multinucleated. Although there is subjectivity in the accurate mechanism that causes these cells to degrade the bone, yet it definitely comprises lysosomal activity. These cells consist of enzymes like collagenases and acid phosphatase in abundance. The precursor of osteoclast, the circulating monocyte, also consists of these enzymes and can cause the bone to degrade in vitro. Osteoclasts also resorb individual bone packets morphologically. The matrix’s biochemical make-up is very important in this regard; osteoclasts cannot resorb the matrix that has not mineralized before. Bone disorders have significant negative impact on the lifestyle of the people suffering from them. Bone disorders cause hindrance in movement and physical activity. Patients having bone disorders have limited mobility and have to bear excruciating pain. Bone disorders may also disfigure the skeleton, and pose problems in gait. Bone disorders cause pain during walking, sitting, and changing posture or position. Many older adults with bone disorders cannot walk without aid. Just like the large impact of bone disorders on the lifestyle of patients, patients’ lifestyle can also affect bone disorders and their ability to deal with them. For example, for the people suffering from osteoporosis, while medication does not restore all of the bone lost, there are certain lifestyle measures that the patients of osteoporosis can take for treating this bone disorder. Such lifestyle measures include but are not limited to muscle strengthening exercises, weight-bearing exercises, deterrence from smoking, and limited intake of alcohol (Kenny, 2012). “Since bone is a dynamic living tissue that gets stronger when stressed and weaker when not used, physically active people generally have higher BMD at all ages than people who are sedentary” (Higdon, 2005). Moderate exposure to sunlight on regular basis helps the body produce vitamin D that is good for bones (Southern Cross, 2013). Physical activity offers primary prevention of different kinds of chronic diseases. Physical activity is also effective in the treatment and rehabilitation of patients. Physical activity optimizes an individual’s well-being and health. The influence of physical activity on the strength of bones and mineral density is evident from the review of literature (Chien et al., 2000). Skeletal muscle activity has a very positive effect on the bone turnover (Langberg et al., 2000). Lindsey et al. (2005) carried out a research on 116 healthy elder women to evaluate the relationship between the measures of physical performance and bone mineral density. Their study led them to the identification of a significant association between walking speed, step length, grip strength and balance on the bone mineral density; women with faster normal speeds, longer step lengths, and brisk gait speeds were found to have greater bone density. A number of studies completed over the last few years have observed the important role of physical activity in the improvement of different kinds of variables assessed in the patients of osteoporosis (Uusi-Rasi et al., 2006, and Liu-Ambrose et al., 2005). A study of 110 control subjects and 107 gymnasts ranged over a period of six years led Uusi-Rasi et al. (2006) to the conclusion that recreational gymnastics has long-term beneficial impact on the decline of bone density and bone loss associated with the process of ageing. In their research, Liu-Ambrose et al. (2005) found positive influence of the physical exercise programs on psychological health and well-being and their tendency to reduce the back pain and chronic osteoporosis pain in the postmenopausal women having lower bone mass. The researchers stated that even agility training and resistance can have significant correlation with changes in the quality of life related to health as determined by the social, emotional, and physical well-being of an individual. References: Beyens, G, and Van Hul, W 2007, Pathophysiology and genetics of metabolic bone disorders characterized by increased bone turnover, Critical Reviews in Eukaryotic Gene Expression, Vol. 17, No. 3, pp. 215-240. Chien MY, Wu YT, Hsu AT, et al 2000, Efficiacy of a 24-week aerobic exercise program for osteopenic postmenopausal women, Calcif Tissue Int, Vol. 67, pp. 443-448. Higdon, J 2005, Preventing Osteoporosis through Diet and Lifestyle, [Online] Available at http://lpi.oregonstate.edu/ss05/osteoporosis.html [accessed: 12 April 2014]. Kenny, T 2012, Osteoporosis, [Online] Available at http://www.patient.co.uk/health/osteoporosis-leaflet [accessed: 12 April 2014]. Langberg H, Skovgaard D, Asp S, et al 2000, Time pattern of exercise-induced changes in type I collagen turnover after prolonged endurance exercise in humans, Calcif Tissue Int, Vol. 67, pp. 41-44. Lindsey C, Brownbill RA, Bohannon RA, et al 2005, Association of physical performance measures with bone mineral density in postmenopausal women, Arch Phys Med Rehabil, Vol. 86, pp. 1102-1107. Liu-Ambrose TYL, Khan KM, Eng JJ, et al 2005, Past resistance and agility training reduce back pain and improve health-related quality of life in older women with low bone mass, Osteoporosis Int, Vol. 16, pp. 1321-1329. Parfitt, AM 2001, ‘Skeletal heterogeneity and the purposes of bone remodelling: implications for the understanding of osteoporosis’, In: Marcus R, Zfeldman D, Kelsey J, eds. Osteoporosis. San Diego: Academic Press. Southern Cross 2013, Osteoporosis - symptoms, treatment, prevention, [Online] Available at https://www.southerncross.co.nz/AboutTheGroup/HealthResources/MedicalLibrary/tabid/178/vw/1/ItemID/131/Osteoporosis-symptoms-treatment-prevention.aspx [accessed: 12 April 2014]. Teitelbaum, SL, and Bullough, PG 1979, The pathophysiology of bone and joint disease, American Journal of Pathophysiology, Vol. 96, No. 1, pp. 282-354. Uusi-Rasi K, Sievänen H, Heinonen A, et al 2006, Long-term recreational gymnastics provides a clear benefit in age-related functional decline and bone loss. A prospective 6-year study, Oteoporos Int, Vol. 17, pp. 1154-1164. Zallone, A 2006, Direct and indirect estrogen actions on osteoblasts and osteoclasts. Annals of the New York Academy of Science, Vol. 1068, pp. 173-179. Read More