Osteoporosis

1. The remodelling of bone is a normal process, and reaches its peak at age 30 known as the peak bone mass. After this age the rate of osteoclast activity begins to gradually remove more bone than osteoblasts can make. This causes the development of osteoporosis, a condition caused by weakened bones, resulting in soft bones that are more prone to fractures (Nucleus Medical Media, 2014).

2. Clarke, B. (2008). Normal Bone Anatomy and Physiology. Clinical Journal of the American Society of Nephrology : CJASN, 3(Suppl 3), S131–S139. Normal Bone Anatomy and Physiology International Osteoporosis Foundation. (2017). Secondary Osteoporosis. Retrieved from https://www.iofbonehealth.org/secondary-osteoporosis Lab Tests Online. (2013). Osteoporosis. Retrieved from http://www.labtestsonline.org.au/learning/index-of-conditions/osteoporosis/tests Lee, J., & Vasikaran, S. (2012). Current recommendations for laboratory testing and use of bone turnover markers in management of osteoporosis. Annals of laboratory medicine, 32(2), 105-112. Metcalfe, D. (2008). The pathophysiology of osteoporotic hip fracture. McGill Journal of Medicine : MJM, 11(1), 51–57. Medscape. (2017). Osteoporosis. Retrieved from https://emedicine.medscape.com/article/330598-overview#a3 Nucleus Medical Media. (2014). Osteoporosis, Nucleus Health. [YOUTUBE]. Retrieved from https://www.youtube.com/watch?v=eYGkT6OrBk0 Office of the Surgeon General. (2004). Bone Health and Osteoporosis: A Report of the Surgeon General. Retrieved form https://www.ncbi.nlm.nih.gov/books/NBK45504/ Osteoporosis. (2017). The Mayo Clinic. Retrieved from https://www.mayoclinic.org/diseases-conditions/osteoporosis/symptoms-causes/syc-20351968 Osteoporosis Australia. (2014). Diagnosis. Retrieved from https://www.osteoporosis.org.au/diagnosis Parathyroid. (2016). Osteoporosis and Parathyroid Disease (Hyperparathyroidism). Retrieved from http://www.parathyroid.com/osteoporosis.htm

2.1. Reference List

3. Aetiology

3.1. Osteoblasts are cells that make new bone tissue using minerals such as calcium and phosphate from the blood

3.2. Osteoclasts are cells that break down bone tissue

3.3. Osteoporosis develops when osteoblast activity can no longer keep up with the rate of osteoclast activity

3.4. Primary Osteoporosis - related to older age, and is more prone in women during menopause due to the lack of oestrogen Secondary Osteoporosis- affects both children and adults and is related to other diseases or conditions, including cancer, hormonal complications or use of certain medications (International Osteoporosis Foundation, 2014).

4. Risk Factors

4.1. Secondary Osteoporosis - Anorexia - Multple Sclerosis - Rheumatoid Arthritis - Coeliac Disease - Hormonal issues (PTH, oestrogen, testosterone) - Lifestyle Factors (cigarette smoking, excessive alcohol consumption) -Cystic Fibrosis

4.2. Primary Osteoporosis -LBM before age 30 - Genetic Predisposition - Female - Poor diet and and lack of weight bearing exercise - Vitamin Deficiencies - Certain Medications (steroids or seizure medications) - Lifestyle Factors (cigarette smoking, excessive alcohol consumption) - Menopause -Hormonal Issues (PTH, oestrogen, testosterone) (International Osteoporosis Foundation, 2014).

5. Impact of aetiologies in the pathogenesis of osteoporosis at a structural and cellular level

5.1. Bones are constantly undergoing a process of remodelling during life, due to the activity of osteoblast and osteoclast activity. Bones are hollow, with the outer dense shell known as the cortical bone. Inside the cortical bone is a fine network of connecting rods and plates called the trabecular bone.

5.2. Under normal conditions, osteoclast activity requires weeks to resorb bone, whereas osteoblast activity requires months. Therefore, any process that increases the rate of bone remodelling will result in net bone loss over time. (Medscape, 2017).

5.3. Accelerated bone loss can be affected by hormonal status, as seen in older men or women, or can be secondary to various diseases.

