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��ࡱ�>��	�����������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������e�	��?[bjbj��	Ix�di\�di\�j,���������8&p|�������8���$��k��&Z
+ + + +,,,CjEjEjEjEjEjEj$bn�q2ij�&,,,!,-,ij + +�kB�6�6�65,~ + +�e~�6,Cj�6�6��F�kH +�����4��������3�kG�e\kH�kG�JqQ64Jq(kHkH�Jq^J�,,�6,,,,,ijij�6,,,�k,,,,��������������������������������������������������������������������Jq,,,,,,,,,�>�:	�Osteoporosis: Pathogenesis, Treatment and Opportunities� 
University Institute of Pharmaceutical Sciences
Panjab University, Chandigarh-160014



Address for correspondence:
Supriya Verma
Email id:  HYPERLINK "mailto:supriya_punjab@yahoo.com" supriya_punjab@yahoo.com
Phone No: 9463453377
















ABSTRACT  

The term �Osteoporosis� is a combination of two words �osteo� and �porosis� which means bone and porous respectively, so osteoporosis literally means porous bone.  It makes the bone more fragile and easily susceptible to fracture. It may be due to an abnormal increase in bone loss, which results in the loss of normal bone strength. Bone loss increases in women after  HYPERLINK "https://en.wikipedia.org/wiki/Menopause" \o "Menopause" menopause,�due to lower levels of� HYPERLINK "https://en.wikipedia.org/wiki/Estrogen" \o "Estrogen" estrogen. On the other hand, men also undergo gradual bone loss with aging, which results into fragile bones. The root cause is the reduction of free testosterone. Osteoporosis may also occur due to a number of diseases (cancer, diabetes), medication (steroids) or treatment. The porosity in this disease may weaken the bone to such a degree, a break may occur with minor stress (fall) and spontaneously. It leads to various types of fractures i.e., vertebral, nonvertebral and hip fractures.�In fact, a fracture is typically the first outward sign of the disease, and advanced osteoporosis is potentially very painful and disabling. There is imbalance between the bone cells i.e., osteoclasts and osteoblasts, which effect the bone remodeling process, which plays a major contribution in the development of osteoporosis. The number of women with osteoporosis is increasing in India. Thus, osteoporosis is a major public health problem in Indian women. Different types of drugs are available in the market, but calcium, estrogen, vitamin D and bisphosphonates are the first-line drugs for the treatment of osteoporosis. Some drugs are antiresorptive i.e., bisphosphosphonates, while the others are osteoanabolic by nature i.e., teriparatide. In order to treat vertebral compression fractures (spine fracture), a surgical treatment (noninvasive) is carried out, which is known as vertebroplasty and kyphoplasty.
Keywords:
Osteoporosis, Osteoblasts, Osteoclasts, Bone remodeling, Bisphosphonates.













INTRODUCTION
Osteoporosis is the most common metabolic and systemic disease of bone that affects the entire skeleton, which leads to an increased level of bone fragility and susceptibility to fracture. It is characterized by micro-artectural deterioration of the skeleton and a condition of low bone mass  ADDIN EN.CITE <EndNote><Cite><Author>Che CT</Author><Year>2015</Year><RecNum>19</RecNum><record><rec-number>19</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">19</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Che CT,</author><author>Wong MS,</author></authors></contributors><titles><title>Ligustrum lucidum and its Constituents: A Mini-Review on the Anti-Osteoporosis Potential</title><secondary-title>Nat Prod Commun</secondary-title></titles><periodical><full-title>Nat Prod Commun</full-title></periodical><pages>2189-94.</pages><volume>10</volume><number>12</number><dates><year>2015</year></dates><isbn>1934-578X (Print)&#xD;1555-9475 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Khajuria DK</Author><Year>2011</Year><RecNum>2</RecNum><record><rec-number>2</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">2</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Khajuria DK,</author><author>Razdan R,</author><author>Mahapatra DR,</author></authors></contributors><titles><title>Drugs for the management of osteoporosis: a review</title><secondary-title>Rev Bras Reumatol</secondary-title></titles><periodical><full-title>Rev Bras Reumatol</full-title></periodical><pages>365-71</pages><volume>51</volume><number>4</number><keywords><keyword>0 (Diphosphonates)</keyword><keyword>Diphosphonates/adverse effects/therapeutic use</keyword><keyword>Humans</keyword><keyword>Osteoporosis/diagnosis/*drug therapy</keyword></keywords><dates><year>2011</year></dates><isbn>1809-4570 (Electronic)&#xD;0482-5004 (Linking)</isbn><urls></urls></record></Cite></EndNote>(1, 2). Osteoporosis or porous bone condition is a silent disease which has  no symptoms until a fracture occurs. The World Health Organization (WHO) has defined  �Osteoporosis as a condition in which a bone mineral density (BMD) is more than 2.5 standard deviations below the mean of normal, healthy individuals at their peak bone mass�  ADDIN EN.CITE <EndNote><Cite><Author>Gronholz MJ</Author><Year>2008</Year><RecNum>9</RecNum><record><rec-number>9</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">9</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Gronholz MJ,</author></authors></contributors><titles><title>Prevention, diagnosis, and management of osteoporosis-related fracture: a multifactoral osteopathic approach</title><secondary-title>J Am Osteopath Assoc.</secondary-title></titles><periodical><full-title>J Am Osteopath Assoc.</full-title></periodical><pages>575-85.</pages><volume>108</volume><number>10</number><keywords><keyword>Aged</keyword><keyword>Aged, 80 and over</keyword><keyword>Female</keyword><keyword>Fractures, Bone/diagnosis/*etiology</keyword><keyword>Health Status Indicators</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>*Osteopathic Medicine</keyword><keyword>Osteoporosis/complications/*diagnosis/prevention &amp; control/therapy</keyword><keyword>Risk Factors</keyword></keywords><dates><year>2008</year></dates><isbn>1945-1997 (Electronic)&#xD;0098-6151 (Linking)</isbn><urls></urls></record></Cite></EndNote>(3).  This term �osteoporosis� was used by Jean Lobstein (French pathologist and surgeon)  first time  in 1835 ADDIN EN.CITE <EndNote><Cite><Author>Lorentzon M</Author><Year>2015</Year><RecNum>5</RecNum><record><rec-number>5</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">5</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Lorentzon M,</author><author>Cummings SR,</author></authors></contributors><titles><title>Osteoporosis: the evolution of a diagnosis</title><secondary-title>J Intern Med</secondary-title></titles><periodical><full-title>J Intern Med</full-title></periodical><pages>650-61</pages><volume>277</volume><number>6</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>X1J18R4W8P (Alendronate)</keyword><keyword>*Absorptiometry, Photon/methods</keyword><keyword>*Aging</keyword><keyword>Alendronate/therapeutic use</keyword><keyword>*Bone Density</keyword><keyword>Bone Density Conservation Agents/therapeutic use</keyword><keyword>Fractures, Bone/etiology/prevention &amp; control</keyword><keyword>Hip Fractures/etiology</keyword><keyword>Humans</keyword><keyword>Osteoporosis/complications/*diagnosis/drug therapy</keyword><keyword>Risk Factors</keyword><keyword>Treatment Outcome</keyword></keywords><dates><year>2015</year></dates><orig-pub>aetiology&#xD;fracture&#xD;osteoporosis</orig-pub><isbn>1365-2796 (Electronic)&#xD;0954-6820 (Linking)</isbn><urls></urls></record></Cite></EndNote>(4). There are various types of osteoporosis. These are:
Primary osteoporosis: It is divided into type I (postmenopausal) & type II (senile) osteoporosis  ADDIN EN.CITE <EndNote><Cite><Author>Marcucci G</Author><Year>2010</Year><RecNum>4</RecNum><record><rec-number>4</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">4</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Marcucci G,</author><author>Brandi ML,</author></authors></contributors><titles><title>Kyphoplasty and vertebroplasty in the management of osteoporosis with subsequent vertebral compression fractures</title><secondary-title>Clin Miner Bone Metab.</secondary-title></titles><periodical><full-title>Clin Miner Bone Metab.</full-title></periodical><pages>51-60.</pages><volume>7</volume><number>1</number><dates><year>2010</year></dates><isbn>1724-8914 (Print)&#xD;1724-8914 (Linking)</isbn><urls></urls></record></Cite></EndNote>(5).  
