Abstract

Osteoporosis was first described more than 150 years ago by the English surgeon Sir Astley Cooper. He observed a connection between reduced bone volume or grade and hip fractures. In 1940, American endocrinologist Fuller Albright found a link between menopausal women’s bone loss and estrogen insufficiency.There are two types of osteoporosis: primary and secondary. Menopausal osteoporosis (type I) and senile osteoporosis (type II) are the two main types. Postmenopausal osteoporosis is associated with decreased estrogen levels following menopause and mostly affects the bones of the trabecular region.Kits were used in determination of Parathyriod hormon , Vitamin D level and minirals ( Ca, P and Mg).The physiological investigation involved measuring the levels of minerals (Ca, P, and Mg), vitamin D, and parathyriod hormone. According to the physiological results, there was a significant correlation (p ≤ 0.05) between the study groups in terms of residence, occupation, BMI, mother history, marital status, number of births, menopause state, medication taken, other diseases, soft drink, parathyroid (PTH), vitamin D, and P mineral..

Keywords: Vitamin D, and P mineral, Osteoporosis

Introduction
Osteoporosis is characterized by a decrease in bone mass and microstructural degradation of the bone tissue, which leads to increased fracture risk and bone fragility. (Eараhоb et al,2009).
There are two types of osteoporosis: primary and secondary. Postmenopausal osteoporosis (type I) and senile osteoporosis (type II) are the two main types. Postmenopausal osteoporosis is associated with decreased estrogen levels following menopause and mostly affects the trabecular bone. Senile osteoporosis, on the other hand, is common in older men and women and is characterized by both cortical thinning and trabecular bone loss. Renal failure, hyperparathyroidism, anorexia nervosa, Cushing’s syndrome, and glucocorticoid substitution are among the factors linked to secondary osteoporosis type, which affects both cortical and trabecular bone. (Riggs et al, 1982).
Serum calcium levels can be affected by hyperparathyroidism either directly or indirectly. About 3–4% of postmenopausal women have primary hyperparathyroidism, which frequently goes years without showing any symptoms. It significantly results in cortical bone loss in the skeleton, which subsequently causes the disease to develop (Dempster et al, 2007). The length of time the illness should be observed prior to medicinal or surgical intervention is debatable (Rubin et al., 2008).
By encouraging intestine absorption of these ions and stimulating bone resorption, vitamin D metabolites primarily maintain blood calcium and phosphate levels. Vitamin D is also important for maintaining the strength of an adult’s skeleton. Elderly individuals typically have low intakes of calcium and vitamin D from dairy products, less usage of sunshine and skin production of vitamin D, and reduced production of 1,25(OH)2 D3 with secondary hyperparathyroidism (Rizzoli et al., 2001).
Like calcium, phosphorus is one of the key minerals that make bones, and bone requires a sufficient amount of phosphorus throughout life. The proper skeletal mineralization depends on phosphorus, and low serum phosphate levels result in poor bone mineralization and weakened osteoblast function. surprisingly, there is minimal proof that phosphorus consumption in the diet influences the occurrence of osteoporosis in individuals in good health, with the exception of very low birth weight infants (Prentice, 2004).
Magnesium plays a crucial role in bone crystal formation and stabilization as well as bone and mineral homeostasis. Additionally, it affects the parathyroid hormone-vitamin D axis. It is currently unknown how magnesium affects the risk of osteoporotic fractures. Magnesium consumption has been shown in a few studies to be favorably correlated with bone resorption indicators and BMD in middle-aged females, and magnesium supplementation has been linked to short-term increases in BMD. The comprehension of these data may be complicated by size effects and bone remodeling transients (Robins et al., 2000).
When PTH is administered intermittently, osteoblast activity and number rise, increasing bone mass and improving skeletal architecture in both trabecular and cortical bone. PTH receptors are found in osteoblasts, bone lining cells, and bone marrow stromal cells. Infrequent PTH stimulates these cells by altering cAMP concentrations and cAMP-dependent protein kinase A. Additionally, the PTH receptor stimulates the growth of osteoblastic lineage cells by activating the calcium protein kinase C pathway (Victoria et al., 2010).
Material and Methods
Study Design , Setting and Data Collection Time
Between January and April of 2015, a case-control study was carried out in the rheumatology unit of Merjan Teaching Hospital in Babylon, Iraq, involving 70 Iraqi patients with osteoporosis and 30 healthy individuals. All patients and controls belonged to the same ethnic group (Arabic). The research project included 70 female patients with ages ranging from 20 to 82 who were chosen from Merjan Teaching Hospital. Thirty females between the ages of 20 and 71 who appeared to be in good health were enrolled in the control group trial. Prior to their involvement in the study, each individual provided written consent.

