**5. Osteoporosis**

Osteoporosis is regarded as a silent bone disorder. Though it is silent and associated with least symptoms, it seeks the most attention. It is reported that osteoporosis targets every third woman and every fifth man beyond 50 years of their ages [44]. Osteoporosis is a pathological condition in which bone mineral density is severely diminished with weakened bone microarchitecture [45]. Bones at the areas specific to hip, wrist and spine are highly vulnerable for the osteoporotic fractures. The occurrence ratio in female to male for the osteoporosis is 1:6 with 61% of fractures befalling in the women [46]. Besides, postmenopausal women have a greater tendency towards osteoporosis [47]. It is predicted that there would be around 6 million victims having osteoporosis by the year 2050 [48]. Osteoporosis is categorized into two major types mentioned as follows:

#### **5.1 Primary osteoporosis**

Primary osteoporosis is the most usual type of osteoporosis. It has two subcategories: Type-I osteoporosis/postmenopausal osteoporosis, is a well-recognized bone issue in the postmenopausal women that is chiefly instigated by estrogen deficit due to menopause, while type-II osteoporosis/age-related osteoporosis is mainly caused as a result of aging in women and men both [49]. In Type-I primary

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*MicroRNAs as Next Generation Therapeutics in Osteoporosis*

osteoporosis, bone loss hastens in the first 5 years of menopause and then slowly becomes constant. Estrogen executes the fundamental role in the bone development. It stimulates pro-collagen synthesis in the osteoblasts while acting against the bone resorbing cytokines [50, 51]. Estrogen is also capable of supporting osteoblast differentiation [52]. Moreover, estrogen deficiency induces the production of reactive oxygen species that results in increased osteoclast differentiation [53]. Thus, a shortage of estrogen after menopause is one prime cause of osteoporosis majorly in women. In the case of type II primary osteoporosis, age is the main cause that leads to fractures. With growing age, availability of minerals decreases, oxidants production increases while the body becomes less active and does not absorb calcium and vitamin D efficiently that overall thins out the density of bone and reduces the

Bone disorders which are secondary impediments of other health-related issues, e.g., adverse effects of drugs interventions, fluctuations in the cycle of physical activities, etc. are acknowledged under the category of secondary Osteoporosis [49]. Glucocorticosteroids and anticonvulsant-based interventions are majorly reported in the cases of secondary osteoporosis [55]. Several other disorders, e.g., endocrinopathies, which have the tendency to reduce the bone mass and interfere with normal bone formation, are also capable of inducing secondary osteoporosis. This form of osteoporosis is found in both pre/post- menopausal

With recent advances in technology and knowledge, many therapeutic strategies

**Mechanism/effect Harmful effects**

Severe joint and bone pain, serious allergic reactions, and osteonecrosis

Kidney-related issues, seizure, intense dizziness, and trouble while breathing

Risk of breast cancer, venous thromboembolism,

and leg cramps

by binding to minerals of the bone matrix

mediated bone disruption, also treats hypercalcemic

conditions

effects in the bone that decreases bone resorption and enhances

bone density

are available for the management of osteoporosis (**Table 1**). Broadly, treatment measures against osteoporosis are classified under two classes: anti-resorptive and anabolic. Anti-resorptive agents work to reduce the rate of bone dissolution while

anabolic agents attempt to boost bone formation and development.

**6. Current therapeutic measures for osteoporosis**

**dose of the drug**

Alendronate 5 mg, 10 mg Inhibits osteoclastogenesis

Zoledronic acid 5 mg/ml Diminishes osteoclast

Raloxifene 60 mg Mimics estrogen like

**Drug Administration** 

**Anti-resorptive strategies 1. Bisphosphonates**

**2. Estrogen modulators**

*DOI: http://dx.doi.org/10.5772/intechopen.91223*

strength [54].

**5.2 Secondary osteoporosis**

women and men [55].

*MicroRNAs as Next Generation Therapeutics in Osteoporosis DOI: http://dx.doi.org/10.5772/intechopen.91223*

osteoporosis, bone loss hastens in the first 5 years of menopause and then slowly becomes constant. Estrogen executes the fundamental role in the bone development. It stimulates pro-collagen synthesis in the osteoblasts while acting against the bone resorbing cytokines [50, 51]. Estrogen is also capable of supporting osteoblast differentiation [52]. Moreover, estrogen deficiency induces the production of reactive oxygen species that results in increased osteoclast differentiation [53]. Thus, a shortage of estrogen after menopause is one prime cause of osteoporosis majorly in women. In the case of type II primary osteoporosis, age is the main cause that leads to fractures. With growing age, availability of minerals decreases, oxidants production increases while the body becomes less active and does not absorb calcium and vitamin D efficiently that overall thins out the density of bone and reduces the strength [54].