Secondary osteoporosis: It includes age-independent factors i.e, glucocorticoid-induced osteoporosis, moderate or heavy alcohol intake and cigarette smoking.
Idiopathic osteoporosis: It includes dietary factors, diseases, sedentary lifestyle, pregnancy-related and post-partum osteoporosis  ADDIN EN.CITE <EndNote><Cite><Author>Khadilkar AV</Author><Year>2015</Year><RecNum>10</RecNum><record><rec-number>10</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">10</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Khadilkar AV,</author><author>Mandlik RM,</author></authors></contributors><titles><title>Epidemiology and treatment of osteoporosis in women: an Indian perspective</title><secondary-title>Int J Womens Health.</secondary-title></titles><periodical><full-title>Int J Womens Health.</full-title></periodical><pages>841-50 </pages><volume>7</volume><dates><year>2015</year></dates><orig-pub>Indian perspective&#xD;epidemiology&#xD;osteoporosis&#xD;treatment</orig-pub><isbn>1179-1411 (Electronic)&#xD;1179-1411 (Linking)</isbn><urls></urls></record></Cite></EndNote>(6).
About 200 million people suffer from osteoporosis worldwide. Out of them, one-tenth are women of age 60 years, one-fifth of age 70 years, two-fifth of age 80 years and two-third of age 90 years. Moreover, in India, 1 out of every 3 females and 1 out of every 8 males, suffer from osteoporosis. This disease is also among the most common diseases in the United States, and can result in devastating physical, psychological and economic consequences. In Europe, the disability due to osteoporosis is much greater than that caused by cancer (with the exception of lung cancer) and is comparable or greater than a variety of chronic non-communicable diseases, such as rheumatoid arthritis, asthma and cardiovascular diseases (7). Different types of drugs are used in its treatment like bisphosphonates, strontium ranelate, teriparatide and denosumab.
Bone Cells (Osteoclasts and Osteoblasts):
Bones are living, active tissues that renew themselves via a process called remodeling. This remodeling process is initiated by the �osteoclasts� which removes the old cells from the bone tissue, deposit them in the bloodstream for their removal and also create small holes in the bone. The cells �osteoblasts� fill the holes with the �mortar� of calcium, minerals and collagen. There is an important role of the parathyroid hormone (PTH), as it activates the osteoclasts and osteoblasts and signals the osteoclasts to pull calcium from the bones. The osteoblast cells are stimulated by the calcitonin hormones and deposit calcium into the bones. The osteoblast cells must be able to do their job effectively. Because the exhausted osteoblasts are one of the primary reasons for bone loss  ADDIN EN.CITE  ADDIN EN.CITE.DATA (8,9).
There are specific sites on the bone surface, where bone undergoes the remodeling process and these sites are known as basic multicellular units (BMU). As it is known to us, the remodeling process is carried out by the osteoclasts (bone resorption cells) and osteoblasts (bone forming cells). Moreover, this process is highly dependent on the delicate balance of the regulatory signalling and the cellular activity. If there is loss of capacity to deactivate osteoclasts or to recruit the active osteoblasts, it results in a net bone loss and to the onset of osteoporosis  ADDIN EN.CITE <EndNote><Cite><Author>Martin TJ</Author><Year>2007</Year><RecNum>6</RecNum><record><rec-number>6</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">6</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Martin TJ,</author><author>Seeman E,</author></authors></contributors><titles><title>New mechanisms and targets in the treatment of bone fragility</title><secondary-title>Clin Sci (Lond).</secondary-title></titles><periodical><full-title>Clin Sci (Lond).</full-title></periodical><pages>77-91.</pages><volume>112</volume><number>2</number><keywords><keyword>0 (PTH protein, human)</keyword><keyword>0 (Parathyroid Hormone)</keyword><keyword>0 (Receptors, Parathyroid Hormone)</keyword><keyword>Bone Density</keyword><keyword>Bone Remodeling/*drug effects</keyword><keyword>Bone Resorption</keyword><keyword>Bone and Bones/cytology/metabolism</keyword><keyword>Female</keyword><keyword>Fractures, Bone/prevention &amp; control</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Osteoporosis/*drug therapy</keyword><keyword>Parathyroid Hormone/metabolism/*therapeutic use</keyword><keyword>Patient Selection</keyword><keyword>Receptors, Parathyroid Hormone/metabolism</keyword></keywords><dates><year>2007</year></dates><isbn>1470-8736 (Electronic)&#xD;0143-5221 (Linking)</isbn><urls></urls></record></Cite></EndNote>(9).
Steps of bone remodeling:
1- Stimulation of osteoclasts (bone resorption cells):- The bone resorption cells secrete the enzymes collagenases and proteinases, which solubilizes the bone matrix and releases calcium into circulation for physiological functions.
2- Once osteoclasts die, osteoblasts (bone forming cells) differentiate and lay down new bone matrix at the sites of previous resorption, which is known as osteoid. 
3- Once the process bone formation is completed, the osteoblasts are inactivated and differentiated into osteocytes, on the surface of the new bone. 
4- The new bone is then mineralized with hydroxyapatite (HAP). The complete process of bone  mineralization and hardening  takes several months  ADDIN EN.CITE <EndNote><Cite><Author>McClung MR</Author><Year>2015 </Year><RecNum>26</RecNum><record><rec-number>26</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">26</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>McClung MR,</author></authors></contributors><titles><title>Emerging Therapies for Osteoporosis</title><secondary-title>Endocrinol</secondary-title></titles><periodical><full-title>Endocrinol</full-title></periodical><pages>429-35</pages><volume>30</volume><number>4</number><dates><year>2015 </year></dates><orig-pub>Cathepsin K&#xD;Osteoporosis&#xD;Parathyroid hormone-related protein&#xD;Sclerostin&#xD;Therapy</orig-pub><isbn>2093-596X (Print)&#xD;2093-596X (Linking)</isbn><urls></urls></record></Cite></EndNote>(10).
Bone Markers:
1. Serum osteocalcin, bone specific alkaline phosphatase, total alkaline phosphatase and type I procollagen (C-terminal/ N-terminal) - for bone formation.
2. Tartrate-resistant acid phosphatase (TRAP), type I collagen cross-linked N- (NTX) and C-telopeptide (CTX) - for bone resorption  ADDIN EN.CITE <EndNote><Cite><Author>Henriksen K</Author><Year>2015</Year><RecNum>14</RecNum><record><rec-number>14</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">14</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Henriksen K,</author><author>Christiansen C,</author><author>Karsdal MA,</author></authors></contributors><titles><title>Role of biochemical markers in the management of osteoporosis</title><secondary-title>Climacteric</secondary-title></titles><periodical><full-title>Climacteric</full-title></periodical><pages>10-8</pages><volume>18</volume><number>Suppl 2</number><dates><year>2015</year></dates><orig-pub>Bone quality&#xD;Bone turnover marker&#xD;Fracture&#xD;Prediction&#xD;Response to therapy</orig-pub><isbn>1473-0804 (Electronic)&#xD;1369-7137 (Linking)</isbn><urls></urls></record></Cite></EndNote>(11). 
Increase in the level of alkaline phosphatase (ALP) is the important indicator of the bone formation cells and decrease in tartrate-resistant acid phosphatase (TRAP) is the most important indicator of the bone resorption cells.

Figure No. 1: The diagrammatic representation of different steps of bone remodeling process.
Role of Wingless-type (Wnt) pathway: As shown in the above given figure, it is clear that the bone cells osteoblasts and osteoclasts play a very important role in the bone remodeling process. Moreover, in order to understand this process and to regulate the bone formation properly, it is required to know about the Wnt pathway.
The Wnt pathway recognised as having a major role in the regulation of bone formation. It is a protein signalling pathway for osteoblasts (derived from mesenchymal stem cell). It inhibits differentiation of adipocytes and promotes cell lineages of osteoblast, by controlling its proliferation, maturation, and terminal differentiation. It has Low density Lipoprotein Receptor related Protein (LRP) 5 and 6 as co-receptors to its frizzled receptors. It shows some of the transcription factors, which involves (the bone morphogenetic protein 2 and 7, beta-catenin, Runx2, osterix and nuclear factor of activated T-cells (NFAT). When osteoblasts have done their job, then they may become incorporated into the bone matrix as osteocytes (may transform into living cells on the bone surface or may undergo death/apoptosis/necrosis). 