5.3.1. Hormonal activity plays a major role in the aetiology of osteoporosis. Parathyroid hormone (PTH) controls calcium and phosphorus levels in the blood. When blood calcium levels drop too low, PTH releases calcium from the bones into the bloodstream. This is a tightly regulated process to ensure the amount of calcium in the blood and bones remains at a normal high level. Hyperparathyroidism is the result of too much PTH resulting in the bones releasing excessive amounts of calcium in the blood at a rate that is too high. This causes the bones to lose their source of calcium and results in the aetiology of osteoporosis (Parathyroid, 2016).

5.3.2. Osteoporosis is common in women after menopause, the lack of oestrogen causes osteoclast production to increase. Oestrogen affects bones indirectly through cytokines and local growth factors. Oestrogen deficiency results in excessive bone resorption accompanied by inadequate bone formation (Medscape, 2017).

6. Laboratory Investigations

6.1. Low bone mass is understood through a bone mineral density test. Bone segments are analysed through X-rays. Imaging options include: - single/double-photon absorptiometry (SPA/DPA) - dual-energy X-ray absorptiometry (DEXA) - quantitative computed tomography (QCT) scanning - magnetic resonance imaging (MRI) (Lee, J., & Vasikaran, S, 2012)

6.1.1. Various tests are used to determine the reasoning behind low bone mass - complete blood count - measure serum calcium level - urine calcium estimation - renal and liver function tests - vitamin D levels - hormone level

6.1.1.1. Osteoporosis diagnostic criteria: T score: 1 to -1 = Normal -1 to -2.5 = Osteopenia (at risk of developing osteoporosis -2.5 or lower = Osteoporosis (Osteoporosis Australia, 2014).

7. Final Nutritional Considerations

7.1. reduced animal protein * animal protein contains high amounts of sulphur-containing amino acids - increased fruit and vegetable intake - reduced sodium intake - low fat diet (specifically omega 6 polyunsaturated) - minimal caffeine and alcohol - vitamin D & calcium supplements *calcium is a main component in bone-forming. * vitamin D deficiency is the cause of rickets in children and osteomalacia in adults. It is gained from foods or sunlight.

8. How do structural changes in osteoporosis alter the physiological function of the bone tissue?

8.1. Osteoporosis results in thin and brittle bones, making one more prone to fractures. Bones are no longer able to provide the strength and support they are built to do, therefore hip, wrist and vertebral fractures are common.(Medscape, 2017).

8.2. The hip is a multi-axial ball-and-socket synovial joint in which the rounded head of the femur articulates with the concave acetabulum of the pelvis. The hip supports the entire weight of the upper body when standing, and in a healthy person should not fracture without considerable high-energy trauma (Metcalfe, D., 2008).

8.3. Vertebral compression fractures affect the lumbar vertebrae - the five vertebrae between the lungs and the pelvis - and are known to "crumble" under the weight of the individual's upper body due to significant bone loss. The reduced density and strength of osseous tissue in pivotal, supportive joints such as the hip and lumbar vertebrae compromise the physiological capabilities of osteoporosis sufferers even before injuries occur. This includes reduced range of motion, joint stiffness and pain, or frailty overall that can disable an individual or compromise their quality of life over time (Metcalfe, D., 2008).

9. How Functional Changes Manifest

9.1. Osteoporosis is often referred to as the “silent disease” as the pathological symptom - bone loss (a structural reduction in bone density) - often goes unnoticed until a minor pump, strain or fall causes a bone fracture or collapsed vertebra. Bone loss manifests over time due to slow or incomplete bone remodeling processes caused by a variety of factors (hormonal changes, corticosteroid use, diet and lifestyle factors) whilst recovery depends on the persons’ age, sex and general health status and the extent of bone loss leading up to the fracture.

9.2. Hip fractures are a common consequence of osteoporosis, usually as a result of a fall and often leading to disability and an increased risk of mortality within one year of the injury for elderly individuals ("Osteoporosis", 2017). Osteoporotic hip fractures may be also attributed to extra-skeletal factors such as frailty, failing eyesight, and a tendency to fall usually associated with elderly populations (Metcalfe, D., 2008).

9.3. Vertebral fractures on the other hand can occur even without a fall or obvious injury, as extensive structural bone loss over time can weaken the vertebrae to the point that they may crumple, causing severe back pain, a hunched or stooped posture and height loss over time ("Osteoporosis", 2017).

9.4. Low bone turnover leads to accumulation of microfractures, whereas high bone turnover - where bone resorption is greater than bone formation - is the main cause of microarchitectural deterioration seen in osteoporosis affected bones (Clarke, 2008).