Osteoporosis from an Endocrine Perspective: The Role of Hormonal Changes in the Elderly

Abstract

Introduction: Osteoporosis is increasingly prevalent in the elderly, with fractures mostly occurring in women and men who are older than 55 and 65 years of age, respectively. The aim of this review was to examine the evidence regarding the influence of hormones on bone metabolism, followed by clinical data of hormonal changes in the elderly, in the attempt to provide possible poorly explored diagnostic and therapeutic candidate targets for the management of primary osteoporosis in the aging population. Material and methods: An extensive Medline search using PubMed, Embase, and Cochrane Library was performed. Results: While the rise in Thyroid-stimulating hormone (TSH) levels has a protective role on bone mass, the decline of estrogen, testosterone, Insulin-like growth factor 1 (IGF1), and vitamin D and the rise of cortisol, parathyroid hormone, and follicle-stimulating hormone (FSH) favor bone loss in the elderly. Particularly, the AA rs6166 FSH receptor (FSHR) genotype, encoding for a more sensitive FSHR than that encoded by the GG one, is associated with low total body mass density (BMD), independently of circulating estrogen. A polyclonal antibody with a FSHR-binding sequence against the β-subunit of murine FSH seems to be effective in ameliorating bone loss in ovariectomized mice. Conclusions: A complete hormonal assessment should be completed for both women and men during bone loss evaluation. Novel possible diagnostic and therapeutic tools might be developed for the management of male and female osteoporosis.

Sex differences in body composition, metabolism‐related hormones, and energy homeostasis during aging in Wistar rats

“…Sex differences found in BMC is mediated by testosterone, which promotes male growth, acting on both bone size and mass, while estrogens limit the female growth of the appendicular skeleton (Zhang et al., 1999). Also, estradiol stimulates osteoblast proliferation and differentiation and inhibits osteoclast differentiation, so the decrease of BMC and BMD in 18‐month‐old female rats may be due to decreased estrogen and high CORT levels, which reduce maturation, lifespan, and function of osteoblast (Cannarella et al., 2019). On the other hand, the fact that at 18‐month‐old male rats kept BMD could be because estrogen is a major regulator of bone in male, and estradiol levels do not change in the aged male (Greenblatt et al., 1976; Khosla & Monroe, 2001; Van Pottelbergh et al., 2003).…”

Trabecular bone scores in young HIV-infected men: a matched case-control study

“…The pathogenesis of bone loss in HIV-infected individuals is a complex and multifactorial process, with HIV itself, the use of antiretroviral agents, hypogonadism in men, menopause in women, low body mass index (BMI), aging, malnutrition, steroid use, and smoking all associated with bone disease [2]. Hormonal changes in postmenopausal women or in elderly people are associated changes in the bone remodeling cycle, which leads to bone fragility and an increased risk of bone fracture [3,4].…”

Molecular Basis of Bone Aging

“…Osteoblastic cells derived from aged human donors exhibit decreased proliferative responses to GH and to the platelet-derived growth factor compared with younger donor cells [36]. Cultured osteoblasts deriving from younger subjects show a greater increase in idroxyproline production in response to estrogen stimulation compared to osteoblasts obtained from older subjects [37]. Many studies proved that 1.25 (OH)Vitamin D 3 stimulation was less effective in increasing the expression of the osteoblastic markers osteocalcin and ALP in osteoblasts derived from aged subjects [38,73].…”