Osteoblasts synthesize RANKL (receptor activator of NF-Kappa B ligand) which is necessary for osteoclasts formation and function. But osteoprotegerin (OPG) is its decoy receptor. Ratio of RANKL/OPG is used to predict the induction or suppression of osteoclastogenesis, the decreased ratio represents induction of osteoclastogenesis and vice versa  ADDIN EN.CITE  ADDIN EN.CITE.DATA (12, 13). Moreover, female hormone estrogen may exert its effect on bone by OPG expression in osteoblasts  ADDIN EN.CITE <EndNote><Cite><Author>Bord S</Author><Year>2003</Year><RecNum>25</RecNum><record><rec-number>25</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">25</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bord S,</author><author>Ireland DC,</author><author>Beavan SR,</author><author>Compston JE,</author></authors></contributors><titles><title>The effects of estrogen on osteoprotegerin, RANKL, and estrogen receptor expression in human osteoblasts</title><secondary-title>Bone.</secondary-title></titles><periodical><full-title>Bone.</full-title></periodical><pages>136-41.</pages><volume>32</volume><number>2</number><keywords><keyword>0 (Estrogen Antagonists)</keyword><keyword>0 (Estrogens)</keyword><keyword>0 (Glycoproteins)</keyword><keyword>0 (Osteoprotegerin)</keyword><keyword>0 (Receptors, Cytoplasmic and Nuclear)</keyword><keyword>0 (Receptors, Estrogen)</keyword><keyword>0 (Receptors, Tumor Necrosis Factor)</keyword><keyword>0 (TNFRSF11B protein, human)</keyword><keyword>Cells, Cultured</keyword><keyword>Estrogen Antagonists/pharmacology</keyword><keyword>Estrogens/*pharmacology</keyword><keyword>Female</keyword><keyword>Gene Expression Regulation, Developmental/drug effects/physiology</keyword><keyword>Glycoproteins/*biosynthesis/genetics</keyword><keyword>Humans</keyword><keyword>Infant</keyword><keyword>Infant, Newborn</keyword><keyword>Osteoblasts/*drug effects/*metabolism</keyword><keyword>Osteoprotegerin</keyword><keyword>Receptors, Cytoplasmic and Nuclear/*biosynthesis/genetics</keyword><keyword>Receptors, Estrogen/agonists/antagonists &amp; inhibitors/*biosynthesis/genetics</keyword><keyword>Receptors, Tumor Necrosis Factor</keyword><keyword>Up-Regulation/drug effects</keyword></keywords><dates><year>2003</year></dates><isbn>8756-3282 (Print)&#xD;1873-2763 (Linking)</isbn><urls></urls></record></Cite></EndNote>(14).
Inhibitors of Wnt signaling pathway:
Sclerostin, is a protein which is secreted by osteocytes, it binds to co-receptors LRP5/6 and inhibits their association with Wnt pathway, thus acting as an inhibitor of this pathway. Dickkopf1 (DKK1) is another negative regulator of the Wnt signaling pathway that acts by directly binding to LRP5 and LRP6 (12). 
PATHOGENESIS 
Senescence of bone cells 
Lifestyle factors i.e., primary exercise and nutrition
Loss of vitamin D metabolism with age
Poor vitamin D metabolism leads to a decrease in the absorption of intestinal calcium and, results in the signalling of parathyroid hormone, to withdraw calcium from the bones. Overtime, this continuous removal of calcium from the bones lead to a stage of decreased bone mass and development of osteoporosis  ADDIN EN.CITE  ADDIN EN.CITE.DATA (6, 15, 16).
Skeletal fracture can result from: 
(a) Failure to produce optimal mass and strength during growth. 
(b) Excessive bone resorption which leads to decreased bone mass. 
(c)  An inadequate formation response to increased resorption during remodeling process. 
Moreover, the larger number of unfilled Howship s lacuna (tiny depressions, pits, or irregular grooves in bone that is being resorbed by osteoclasts) and haversian canals (minute tubes which form a network in bone and contain blood vessels) further weaken the bone. Excessive resorption can also result in complete loss of trabecular structures, so that there is no template for bone formation  ADDIN EN.CITE  ADDIN EN.CITE.DATA (13, 17). 
Central role of estrogen:
Estrogen deficiency plays a major role in the pathogenesis of osteoporosis. In postmenopausal women, whose estrogen levels decline naturally, are at the highest risk for developing this disease. Morphological studies and measurements of certain bone markers have indicated that the process of bone remodeling is accelerated at the menopause.
Moreover, fracture risk is inversely related to estrogen levels in the postmenopausal women. Estrogen is critical for epiphyseal closure in puberty, and is required for the regulation of bone turnover in both sexes. Although androgen play a role, but estrogen has a greater effect than androgen in inhibiting bone resorption in men  ADDIN EN.CITE  ADDIN EN.CITE.DATA (13). Estrogen may also have an important role in the acquisition of peak bone mass in men. Moreover, in older men osteoporosis is closely associated with low level of estrogen than with low androgen. Estrogen treatment decreases the rate of bone remodeling, as well as the amount of bone loss with each remodeling cycle  ADDIN EN.CITE  ADDIN EN.CITE.DATA (18, 19). 
Animal models and cell culture studies have suggested that, multiple sites are involved for the estrogen action, not only the cells of the BMU, but other marrow cells are also involved in it. Estrogen acts through 2 receptors: estrogen receptor alpha and beta, i.e., ER� and ER�. 
ER� appears to be the primary mediator of estrogen s actions on the skeleton. Osteoblasts do express ER�, but the actions of ER� agonists on bone are not much clear. Single nucleotide polymorphisms (SNPs) of ER� may affect the fragility of bone. An orphan nuclear receptor  i.e., estrogen receptor-related receptor � (ERR�), having sequence homology to ER� and ER� is also present in bone cells. Despite its inability to bind estrogens, this receptor may interact with ER� and ER� or act directly to alter bone cell function. Sex hormone-binding globulin (SHBG) is the major binding protein for sex steroids in plasma, which not only alter the bioavailability of estrogen to hormone responsive tissues, but also affect its entry into cells  ADDIN EN.CITE  ADDIN EN.CITE.DATA (20).
Diagnosis of osteoporosis: Computed tomography, x-ray and dual energy x-ray absorptiometry (DXA) images are used in cross-sectional and longitudinal studies in osteoporosis. Fracture Risk Assessment Tool (FRAX), an absolute risk assessment tool, which includes BMD testing based on age and fracture probability by using predetermined assessment thresholds  ADDIN EN.CITE  ADDIN EN.CITE.DATA (21, 22).
Animal model: The suitable animal model used for the study of osteoporosis is ovariectomized (OVX) rats or mice; by making use of this model, we can quantify the drug levels in the desired part of the body. The findings will be assessed on the basis of animal weight, morphology of target bone, and histochemical localization of ALP (an osteoblastic marker) and TRAP (an osteoclastic marker).�In the target bone sections, the osteoclastic activity will be confirmed by TRAP staining, and the bone formation is assessed by making use of ALP staining. The color intensity of  the enzymes TRAP and ALP  will be evaluated from the images by the image analysis software, which is developed locally  ADDIN EN.CITE <EndNote><Cite><Author>Komori T</Author><Year>2015</Year><RecNum>23</RecNum><record><rec-number>23</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">23</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Komori T,</author></authors></contributors><titles><title>Animal models for osteoporosis</title><secondary-title>Eur J Pharmacol</secondary-title></titles><periodical><full-title>Eur J Pharmacol</full-title></periodical><pages>287-94</pages><volume>759</volume><keywords><keyword>0 (Estrogen Receptor alpha)</keyword><keyword>0 (Glucocorticoids)</keyword><keyword>Animals</keyword><keyword>Apoptosis/drug effects</keyword><keyword>Bone Resorption</keyword><keyword>*Disease Models, Animal</keyword><keyword>Estrogen Receptor alpha/genetics</keyword><keyword>Female</keyword><keyword>Glucocorticoids/administration &amp; dosage</keyword><keyword>Hindlimb Suspension</keyword><keyword>Humans</keyword><keyword>Osteoblasts/drug effects/pathology</keyword><keyword>Osteoclasts/drug effects/pathology</keyword><keyword>Osteoporosis/*etiology/genetics/immunology/pathology</keyword><keyword>Ovariectomy</keyword><keyword>Species Specificity</keyword></keywords><dates><year>2015</year></dates><orig-pub>Estrogen&#xD;Glucocorticoid&#xD;Osteocyte&#xD;Osteoporosis&#xD;Sympathetic nerve&#xD;Unloading</orig-pub><isbn>1879-0712 (Electronic)&#xD;0014-2999 (Linking)</isbn><urls></urls></record></Cite></EndNote>(23).