Determination of Parathyroid hormone (PTH) concentration in serum
TEST PROCEDURE
Strictly follow the fully automatic chemiluminescence immunoassay (CLIA) analyzer MAGLUMI’s operating directions to guarantee accurate test performance. An RFID tag on the Reagent Integral is used to identify each test parameter. See the Fully-auto Chemiluminescence Immunoassay (CLIA) analyzer MAGLUMI Operating Instruction kit for more details.

Determination of Vitamin D concentration in serum ( CLIA )
TEST PROCEDURE
Follow the MAGLUMI Fully-auto chemiluminescence immunoassay (CLIA) analyzer’s operating instructions to the letter to guarantee accurate test performance. An RFID tag on the Reagent Integral is used to identify each test parameter. Refer to the MAGLUMI kit Fully-auto chemiluminescence immunoassay (CLIA) analyzer’s usage manual for more details.
Diagnostic kit for determination of calcium concentration
PROCEDURE
The ACCENT-200 and ACCENT-200 II GEN automated analyzers can use this reagent. 1. The reagent is prepared for usage. It is advised to use deionized water as a reagent blank.
APPLICATION for ACCENT – 200
Diagnostic kit for the determination of magnesium concentration
PROCEDURE The ACCENT-200 and ACCENT-200 II GEN automated analyzers can use this reagent. 1. The reagent is prepared for usage.
a foaming void.
It is advised to use deionized water as a reagent blank.
Diagnostic kit for determination of phosphorus concentration
PROCEDURE Automatic analyzers may employ this reagent. The ACCENT-200 II GEN 1-Reagent is prepared for use. It is advised to use deionized water as a reagent blank for ACCENT-200 and ACCENT-200 II GEN applications.
Results and Discussion
Mean Differences of PTH by Study Groups
The mean variations in parathyroid (PTH) serum concentrations are displayed in Table 1. The study groups’ mean parathyroid (PTH) levels differed significantly (p < 0.05). There is a connection between vitamin D and the PTH hormone. It is widely accepted that vitamin D’s effects on bone are closely related to PTH activity because PTH is necessary for vitamin D to function on bone and because vitamin D inhibits PTH synthesis both directly (by activating a VDRE in the PTH gene promoter) and indirectly (by raising calcium concentration). Additionally, vitamin D affects calcium sensitivity by increasing the transcription of CasR (Calcium Sensitivity Receptor) and suppresses the proliferation of parathyroid cells39 (Mattia et al., 2015).
Each region should try to determine the lowest limit of normality for serum 25OHD, which is defined as the level at which mean serum PTH levels start to rise, indicating secondary hyperparathyroidism, since a lack of vitamin D may be asymptomatic but predisposes to a greater loss of bone alongside consequent elevated likelihood of fractures (Thomas et al., 1998).
Sambrook, P.N., et al. accepted the results (Sambrook et al. 2004). Regardless of the rise in the frequency of falls, a rise in fractures is linked to a drop in vitamin D levels and an increase in PTH levels (Pasco et al. 2004).
Other factors, such as a rise in parathyroid hormone (PTH) concentration with age, were also deemed significant in both men and women. The gradual but unstoppable loss of bone mass linked to aging in both sexes has been linked to the age-related increase in PTH and other homeostatic “breakdowns.” In contrast to estrogen-deficient women who do not develop osteoporosis, dietary calcium deficiencies combined with vitamin D deficiency can significantly contribute to the increases in PTH associated with aging (John 1998), which is comparable to the results in figures (1), (2).
In contrast, normal vitamin D levels promote adequate calcium levels in the bloodstream. The parathyroid gland cells are sensitive to these two elements by having VDR and calcium-sensing receptors, which act by combating PTH hypersecretion and the resulting bone resorption (Cunningham et.al, 2011; Diamond et.al,2013; Flávia and Josefina,2014).
According to Jeri (2005), hyperparathyroidism is linked to inadequate nutrition, which increases the risk of osteoporosis. This usually results in table (1), which shows the correlation between PTH and P. Heaney RP accepts the substantial mean difference of P (0.000) caused by poor nutrition. Table (1) displays the mean differences of serum concentration of P by study groups. Mineralization and bone growth will be restricted by low serum phosphate (Heaney 2004). Thus, a lack of phosphorus may restrict osteoblast activity and promote osteoclastic bone breakdown (Heaney 2002).

