Axial and Appendicular Skeleton

Osteoporosis is a condition that affects approximately 44 million individuals in the United States alone and worldwide affects more than 200 million (Facts and Statistics, n.d). This condition usually affects mostly women; however, men are also affected. Fractures in adults aged 65 and over can be of big detriment to their overall health and life expectancy, with fractures occurring nearly 600 per 1000,000 and 1400 per 100,000 in hip and vertebra, respectively (Lewiecki, 2018).

Osteoporosis is a loss of bone strength that leads to increased risk of fractures in the adult (Lindsay & Cosman, 2015, p.

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2488). Osteoporosis can be diagnosed clinically with fragility fractures that are present in particular sites such as in the spine, hip, wrist, humerus, rib, and pelvis (Lewiecki, 2018). However, Dual-energy X-ray absorptiometry (DEXA) is gold standard for diagnosis of this condition and it is diagnosed when the bone density is below 2.5 standard deviation, or a T-score of -2.5 as it is also referred to.

Our axial and appendicular skeleton is composed of bone that’s is a complex mixture of collagen with calcium and phosphate.

Before the skeleton reaches maturity, bone achieves its shape via modeling made by two specific cells called osteoblasts and osteoclast (Manolagas, 2018). After it has reached its maturity bone remodeling starts. As adults we get the maximum bone mass around the third decade of life. As stated by Lindsay and Cosman, after the phase of bone modeling that happens during the periods of growth during youth, “bone remodeling [in adults] repair microdamage within the skeleton to maintain skeletal strength and ensure relative youth of the skeleton and to supply calcium form the skeleton to maintain serum calcium” (Lindsay & Cosman, 2015, p. 2489)

Several factors affect the development of healthy bone, such as diet, hormones, growth factors, cytokines and local signals (Manolagas, 2018). Even though, diet and lifestyle adequate for healthy bone development is very important at an early age, heredity plays a role into the development of osteoporosis. As indicated by Lindsay and Cosman, peak bone mass is lower in patients with family history of osteoporosis and hereditability counts for about 50-80% of bone density (Lindsay & Cosman, 2015, p. 2489). As stated by Manolagas (2018), studies that have looked into genetics and its association with bone mineral density have found about 80 genetic loci that impacts BMD (Manolagas, 2018). Genes such as Vitamin D receptor, type I collagen and estrogen receptor and interleukin 6 and insulin-like growth factor play a role along with bone mass, and bone turnover (Lindsay & Cosman, 2015, p. 2489). Other genes related to low bone loss have had found to have a mutation in in LRP5, which is a low density lipoprotein receptor-related protein, which with this mutation osteoblast formation is stimulated leading to increased bone formation (Lindsay & Cosman, 2015, p. 2489).

According to Lindsay and Cosman, “nutrition and lifestyle…play an important role in growth” of skeletal bone (Lindsay & Cosman, 2015, p. 2489). Nutrients such as protein, minerals such as Calcium, vitamin D and hormones help maintain a healthy bone structure in the adult. As states by Jennings et al. (2018), during adulthood healthy diet such as the Mediterranean that supplies healthy polyunsaturated and monounsaturated fats such as olive oil, margarine, nuts, high intake of fish, protein from legumes and supplement of vitamin D can help with healthy bone (Jennings et al., 2018). On the other hand, an unhealthy diet with high salt intake, excess alcohol consumption, and low calcium intake, a sedentary life style, excessive thinness, long term exposure to corticosteroids, smoking can contribute to osteoporosis and increase risk of fractures (Lindsay & Cosman, 2015, p. 2490)

As stated by the USPFT screening for osteoporosis in the adult population, specially in the postmenopausal women is of paramount importance. Doing it clinically or with DEXA for bone mass starting at age 65 so we can lower the burden of this condition in the adult. Y implementing screenings for this condition, we can recognize it and start treating it if needed to avoid the bone density to become thinner and leading to increased risk of fracture. The different treatments expand from more conservative to use of medicine. Starting with lifestyle measures such as “adequate calcium and vitamin D consumption, exercise, smoking cessation, avoidance of heavy alcohol and fall prevention” (Rosen and Drezner, 2018). Medical treatment is pretty much established at this point for this condition and includes biophosphonates as first line therapy, and also there is the option of anabolic agents, denosumab or SERMs (Rosen and Drezner, 2018).