TREATMENT STRATEGIES: Therapy should be chosen on the basis of thetype of osteoporosis  ADDIN EN.CITE <EndNote><Cite><Author>Kling JM</Author><Year>2014</Year><RecNum>31</RecNum><record><rec-number>31</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">31</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Kling JM,</author><author>Clarke BL,</author><author>Sandhu NP,</author></authors></contributors><titles><title>Osteoporosis prevention, screening, and treatment: a review</title><secondary-title>J Womens Health (Larchmt)</secondary-title></titles><periodical><full-title>J Womens Health (Larchmt)</full-title></periodical><pages>563-72</pages><volume>23</volume><number>7</number><keywords><keyword>0 (Diphosphonates)</keyword><keyword>Absorptiometry, Photon/economics</keyword><keyword>Aged</keyword><keyword>Bone Density/*physiology</keyword><keyword>Cost-Benefit Analysis</keyword><keyword>Diphosphonates/economics/*therapeutic use</keyword><keyword>Female</keyword><keyword>Fractures, Bone/*prevention &amp; control</keyword><keyword>Humans</keyword><keyword>Mass Screening/economics/*methods</keyword><keyword>Osteoporosis/diagnosis/*drug therapy/economics/*prevention &amp; control</keyword><keyword>Risk Assessment</keyword></keywords><dates><year>2014</year></dates><isbn>1931-843X (Electronic)&#xD;1540-9996 (Linking)</isbn><urls></urls></record></Cite></EndNote>(24):
Antiresorptive drugs, which slow the progressive thinning of bone e.g., hormone replacement therapy (HRT), bisphosphonates (BP), calcitonin, and estrogen agonists.
Bone forming drugs e.g., teriparatide which helps to rebuild the skeleton, and drugs with a more complex mechanism of action.
Calcium and vitamin D precursors to ensure adequate intake and to ensure maximum effectiveness of the drug therapy  ADDIN EN.CITE <EndNote><Cite><Author>Tsai KS</Author><Year>1984</Year><RecNum>33</RecNum><record><rec-number>33</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">33</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Tsai KS,</author><author>Heath H 3rd,</author><author>Kumar R,</author><author>Riggs BL,</author></authors></contributors><titles><title>Impaired vitamin D metabolism with aging in women. Possible role in pathogenesis of senile osteoporosis</title><secondary-title>J Clin Invest.</secondary-title></titles><periodical><full-title>J Clin Invest.</full-title></periodical><pages>1668-72.</pages><volume>73</volume><number>6</number><keywords><keyword>0 (Parathyroid Hormone)</keyword><keyword>0 (Phosphates)</keyword><keyword>1406-16-2 (Vitamin D)</keyword><keyword>E0399OZS9N (Cyclic AMP)</keyword><keyword>EC 3.1.3.1 (Alkaline Phosphatase)</keyword><keyword>FXC9231JVH (Calcitriol)</keyword><keyword>P6YZ13C99Q (Calcifediol)</keyword><keyword>SY7Q814VUP (Calcium)</keyword><keyword>Aged</keyword><keyword>*Aging</keyword><keyword>Alkaline Phosphatase/blood</keyword><keyword>Calcifediol/blood</keyword><keyword>Calcitriol/blood</keyword><keyword>Calcium/blood</keyword><keyword>Cyclic AMP/urine</keyword><keyword>Female</keyword><keyword>Glomerular Filtration Rate</keyword><keyword>Humans</keyword><keyword>Osteoporosis/etiology/*physiopathology</keyword><keyword>Parathyroid Hormone/blood</keyword><keyword>Phosphates/blood</keyword><keyword>Vitamin D/*metabolism</keyword></keywords><dates><year>1984</year></dates><isbn>0021-9738 (Print)&#xD;0021-9738 (Linking)</isbn><urls></urls></record></Cite></EndNote>(15).
Drugs used in the treatment of osteoporosis:
1. Bisphosphonates e.g., alendronate, ibandronate, etiodronate, zoledronate and risedronate
2. Teriparatide or Parathyroid Hormone
3. Raloxifene (Selective Estrogen Receptor Modulator, SERM)
4. Calcitonin
5. Strontium Ranelate
6. Hormone Replacement Therapy 
7. Calcium and Vitamin D
8. Denosumab	
1. Bisphosphonates: They are called bisphosphonates because they have phosphonate groups (PO (OH) 2) linked by phosphoether bonds. This arrangement makes BP stable by nature and resistant to the biological degradation. They inhibit the osteoporosis by having antiresorptive action or by slowing bone loss, as they encourages the osteoclasts to undergo apoptosis, or cell death. 
They appear to stimulate the proliferation of preosteoblast cells transiently and to increase their differentiation. They may increase the production of antiresorptive protein (osteoprotegerin) by osteoblasts. Drugs of bisphosphonate class are divided into two categories based on their chemical structure, one is the nitrogen containing while the other is non-nitrogen containing bisphosphonates. Nitrogen containing bisphosphonates i.e., alendronate are more potent than the non-nitrogen containing bisphosphonates i.e., etiodronate, by their ability to suppress osteoclast activity (as measured by biochemical markers of bone turnover). 
Mechanism of Action: Negative charge on the phosphate group of the bisphosphonate nucleus gave these compounds a high affinity for the surface of bone. BPs act on bone metabolism by binding and blocking the enzyme farnesyl pyrophosphate synthase (FPPS), in the HMG-CoA (3-hydroxy-3-methylglutaryl-Coenzyme A) reductase pathway (also known as mevalonate pathway). After binding to the mineralized bone surface, BPs are taken up by the osteoclasts during resorption of bone. It causes lipid modification of many proteins which are found in osteoclast i.e., Ras, Rho and Rac (which play a central role in the regulation of core osteoclasts, cellular activity including stress fibre assembly and membrane ruffling. As a result their survival is inhibited by the loss of the protein prenylation. Because of this loss of protein prenylation, osteoclasts become unable to resorb bone, which ultimately lead to osteoclast apoptosis  ADDIN EN.CITE <EndNote><Cite><Author>Maraka S</Author><Year>2015</Year><RecNum>21</RecNum><record><rec-number>21</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">21</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Maraka S,</author><author>Kennel KA,</author></authors></contributors><titles><title>Bisphosphonates for the prevention and treatment of osteoporosis</title><secondary-title>BMJ (Clinical research ed.)</secondary-title></titles><periodical><full-title>BMJ (Clinical research ed.)</full-title></periodical><pages>h3783</pages><volume>351</volume><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>Bone Density/drug effects</keyword><keyword>Bone Density Conservation Agents/adverse effects/*therapeutic use</keyword><keyword>Diphosphonates/adverse effects/*therapeutic use</keyword><keyword>Female</keyword><keyword>Fractures, Bone/etiology/prevention &amp; control</keyword><keyword>Humans</keyword><keyword>Osteoporosis/complications/*drug therapy/*prevention &amp; control</keyword></keywords><dates><year>2015</year></dates><isbn>1756-1833 (Electronic)&#xD;0959-535X (Linking)</isbn><urls></urls></record></Cite></EndNote>(25). The BPs also have the ability to inhibit apoptosis in osteocytes, which appears to be mediated through the opening of connexin 3 hemichannels and subsequent activation of extracellular signal-regulated kinases (ERKs).