Table (1) The mean of serum concentration of PTH, Vitamin D, Ca, Mg and P

* significant at 0.05

Correlation factor of PTH ,vitamin D with age, Ca, P, Mg.
Figures (1) and (2) illustrate the relationship among the patient group’s age and serum levels of vitamin D and parathyroid hormone (PTH). There are a number of reasons why the PTH is raised as people age. Renal osteodystrophy (ROD) and chronic kidney disease-mineral and bone disorder (CKD-MBD) are two of these causes, as is persistent kidney disease (CKD), which is most frequently linked to aging and osteoporosis. and the PTH level in accordance with these anomalies (Moe et al., 2006).
Menopause, BMI, and thyroid gland diseases are further causes of this age-related abnormality in PTH levels. Age and estrogen insufficiency have a significant impact on blood PTH and markers of bone repair. It is also possible to discover characteristics that predict changes in serum PTH and bone turnover in older women, which result in the appearance of osteoporosis.
Additionally, estrogen therapy directly decreases bone resorption; this is linked to a compensatory rise in blood PTH levels, which is most common in women with breast cancer (Ledger et al., 1995). Reduced vitamin D blood levels are strongly correlated with raised PTH levels, body fat, and BMI (Noncommunicable illnesses Country Profiles; World Health Organization: Geneva, Switzerland, 2011).

Figure(1)Correlation between PTH and age

Figure(2)Correlation between Vitamin D and age.

It is concerning that vitamin D was found to have an impact on PTH levels. Compared to a bone biopsy to demonstrate greater PTH-mediated bone resorption or a mineralization deficiency, serum vitamin D levels are an increasingly clinically accessible indicator of vitamin D status. Bone mineralization may be hampered by low vitamin D levels below the usual range (Chapuy and Meunier 1997). Concerns about PTH-mediated reduction in bone mass in this study population are raised by the association between vitamin D and PTH. Numerous studies have shown a link between vitamin D and secondary hyperparathyroidism, especially in older individuals (mean age 81 years) in outdoor, homebound, and nursing facility settings (Lips et al., 1995).

Table (2) demonstrates that the studied minerals (Ca, Mg, P) do not correlate with PTH or vitamin D. While numerous searches and research have shown that there is no association between PTH and vitamin D blood level and Ca, Mg, and P, the relationship between PTH and vitamin D level in the blood and P is unclear (BROT et al., 1999; International Society of Nephrology, 1988).

Table(2) Correlation between PTH and vitamin D with (Ca, Mg, P)

p value r Variables
Conclusion
PTH, P, and vitamin D have an impact on how diseases manifest. PTH and vitamin D levels are strongly correlated with patients’ ages. PTH and vitamin D are significant risk factors for illness.

Acknowledgment
Non.
Conflicts Interest
Non.

