Calcium Homeostasis Overview

Calcium Homeostasis

Calcium Homeostasis is referred to the mechanism through which adequate level of calcium is maintained within the body as derangement of the mechanism lead to development of hypocalcaemia or hypocalcaemia that leads to hindered consequences for the individual's health (Veldurthy et al. 2016). The calcium homeostasis is managed through appropriate balance between three organs that are bone, kidney and intestine. The bone acts as the key storage of calcium in the body that is absorbed from the blood with the help of osteoclasts when there is increased calcium in the body. However, the bones release calcium in the blood when the level of calcium becomes too low in the blood helping to maintain homeostasis in the body. This process is managed and regulated through the action of parathyroid and calcitonin hormone along with vitamin D (Meleleo and Picciarelli, 2016).

In the parathyroid gland, the cells have a plasma membrane receptor for calcium ions. During lower calcium levels in the blood, there is lack of calcium ions present to remain bonded with the receptors of the parathyroid gland that triggers release of parathyroid hormone from the gland which stimulates the proliferation of osteoclast (Summers and Macnab, 2017). The osteoclasts function to initiates reabsorption of bones and the demineralisation process by breaking down bone matrix helps to release calcium in the blood. This leads to create an overall increase in the amount of calcium in the blood. The parathyroid hormones act to trigger the kidney and the intestine to reabsorb calcium from the urine to be transferred to the blood to maintain effective level of calcium (Hansen et al. 2018).

As the calcium level normalises in the blood, the parafollicular cells increase secretion of calcitonin from the thyroid glands. Moreover, at the same time, the parathyroid hormone secretion is reduced in the body by the parathyroid glands as a result of trigger of enough calcium in the blood. The increased level of calcitonin leads to trigger osteoblast proliferation (Faour and Gilloteaux, 2017). The osteoblasts are large cells which are responsible for formation and mineralisation of bone by absorbing and removing calcium from the blood plasma (Cao et al. 2016). The calcitonin levels are again lowered when the calcium level in the blood fall, triggering parathyroid hormones to be released from the parathyroid glands and repeat the process to maintain calcium homeostasis (DiMeglio and Imel, 2019).

Vitamin D has a major part to be played in the calcium homeostasis. It is mainly collected from the skin and diets by the liver and kidneys to convert it into calcitriol as the active hormone in the proximal convoluted tubule in the kidney. Calcitriol is released in the blood to manage enhanced level of calcium and phosphate in the blood, in turn, avoiding abrupt reduction of minerals at dangerous level that may disrupt the body functioning. The effective management of calcium level in the blood by calcitriol leads to promote healthy bone growth and remodelling, in turn, stabilising calcium homeostasis (Fleet, 2017). The calcitriol which is the active form of vitamin D also supports increasing amount of calcium absorption by the gut from the food to be transported to the blood. It prevents calcium loss from the kidneys, in turn, acts to support maintaining enhanced calcium level in the blood and ensure calcium homeostasis (Bivona et al. 2018).

Osteoporosis

Osteoporosis is referred to the condition in which the bones become brittle and weak causing hindered physical ability among the patients to execute everyday activities (Sugiyama and Oda, 2017). It mainly results as a result of excessive bone reabsorption, inadequate peak bone mass and inadequate remodelling or formation of bone out of mesenchymal stem cells avoiding to form osteoblast (Ivanova and Vasileva, 2017). The hormonal factor that supports the development of osteoporosis includes reduced estrogen level in the blood as a result of menopause which increases mineralisation and reabsorption of bones along with avoiding to support deposition of new bones that normally develops in weight-bearing bones (Ferrari, 2019). The other factor that supports development of osteoporosis is hindered calcium homeostasis in which the overall production of parathyroid hormone that stimulates breakdown of bone is triggered out of reduce calcium and vitamin D level in the blood in the patients (Awasthi et al. 2018). The role of calcitonin is found to be less significant in causing osteoporosis among individuals (Awasthi et al. 2018).

Risk Factor

The risk factor for osteoporosis include sex and age that is compared to men, the women are more prone to get affected by the disorder with increasing age after menopause. This is because the estrogen levels which support menstruation and functional capacity of osteoblasts are lowered leading the women to lose increased bone mass (El-Tawab et al. 2016).

The individuals of White or Asian descent are considered to be at increased risk of osteoporosis. This is mainly due to presence of higher bone mass among the other races such as African American and others (Du et al. 2017).

The family history of osteoporosis also creates risk of the disease and the increased body size has also effect on worst condition regarding the disorder. This is because one of the genes that is DARC gene which is responsible to stimulate production of protein that support bone breakdown may be present among parents that are transferred among the children through heredity (Zhang et al. 2019).

The presence of poor calcium diet along with reduced exercise creates risk for osteoporosis as exercise helps to reduce bone loss and increased calcium in the diet that enters the body support effective calcium homeostasis and bone formation (Pu et al. 2016).

Diagnosis

Sign and Symptoms

Increased back pain caused due to collapsed vertebrae or fracture (Watts, 2018)

Loss of height (Watts, 2018)

Stooped posture (Watts, 2018)

Unexpected bone fracture (Watts, 2018)

Diagnostic Test

The bone density test is performed for detecting osteoporosis in which the density of bones and its chance of breaking down are determined. This is executed with the help of Dual Energy X-ray absorptiometry (DXA) machine (Nakanishi et al. 2018).

The blood test is performed to determine the calcium level in the body and rule out other diseases that have similar signs and symptoms like osteoporosis (Nakanishi et al. 2018).