Different types of BPs with its dosage, uses and marketed products are mentioned in the   table given below. Out of them, alendronate and ibandronate are the second generation derivatives of bisphosphonates, which localizes preferentially on bone resorption surfaces by binding to the exposed calcium phosphate bone mineral. Osteoclasts attach to these surfaces by a tight seal enclosing a space into which they secrete acid and dissolve the mineral. During this process, the bisphosphonates are released and can reach local concentration in high micromolecular range  ADDIN EN.CITE <EndNote><Cite><Author>Drake MT</Author><Year>2008</Year><RecNum>12</RecNum><record><rec-number>12</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">12</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Drake MT,</author><author>Clarke BL,</author><author>Khosla S,</author></authors></contributors><titles><title>Bisphosphonates: mechanism of action and role in clinical practice</title><secondary-title>Mayo Clin Proc.</secondary-title></titles><periodical><full-title>Mayo Clin Proc.</full-title></periodical><pages>1032-45</pages><volume>83</volume><number>9</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>Bone Density Conservation Agents/administration &amp; dosage/*pharmacology</keyword><keyword>Bone Resorption/drug therapy</keyword><keyword>Bone and Bones/drug effects</keyword><keyword>Breast Neoplasms/drug therapy</keyword><keyword>Diphosphonates/administration &amp; dosage/*pharmacology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Multiple Myeloma/drug therapy</keyword><keyword>Osteitis Deformans/*drug therapy</keyword><keyword>Osteoclasts/*drug effects</keyword><keyword>Osteoporosis/*drug therapy</keyword><keyword>Prostatic Neoplasms/drug therapy</keyword></keywords><dates><year>2008</year></dates><isbn>1942-5546 (Electronic)&#xD;0025-6196 (Linking)</isbn><urls></urls></record></Cite></EndNote>(26). Zoledronic acid which is one of the third generation derivative of bisphosphonates, is the only BP that has been developed exclusively for i.v. but not for oral use, which has led to an attractive once-yearly regimen in the treatment for osteoporosis. It has fastest onset of action among the bisphosphonates on different types of fracture, a rapid effect appears for vertebral fractures and not for reduction of hip and nonvertebral fractures (44,45).
Table No.1: The different drugs of the class bisphosphonates  ADDIN EN.CITE <EndNote><Cite><Author>Banu J</Author><Year>2013</Year><RecNum>7</RecNum><record><rec-number>7</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">7</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Banu J,</author></authors></contributors><titles><title>Causes, consequences, and treatment of osteoporosis in men</title><secondary-title>Drug Des Devel Ther</secondary-title></titles><periodical><full-title>Drug Des Devel Ther</full-title></periodical><pages>849-60 </pages><volume>7</volume><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>3XMK78S47O (Testosterone)</keyword><keyword>Aging</keyword><keyword>Animals</keyword><keyword>*Bone Density</keyword><keyword>Bone Density Conservation Agents/therapeutic use</keyword><keyword>Dietary Supplements</keyword><keyword>Diphosphonates/therapeutic use</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Mass Screening/methods</keyword><keyword>Nutritional Status</keyword><keyword>Osteoporosis/*epidemiology/etiology/therapy</keyword><keyword>Osteoporotic Fractures/*epidemiology</keyword><keyword>Risk Factors</keyword><keyword>Testosterone/administration &amp; dosage/metabolism</keyword></keywords><dates><year>2013</year></dates><orig-pub>antibodies&#xD;bisphosphonates&#xD;hormones&#xD;male osteoporosis&#xD;nutritional supplements&#xD;protein inhibitors&#xD;risk factors</orig-pub><isbn>1177-8881 (Electronic)&#xD;1177-8881 (Linking)</isbn><urls></urls></record></Cite></EndNote>(27).
DrugDosage/FrequencyAdvantagesSide effectsMarketed ProductEtiodronate400 mg daily�! BMD in lumbar vertebraeGI tract intolerance,  bone, joint and muscle pain, jaw pain, severe diarrhoea, numbness or swellingDidronelIbandronate2.5 mg daily or 150 mg monthly or 3 mg every 3 months (IV)�! BMD spine, trochanter, femur neckGI tract intolerance, hives, swelling of mouth and throat, flu-like symptoms, osteonecrosis of jawBonivaAlendronate10 mg daily or 70 mg weekly�! BMD in vertebre, femoral neckGI tract intoleranceFosamax or Fosamax PlusRisedronate5 mg daily or 35 mg weekly or 75 mg monthly or 150 mg monthly�! Bone massGI tract intoleranceActonelZoledronate5 mg yearly (IV)�! Bone massFlu-like symptoms, osteonecrosis of jawReclast,
ZomediaAmongst a wide range of drugs available in the treatment of osteoporosis, bisphosphonates are known as first-line drugs, on account of their reasonable efficacy, while cost benefits also matter to a sizable extent (28). Drugs of this class are commercially available as oral tablets and/or i.v. infusion viz., ibandronate (Boniva), alendronate (Fosamax), risedronate (Actonel) and zoledronate (Zometa). However, these often lead to adverse side-effects, which include severe gastrointestinal (GI) disturbances, inflammation, pain and osteonecrosis of jaw. It also sometimes leads to transient post-infusion influenza-like illness, arrhythmia, serious atrial fibrillation, mild transient hypocalcemia and renal failure. 
The major challenge of a vast majority of drugs of this class, is patient non-compliance and intolerance, while their bioavailability is also considerably sub-optimal. The poor GI absorption and decreased bioavailability demand more number of molecules (i.e., high dose) to be administered, which eventually leads to multiple side-effects involving GI tract, and beyond. These observations call for research to bring novelty in terms of enhanced absorption, reduced dosage and bio-acceptable interactions with the absorbing GI mucosal membrane. This can be worked out either by chemical modification or by modifying the surface characteristics of the molecules, without tampering its original chemistry. The latter is more feasible, less time-consuming and economically viable option, which attracts the interest and attention of the formulation scientists. The present time is quite conducive and encouraging, as it provides the advancements in the field of drug delivery coupled with the relevant development in engineering and technology to support research and development in this domain.
RISEDRONATE (RSD)
RSD is a FDA-approved third generation bisphosphonate, which is an antiresorptive agent, for the treatment of osteoporosis, available in the market as oral tablet dosage forms. It has considered to possess strong affinity for bone, prolonged stay period, high potency in blocking the bone dissolution, and versatile usage, i.e., in the treatment of Postmenopausal Osteoporosis (PMO), Male Osteoporosis (MO), Glucocorticoid-induced Osteoporosis (GIOP) and Paget�s Disease (resulting in enlarged and mis-shaped bones). However, the patients show poor compliance to its regimen due to GI irritation or ulceration with its oral administration, while permeation remains the challenge  ADDIN EN.CITE  ADDIN EN.CITE.DATA (29-31). Moreover, all the marketed products are based on age-old formulation approaches (empirical practices), made up of conventional materials like crospovidone, hydroxypropyl cellulose, hypromellose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, silicon dioxide and titanium dioxide (www.fda.gov.), which have no capacity to overcome the bio-hurdles present therein. 
Mechanism of Action
RSD is a bone resorption inhibitor. It has good affinity for hydroxyapatite crystals in bone and acts as an antiresorptive agent, as it is an inhibitor of farnesyl pyrophosphate synthase (FPPS) enzyme in osteoclasts. FPPS is a key enzyme in the mevalonate pathway, which generates isoprenoid lipids utilized for the post-translational modification of small GTP- binding proteins that are essential for osteoclast function, which results in downstream inhibition of osteoclast activity and reduced bone resorption and turnover  ADDIN EN.CITE <EndNote><Cite><Author>Russell</Author><Year>2008</Year><RecNum>11</RecNum><record><rec-number>11</rec-number><foreign-keys><key app="EN" db-id="wrrwztps82zperewsevpvpph0a0r2rfwpp00">11</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Russell , R.G.</author><author>Watts , N.B.</author><author>Ebetino , F.H.</author><author>Rogers , M.J.</author></authors></contributors><titles><title>Mechanisms of action of bisphosphonates: similarities and differences and their potential influence on clinical efficacy</title><secondary-title>Osteoporos Int.</secondary-title></titles><periodical><full-title>Osteoporos Int.</full-title></periodical><pages>733-59</pages><volume>19</volume><number>6</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>Animals</keyword><keyword>Bone Density/drug effects</keyword><keyword>Bone Density Conservation Agents/pharmacokinetics/*pharmacology/therapeutic use</keyword><keyword>Bone Resorption/prevention &amp; control</keyword><keyword>Bone and Bones/*drug effects/metabolism/physiology</keyword><keyword>Diphosphonates/pharmacokinetics/*pharmacology/therapeutic use</keyword><keyword>Humans</keyword><keyword>Osteoclasts/drug effects</keyword><keyword>Osteocytes/drug effects</keyword><keyword>Osteoporosis/drug therapy/metabolism/physiopathology</keyword><keyword>Structure-Activity Relationship</keyword></keywords><dates><year>2008</year></dates><isbn>0937-941X (Print)&#xD;0937-941X (Linking)</isbn><urls></urls></record></Cite></EndNote>(32).