References
• BROT, C.N. JéRGENSEN, O. R. MADSEN, L. B. JENSEN & O. H. SéRENSEN, (1999). Relationships between bone mineral density, serum vitamin D metabolites and calcium:phosphorus intake in healthy perimenopausal women. Journal of Internal Medicine 1999; 245: 509]516
• Cunningham, J.; Locatelli, F.; Rodriguez, M. (2011). Secondary hyperparathyroidism: Pathogenesis,disease progression, and therapeutic options. Clin. J. Am. Soc. Nephrol., 6, 913–921.
• Diamond, T.; Wong, Y.K.; Golombick, T. (2013). Effect of oral cholecalciferol 2000 vs. 5000 IU onserum vitamin D, PTH, bone and muscle strength in patients with vitamin D deficiency.Osteoporos. Int., 24, 1101–1105.
• Eараhоb ВС, Hbаmеhkо Тe, Eараhоbа ЕВ, H др. (2009). Генетhескhh nасnорт основа индивидуальной и предиктивной медицины. Баранов ВС (ред.). Санкт- Петербург: Н-Л, 527 с.
• Flávia Galvão Cândido * and Josefina Bressan (2014). Vitamin D: Link between Osteoporosis, Obesity, and Diabetes?. Int. J. Mol. Sci, 15, 6569-6591; doi:10.3390/ijms15046569
• Heaney RP, Nordin BE. (2002). Calcium effects on phosphorus absorption:implications for the prevention and co-therapy of osteoporosis. J AmColl Nutr;21:239–44.
• International Society of Nephrology, (1988). Parathyroid hormone and 1 ,25(OH)2D3 in chronic renal failure. Kidney International, Vol. 33, pp. 1049—1 058
• Ledger GA, Burritt MF, Kao PC, O’Fallon WM, Riggs BL, Khosla S. 1995 Role of parathyroid hormone in mediating nocturnal and age-related increases in bone resorption. J Clin Endocrinol Metab. 80:3304 –3310.
• Lips P, Chapuy MC, Dawson-Hughes B, Pols HAP (1995). International comparison of serum 25-hydroxyvitamin D measurements. J Bone Miner Res 10:S496
• Mattia Bellana, Mario Pirisi a,b, Pier Paolo Sainaghi,(2015). Osteoporosis in rheumatoid arthritis: role of the vitamin D/parathyroid hormone system. r e v b r a s r e u m a t o l . 201 5; 5 5(3):256–263
• Moe SM, Drüeke T, Cunningham J, et al. Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGOR). Kidney Int. 2006;69:1945-1953.
• Pasco, J.A., (2004). Seasonal periodicity of serum vitamin D and parathyroid hormone, bone resorption, and fractures: the Geelong OsteoporosisStudy. J. Bone Miner. Res. 19:752–758.
• Prentice A. (1997). Is nutrition important in osteoporosis? Proceedings of the Nutrition Society; 56: 357–67.
• PrenticeA, (2004), Diet, nutrition and the prevention of osteoporosis. Public Health Nutrition: 7(1A), 227–243.
• Raisz, L.G., (2005). Pathogenesis of osteoporosis: concepts, conflicts, and prospects. J Clin Invest. 115(12): p. 3318-25.
• Riggs BL, Melton LJ: Evidence for two distinct syndromes of involutional osteoporosis. AmJ Med, 1982; 75: 899-901.
• Rizzoli, J-P Bonjour and S L Ferrari(2001), Osteoporosis, genetics and hormones. Journal of Molecular Endocrinology (2001) 26, 79–94.
• Robins SP, New SA, Campbell MK, (2000). Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable intake and bone health? American Journal of Clinical Nutrition; 71:142–51.
• Rubin, M.R., (2008). The natural history of primary hyperparathyroidism with or without parathyroid surgery after 15 years. J Clin Endocrinol Metab,. 93(9): p. 3462-70.
• Sambrook, P.N., et al. 2004. Serum parathyroid hormone is associated with increased mortality independent of 25-hydroxy vitamin d status, bone mass, and renal function in the frail and very old: a cohort study. J. Clin. Endocrinol. Metab. 89:5477–5481.
• Thomas MK, Lloyd-Jones DM, Thadhani RI, Demay MB. Hypovitaminosis D in medical inpatients. N Engl J Med. 1998;338:777-83.
• Victória Z. Cochenski Borba1, Nádila Cecyn Pietszkowski Mañas1(2010), The use of PTH in the treatment of osteoporosis. Arq Bras Endocrinol Metab. 2010;54/2