Treatment

The treatment of osteoporosis includes:

The use of biphosphonates is suggested to be orally taken by osteoporosis patients. This is because they reduce the bone reabsorption by osteoclasts and may affect osteoblast proliferation at times (Imai et al. 2019). However, side effects of biphosphonates include abdominal pain, nausea and heartburn symptoms. The side effects can be resolved by intravenously administering bisphosphonates to patients with osteoporosis (Walker, 2020). As criticised by Deeks (2018), monoclonal antibody medications like denosumab act in a better way compared to biphosphonates. This is because denosumab inhibits RANKL (receptor activator of nuclear factor κB) which regulate osteoclastogenesis, in turn, avoiding increased bone loss.

The hormonal therapy such as supporting production of estrogen immediately after menopause is effective to treat osteoporosis. In this purpose, the raloxifene which mimics estrogen can be delivered to avoid osteoporosis (Gupta et al. 2019).

The change in everyday activities such as increasing physical exercise, avoiding smoking and alcohol intake also supports treating osteoporosis (Kerr et al. 2017).

Conclusion

The above discussion informs that for management of calcium homeostatic, the hormones released from the thyroid and parathyroid along with vitamin D play an effective role. The Osteoporosis is developed due to disruption in calcium homeostasis as a result of which bone becomes brittle creating hindered physical efficiency of the individual in performing physical activities. The diagnostic test for Osteoporosis includes bone imaging and blood test and the treatment includes use of medication, hormonal therapy and control of everyday lifestyle.

References

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Bivona, G., Agnello, L. and Ciaccio, M., 2018. The immunological implication of the new vitamin D metabolism. Central-European Journal of Immunology, 43(3), p.331.

Cao, Z., Liu, D., Zhang, Q., Sun, X. and Li, Y., 2016. Aluminum chloride induces osteoblasts apoptosis via disrupting calcium homeostasis and activating Ca 2+/CaMKII signal pathway. Biological trace element research, 169(2), pp.247-253.

Deeks, E.D., 2018. Denosumab: A review in postmenopausal osteoporosis. Drugs & aging, 35(2), pp.163-173.

DiMeglio, L.A. and Imel, E.A., 2019. Calcium and phosphate: hormonal regulation and metabolism. In Basic and applied bone biology (pp. 257-282). Academic Press.

Du, Y., Zhao, L., Xu, Q. and Deng, H., 2017. Osteoporosis Preventive Behaviors and Bone Mineral Density among Older White and Asian Women. Innovation in aging, 1(1), pp.143-143.

El-Tawab, S.S., Saba, E.K.A., Elweshahi, H.M.T. and Ashry, M.H., 2016. Knowledge of osteoporosis among women in Alexandria (Egypt): A community based survey. The Egyptian Rheumatologist, 38(3), pp.225-231.

Faour, O. and Gilloteaux, J., 2017. Calcitonin: Survey of new anatomy data to pathology and therapeutic aspects. Translational Research in Anatomy, 6, pp.4-15.

Ferrari, S.L., 2019. Pathophysiology of Osteoporosis. In Pocket Reference to Osteoporosis (pp. 1-10). Springer, Cham.

Fleet, J.C., 2017. The role of vitamin D in the endocrinology controlling calcium homeostasis. Molecular and cellular endocrinology, 453, pp.36-45.

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Hansen, T.H., Madsen, M.T., Jørgensen, N.R., Cohen, A.S., Hansen, T., Vestergaard, H., Pedersen, O. and Allin, K.H., 2018. Bone turnover, calcium homeostasis, and vitamin D status in Danish vegans. European journal of clinical nutrition, 72(7), pp.1046-1054.

Imai, N., Endo, N., Shobugawa, Y., Oinuma, T., Takahashi, Y., Suzuki, K., Ishikawa, Y., Makino, T., Suzuki, H., Miyasaka, D. and Sakuma, M., 2019. Incidence of four major types of osteoporotic fragility fractures among elderly individuals in Sado, Japan, in 2015. Journal of bone and mineral metabolism, 37(3), pp.484-490.

Ivanova, S. and Vasileva, L., 2017. Current and emerging strategies in osteoporosis management. Current Pharmaceutical Design, 23(41), pp.6279-6287.

Kerr, C., Bottomley, C., Shingler, S., Giangregorio, L., de Freitas, H.M., Patel, C., Randall, S. and Gold, D.T., 2017. The importance of physical function to people with osteoporosis. Osteoporosis International, 28(5), pp.1597-1607.

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Nakanishi, K., Shishido, K., Kumata, C., Ito, K., Nakashima, Y. and Wakasa, M., 2018. Bone density of the femoral neck in patients on maintenance dialysis. PloS one, 13(5), p.e0197965.

Pu, F., Chen, N. and Xue, S., 2016. Calcium intake, calcium homeostasis and health. Food Science and Human Wellness, 5(1), pp.8-16.

Sugiyama, T. and Oda, H., 2017. Osteoporosis therapy: bone modeling during growth and aging. Frontiers in endocrinology, 8, p.46.

Summers, R. and Macnab, R., 2017. Thyroid, parathyroid hormones and calcium homeostasis. Anaesthesia & Intensive Care Medicine, 18(10), pp.522-526.

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Walker, J., 2020. Osteoporosis and fragility fractures: risk assessment, management and prevention. Nursing older people, 32(2).pp.34-56.

Watts, N.B., 2018. Postmenopausal osteoporosis: a clinical review. Journal of women's health, 27(9), pp.1093-1096.

Zhang, L., Zhao, Y., Wen, Y., Ma, M., Cheng, S., Cheng, B., Liu, L., Li, P., Qi, X., Liang, C. and Zhang, F., 2019. Linkage disequilibrium score regression distinguishes associations between lean body mass and blood plasma proteome.Molecular Genetics. 3(2). pp.90-122.