Pharmacokinetics
The pharmacokinetics of RSD is not influenced by age or gender. Though the drug inherently is reported to be well-absorbed, but, the hindrances occur due to the varied complex interactions in GI environment majorly, on account of bivalent ions like calcium or other polyvalent cations. It has low plasma protein binding (~ 24%), with no evidence of systemic metabolism. It is excreted unchanged primarily via the kidney. Insignificant amounts (<0.1% of intravenous dose) of drug are excreted in the bile in rats. It has a short biological/elimination half life (~ 1.5 hours) and faster clearance rate (122 mL/min)  ADDIN EN.CITE <EndNote><Cite><Author>Kim</Author><Year>2016</Year><RecNum>200</RecNum><record><rec-number>200</rec-number><foreign-keys><key app="EN" db-id="wrrwztps82zperewsevpvpph0a0r2rfwpp00">200</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Kim , J.S.</author><author>Jang , S.W.</author><author>Son , M.</author><author>Kim , B.M.</author><author>Kang , M.J.</author></authors></contributors><titles><title>Enteric-coated tablet of risedronate sodium in combination with phytic acid, a natural chelating agent, for improved oral bioavailability</title><secondary-title>Eur J Pharm Sci.</secondary-title></titles><periodical><full-title>Eur J Pharm Sci.</full-title></periodical><pages>45-51</pages><volume>82</volume><dates><year>2016</year></dates><orig-pub>Chelating agent&#xD;Enteric-coated&#xD;Oral bioavailability&#xD;Phytic acid&#xD;Risedronate sodium</orig-pub><isbn>1879-0720 (Electronic)&#xD;0928-0987 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Sweetman</Author><RecNum>297</RecNum><record><rec-number>297</rec-number><foreign-keys><key app="EN" db-id="wrrwztps82zperewsevpvpph0a0r2rfwpp00">297</key></foreign-keys><ref-type name="Edited Book">28</ref-type><contributors><authors><author>Sweetman, S.C.</author></authors><secondary-authors><author> </author></secondary-authors></contributors><titles><title>Martindale: The Complete Drug Reference</title></titles><dates><year>2009</year><pub-dates><date>Sep&#xD;2014 Sep</date></pub-dates></dates><publisher>thirty sixth</publisher><isbn>1354-5752 (Print)&#xD;1354-5752 (Linking)</isbn><urls></urls></record></Cite></EndNote>(33,34).
Adverse effects and Contraindications
The GI disturbance (irritation and ulceration) is the major adverse effect. There is no reported drug interaction with the orally administered drug. The drug is contraindicated in individuals with a history of renal disease i.e., creatinine clearance less than 30 mL/min  ADDIN EN.CITE <EndNote><Cite><Author>Crandall</Author><Year>2001</Year><RecNum>40</RecNum><record><rec-number>40</rec-number><foreign-keys><key app="EN" db-id="psta9xsv2fv2dhextr0vwzrkap59rvtp9dx2">40</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Crandall, C.,</author></authors></contributors><titles><title>Risedronate: a clinical review</title><secondary-title>Arch Intern Med.</secondary-title></titles><periodical><full-title>Arch Intern Med.</full-title></periodical><pages>353-60</pages><volume>161</volume><number>3</number><keywords><keyword>0 (Calcium Channel Blockers)</keyword><keyword>0 (Glucocorticoids)</keyword><keyword>M2F465ROXU (Etidronic Acid)</keyword><keyword>OFG5EXG60L (Risedronate Sodium)</keyword><keyword>Animals</keyword><keyword>Bone Density/drug effects</keyword><keyword>Bone and Bones/*drug effects</keyword><keyword>Breast Neoplasms/drug therapy</keyword><keyword>Calcium Channel Blockers/*pharmacology/*therapeutic use</keyword><keyword>Etidronic Acid/analogs &amp; derivatives/*pharmacology/*therapeutic use</keyword><keyword>Female</keyword><keyword>Glucocorticoids/pharmacology/therapeutic use</keyword><keyword>Humans</keyword><keyword>Osteitis Deformans/drug therapy</keyword><keyword>Osteoporosis/*drug therapy</keyword><keyword>Osteoporosis, Postmenopausal/drug therapy</keyword><keyword>Risedronate Sodium</keyword></keywords><dates><year>2001</year></dates><isbn>0003-9926 (Print)&#xD;0003-9926 (Linking)</isbn><urls></urls></record></Cite></EndNote>(34,35).
2.1.2.1. CHALLENGES
 The patient-compliance to current formulations is inadequate due to complications of its oral intake regimen and GI inflammatory reactions. Some of the main challenges with this drug molecule are enlisted below:
Oral bioavailability is less than 1 % (0.63% in fasting)
Adverse effects such as ulcers, esophagitis, gastritis, renal failure, osteonecrosis and musculoskeletal pain 
The presence of Ca2+ or other divalent cations in the GI tract or intestinal lumen hampers its absorption, by forming nonabsorbable complexes with the metal ions
It cannot be given to the patient at bedtime or within 2 hours of food or fluid (except water) 
Patients should not lie down for at least 30 minutes after taking the medication
Absorption is reduced by food, especially by products containing calcium or other polyvalent cations.
2. Teriparatide and Parathyroid Hormone: It is a 34-amino acid polypeptide of the 84 amino acids native parathyroid hormone molecule, it is produced by recombinant DNA technique. It is the only skeletal osteoanabolic agent, which is approved by US Food and Drug Administration (FDA).  But, the teriparatide treatment has limited by FDA to 24 months lifetime, because it can lead to the formation of osteosarcoma. It is given to the patient once a day by subcutaneous injection. But teriparatide treatment alone is more expensive and produced a smaller increase in Quality-adjusted life-year (QALYs) than alendronate. So, combination of teriparatide with other agents i.e., estrogen, alendronate, zoledronate and denosumab increases BMD substantially  ADDIN EN.CITE  ADDIN EN.CITE.DATA (27, 36).
3. Raloxifene (SERM): It is the only marketed SERM which has approved for treatment and prevention of postmenopausal osteoporosis. It prevents bone loss and is indicated for the prevention and treatment of vertebral fractures in postmenopausal women. Post hoc analysis showed a significant reduction of nonvertebral fractures. Bazedoxifene in combination with conjugated estrogens is recently approved by the FDA as �antiosteoporotic drug�  ADDIN EN.CITE <EndNote><Cite><Author>McClung MR</Author><Year>2015 </Year><RecNum>26</RecNum><record><rec-number>26</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">26</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>McClung MR,</author></authors></contributors><titles><title>Emerging Therapies for Osteoporosis</title><secondary-title>Endocrinol</secondary-title></titles><periodical><full-title>Endocrinol</full-title></periodical><pages>429-35</pages><volume>30</volume><number>4</number><dates><year>2015 </year></dates><orig-pub>Cathepsin K&#xD;Osteoporosis&#xD;Parathyroid hormone-related protein&#xD;Sclerostin&#xD;Therapy</orig-pub><isbn>2093-596X (Print)&#xD;2093-596X (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Drake MT</Author><Year>2015</Year><RecNum>37</RecNum><record><rec-number>37</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">37</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Drake MT,</author><author>Clarke BL,</author><author>Lewiecki EM,</author></authors></contributors><titles><title>The Pathophysiology and Treatment of Osteoporosis</title><secondary-title>Clin Ther</secondary-title></titles><periodical><full-title>Clin Ther</full-title></periodical><pages>1837-50</pages><volume>37</volume><number>8</number><dates><year>2015</year></dates><orig-pub>aging&#xD;bisphosphonate&#xD;bone&#xD;bone mineral density&#xD;menopause&#xD;osteoporosis</orig-pub><isbn>1879-114X (Electronic)&#xD;0149-2918 (Linking)</isbn><urls></urls></record></Cite></EndNote>(10, 36).
4. Calcitonin: Calcitonin (hormone) act as a antiresorptive agent, which reduces the occurrence of vertebral fractures in women but has not been shown to reduce the risk of nonvertebral fractures. Supplementation with calcium and vitamin D is mandatory with calcitonin  ADDIN EN.CITE <EndNote><Cite><Author>Khadilkar AV</Author><Year>2015</Year><RecNum>10</RecNum><record><rec-number>10</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">10</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Khadilkar AV,</author><author>Mandlik RM,</author></authors></contributors><titles><title>Epidemiology and treatment of osteoporosis in women: an Indian perspective</title><secondary-title>Int J Womens Health.</secondary-title></titles><periodical><full-title>Int J Womens Health.</full-title></periodical><pages>841-50 </pages><volume>7</volume><dates><year>2015</year></dates><orig-pub>Indian perspective&#xD;epidemiology&#xD;osteoporosis&#xD;treatment</orig-pub><isbn>1179-1411 (Electronic)&#xD;1179-1411 (Linking)</isbn><urls></urls></record></Cite></EndNote>(6).
5. Strontium Ranelate: Marketed and registered for the treatment of postmenopausal osteoporosis. It has dual mechanism of action: it has an antiresorptive action and anabolic action (stimulates osteoblasts to increase bone mass).
Dose:-2 gm sachet once daily by mouth. Strontium ranelate is not given to the patient with a history of thrombophlebitis  ADDIN EN.CITE <EndNote><Cite><Author>Sanchez JA</Author><Year>2015</Year><RecNum>35</RecNum><record><rec-number>35</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">35</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Sanchez JA,</author></authors></contributors><titles><title>Normalization of bone mineral density after five years of treatment with strontium ranelate</title><secondary-title>Clin Cases Miner Bone Metab.</secondary-title></titles><periodical><full-title>Clin Cases Miner Bone Metab.</full-title></periodical><pages>251-2</pages><volume>12</volume><number>3</number><dates><year>2015</year><pub-dates><date>&#xD;</date></pub-dates></dates><orig-pub>osteoporosis&#xD;strontium&#xD;treatment</orig-pub><isbn>1724-8914 (Print)&#xD;1724-8914 (Linking)</isbn><urls></urls></record></Cite></EndNote>(37).
6. Hormone Replacement Therapy (HRT): After menopause, due to the lack of hormone i.e., estrogen, rate of bone turnover increases, which results in accelerated bone loss. Indian guidelines advise that therapy with estrogen may be used for prevention and treatment of osteoporosis in the early postmenopausal period in women who are symptomatic. Thus, therapy with estrogen or estrogen and progesterone is believed to prevent osteoporotic fractures and increase lumbar spine and femoral neck BMD  ADDIN EN.CITE <EndNote><Cite><Author>Khadilkar AV</Author><Year>2015</Year><RecNum>10</RecNum><record><rec-number>10</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">10</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Khadilkar AV,</author><author>Mandlik RM,</author></authors></contributors><titles><title>Epidemiology and treatment of osteoporosis in women: an Indian perspective</title><secondary-title>Int J Womens Health.</secondary-title></titles><periodical><full-title>Int J Womens Health.</full-title></periodical><pages>841-50 </pages><volume>7</volume><dates><year>2015</year></dates><orig-pub>Indian perspective&#xD;epidemiology&#xD;osteoporosis&#xD;treatment</orig-pub><isbn>1179-1411 (Electronic)&#xD;1179-1411 (Linking)</isbn><urls></urls></record></Cite></EndNote>(6). Due to the reduction of free testosterone in men, they may develop gradual bone loss and testosterone replacement is one of the way to treat this condition  ADDIN EN.CITE <EndNote><Cite><Author>Banu J</Author><Year>2013</Year><RecNum>7</RecNum><record><rec-number>7</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">7</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Banu J,</author></authors></contributors><titles><title>Causes, consequences, and treatment of osteoporosis in men</title><secondary-title>Drug Des Devel Ther</secondary-title></titles><periodical><full-title>Drug Des Devel Ther</full-title></periodical><pages>849-60 </pages><volume>7</volume><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>3XMK78S47O (Testosterone)</keyword><keyword>Aging</keyword><keyword>Animals</keyword><keyword>*Bone Density</keyword><keyword>Bone Density Conservation Agents/therapeutic use</keyword><keyword>Dietary Supplements</keyword><keyword>Diphosphonates/therapeutic use</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Mass Screening/methods</keyword><keyword>Nutritional Status</keyword><keyword>Osteoporosis/*epidemiology/etiology/therapy</keyword><keyword>Osteoporotic Fractures/*epidemiology</keyword><keyword>Risk Factors</keyword><keyword>Testosterone/administration &amp; dosage/metabolism</keyword></keywords><dates><year>2013</year></dates><orig-pub>antibodies&#xD;bisphosphonates&#xD;hormones&#xD;male osteoporosis&#xD;nutritional supplements&#xD;protein inhibitors&#xD;risk factors</orig-pub><isbn>1177-8881 (Electronic)&#xD;1177-8881 (Linking)</isbn><urls></urls></record></Cite></EndNote>(27).
7. Calcium and vitamin D:  In order to treat osteoporosis, adequate calcium and vitamin D supplementation is required. The National Osteoporosis Foundation recommends elemental calcium dietary intake of 1200 mg per day for postmenopausal women. The recommended intake for vitamin D is 800�1000 IU per day with a target 25-hydroxy vitamin D level of at least 30 ng/ml  ADDIN EN.CITE <EndNote><Cite><Author>Lim SY</Author><Year>2015</Year><RecNum>13</RecNum><record><rec-number>13</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">13</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Lim SY,</author><author>Bolster MB,</author></authors></contributors><titles><title>Current approaches to osteoporosis treatment</title><secondary-title>Curr Opin Rheumatol</secondary-title></titles><periodical><full-title>Curr Opin Rheumatol</full-title></periodical><pages>216-24</pages><volume>27</volume><number>3</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>Bone Density Conservation Agents/therapeutic use</keyword><keyword>Diphosphonates/*therapeutic use</keyword><keyword>Humans</keyword><keyword>Osteoporosis/*drug therapy</keyword><keyword>Treatment Outcome</keyword></keywords><dates><year>2015</year></dates><isbn>1531-6963 (Electronic)&#xD;1040-8711 (Linking)</isbn><urls></urls></record></Cite></EndNote>(38).
Table No. 2: The comparison of different FDA approved medications and indications.
DrugPMOGIO (Men and Women)MOPreventionTreatmentPreventionTreatmentEstrogen"Alendronate PO""""Risedronate PO"""""Risedronate Delayed Release PO"Ibandronate PO""Ibandronate IV"Zoledronate IV"""""Calcitonin IN"Raloxifene PO""Denosumab SC""Teriparatide SC"""PMO: Postmenopausal osteoporosis, GIO: Glucorticoid Induced Osteoporosis, or MO: Male osteoporosis, PO: Peroral, IV: Intravenous, IN: Intranasal, SC: Subcutaneous.
As it is known to us, there are different types of drugs available for the treatment of osteoporosis. The above given table contains FDA approved drugs with their respective uses in PMO, GIO & MO respectively.
8. Denosumab: It is a human monoclonal antibody, which is very potent antiresorptive drug and blocks RANKL specifically. It is quiet efficacious in reducing the risk of vertebral, hip and nonvertebral fracture.  Moreover, it fully inhibits teriparatide-induced bone resorption at approved doses. Significantly greater treatment adherence is observed for subcutaneous administration, of denosumab every 6 months than for oral alendronate once weekly  ADDIN EN.CITE <EndNote><Cite><Author>Torring O</Author><Year>2015</Year><RecNum>22</RecNum><record><rec-number>22</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">22</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Torring O,</author></authors></contributors><titles><title>Effects of denosumab on bone density, mass and strength in women with postmenopausal osteoporosis</title><secondary-title>Ther Adv Musculoskelet Dis</secondary-title></titles><periodical><full-title>Ther Adv Musculoskelet Dis</full-title></periodical><pages>88-102</pages><volume>7</volume><number>3</number><dates><year>2015</year></dates><orig-pub>Fracture Reduction Evaluation of Denosumab in Osteoporosis Every 6 Months study&#xD;antiresorptive therapy&#xD;bisphosphonate&#xD;bone density&#xD;bone mass&#xD;bone strength&#xD;cortical porosity&#xD;denosumab&#xD;receptor activator of nuclear factor kappaB ligand</orig-pub><isbn>1759-720X (Print)&#xD;1759-720X (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Geusens P</Author><Year> 2015</Year><RecNum>16</RecNum><record><rec-number>16</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">16</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Geusens P,</author></authors></contributors><titles><title>New insights into treatment of osteoporosis in postmenopausal women</title><secondary-title>RMD Open</secondary-title></titles><periodical><full-title>RMD Open</full-title></periodical><pages>e000051</pages><volume>1</volume><number>Suppl 1</number><dates><year> 2015</year></dates><orig-pub>Bone Mineral Density&#xD;Osteoporosis&#xD;Treatment</orig-pub><isbn>2056-5933 (Electronic)&#xD;2056-5933 (Linking)</isbn><urls></urls></record></Cite></EndNote>(39, 40).
Adverse effects of antiosteoporotic drugs  ADDIN EN.CITE <EndNote><Cite><Author>Rizzoli R</Author><Year>2011</Year><RecNum>32</RecNum><record><rec-number>32</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">32</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Rizzoli R,</author><author>Reginster JY,</author><author>Boonen S,</author><author>Breart G,</author><author>Diez-Perez A,</author><author>Felsenberg D,</author><author>Kaufman JM,</author><author>Kanis JA,</author><author>Cooper C,</author></authors></contributors><titles><title>Adverse reactions and drug-drug interactions in the management of women with postmenopausal osteoporosis</title><secondary-title>Calcif Tissue Int</secondary-title></titles><periodical><full-title>Calcif Tissue Int</full-title></periodical><pages>91-104</pages><volume>89</volume><number>2</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>0 (Organometallic Compounds)</keyword><keyword>0 (Thiophenes)</keyword><keyword>04NQ160FRU (strontium ranelate)</keyword><keyword>10T9CSU89I (Teriparatide)</keyword><keyword>Bone Density Conservation Agents/adverse effects/pharmacology</keyword><keyword>Diphosphonates/adverse effects/therapeutic use</keyword><keyword>Drug Interactions/*physiology</keyword><keyword>Drug-Related Side Effects and Adverse Reactions/*epidemiology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Organometallic Compounds/adverse effects/therapeutic use</keyword><keyword>Osteoporosis, Postmenopausal/*drug therapy/*epidemiology</keyword><keyword>Pharmacovigilance</keyword><keyword>Teriparatide/adverse effects/therapeutic use</keyword><keyword>Thiophenes/adverse effects/therapeutic use</keyword></keywords><dates><year>2011</year></dates><isbn>1432-0827 (Electronic)&#xD;0171-967X (Linking)</isbn><urls></urls></record></Cite></EndNote>(41,43):
1. Bisphosphonates: Gastrointestinal Effects i.e., abdominal disturbances, Barrett�s esophagus, Esophageal cancer, Musculoskeletal pain, Acute-phase reaction, Atrial fibrillation, Atypical subtrochanteric fractures, Osteonecrosis of the jaw, Hypersensitivity reactions.
2.  Denosumab: Infections, Osteonecrosis of the jaw, Cancer.
3. Raloxifene: Hot flushes and Leg cramps, Venous thromboembolism, Cardiovascular events and Stroke.
4. Strontium Ranelate: Venous thromboembolism, Hypersensitivity.
5. Teriparatide or Parathyroid hormone: Nervous system disease, Osteosarcoma.
Vertebroplasty and Kyphoplasty (Surgical treatment): Whenever we study osteoporosis induced fracture, then we come to know an invasive surgery i.e., vertebroplasty and kyphoplasty. It is used to treat a vertebral compression fractures (VCFs) in the spinal column, which are a common result of osteoporosis. Physician inject a cement mixture into the fractured bone, in vertebroplasty. On the other hand, a balloon is inserted into the fractured bone to create a space, and then is filled with cement in kyphoplasty  ADDIN EN.CITE <EndNote><Cite><Author>Marcucci G</Author><Year>2010</Year><RecNum>4</RecNum><record><rec-number>4</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">4</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Marcucci G,</author><author>Brandi ML,</author></authors></contributors><titles><title>Kyphoplasty and vertebroplasty in the management of osteoporosis with subsequent vertebral compression fractures</title><secondary-title>Clin Miner Bone Metab.</secondary-title></titles><periodical><full-title>Clin Miner Bone Metab.</full-title></periodical><pages>51-60.</pages><volume>7</volume><number>1</number><dates><year>2010</year></dates><isbn>1724-8914 (Print)&#xD;1724-8914 (Linking)</isbn><urls></urls></record></Cite></EndNote>(5). 
The goals of this surgery:
To reduce pain in the patient from the fracture.
To stabilize the vertebra. 
To restore the vertebra back to its normal height.
New agents for the treatment of osteoporosis: With the evolving understanding of human bone biology, there is development of new approaches, for the treatment of osteoporosis. They are the inhibitors of cathepsin K and sclerostin. Cathepsin K, a cysteine protease expressed by osteoclasts, which mediates bone resorption through its effects on collagen matrix degradation. As already explained, sclerostin is an osteocyte-secreted Wnt signaling antagonist, which suppresses bone formation via its effects on osteoblast differentiation, activity, and survival  ADDIN EN.CITE <EndNote><Cite><Author>Drake MT</Author><Year>2008</Year><RecNum>12</RecNum><record><rec-number>12</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">12</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Drake MT,</author><author>Clarke BL,</author><author>Khosla S,</author></authors></contributors><titles><title>Bisphosphonates: mechanism of action and role in clinical practice</title><secondary-title>Mayo Clin Proc.</secondary-title></titles><periodical><full-title>Mayo Clin Proc.</full-title></periodical><pages>1032-45</pages><volume>83</volume><number>9</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Diphosphonates)</keyword><keyword>Bone Density Conservation Agents/administration &amp; dosage/*pharmacology</keyword><keyword>Bone Resorption/drug therapy</keyword><keyword>Bone and Bones/drug effects</keyword><keyword>Breast Neoplasms/drug therapy</keyword><keyword>Diphosphonates/administration &amp; dosage/*pharmacology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Multiple Myeloma/drug therapy</keyword><keyword>Osteitis Deformans/*drug therapy</keyword><keyword>Osteoclasts/*drug effects</keyword><keyword>Osteoporosis/*drug therapy</keyword><keyword>Prostatic Neoplasms/drug therapy</keyword></keywords><dates><year>2008</year></dates><isbn>1942-5546 (Electronic)&#xD;0025-6196 (Linking)</isbn><urls></urls></record></Cite></EndNote>(25). Some of New agents for the osteoporosis are:
  �anti-resorptive�- Odanacatib, �anabolics�- teriparatide analogues (abaloparatide), �monoclonal antibody to sclerostin�- romosozumab  ADDIN EN.CITE <EndNote><Cite><Author>Miller PD</Author><Year>2015</Year><RecNum>38</RecNum><record><rec-number>38</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">38</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Miller PD,</author></authors></contributors><titles><title>Management of severe osteoporosis</title><secondary-title>Expert Opin Pharmacother</secondary-title></titles><periodical><full-title>Expert Opin Pharmacother</full-title></periodical><pages>473-88</pages><volume>17</volume><number>4</number><dates><year>2015</year></dates><orig-pub>Management of severe osteoporosis&#xD;pharmacological therapy of severe osteoporosis&#xD;severe osteoporosis&#xD;treatment of high risk osteoporotic patients</orig-pub><isbn>1744-7666 (Electronic)&#xD;1465-6566 (Linking)</isbn><urls></urls></record></Cite></EndNote>(42).
Challenges with the drugs of osteoporosis:
Different drugs have different challenges e.g., alendronate drug is hydrophilic by nature and is not able to permeate the lipid barriers of the body. Moreover, the drugs of the BP group are ready to form complexes with the metal ions, as a result the active entity is not able to reach the site of action. Moreover, these drugs highly irritate the gastrointestinal tract by oral route and if given directly by intravenous routes, then they cause osteonecrosis of the jaw. In case of teriparatide treatment, trabecular thickness and trabecular connectivity increases, but there is no effect on cortical thickness, which is also required for the bone formation. Moreover, it induces bone resorption, for which we need denosumab in order to inhibit teriparatide-induced bone resorption at approved doses. Raloxifene (SERM) is specific to vertebral fracture only, it is not effective for the nonvertebral fractures. Calcium and vitamin D supplements are required to treat the disease along with the other drugs, if the patients having less calcium intake through diet.
CONCLUSION 
In the understanding of the bone disease osteoporosis, substantial progress has been made in the past several years, which also includes modification in its management or treatment. The guidelines for the prevention and treatment of osteoporosis have revised and now, it include criteria for commencing medical treatment in addition to, continued diligence in early diagnosis and implementation of treatment. In Indian women, low calcium intakes, vitamin D deficiency, difference in both sexes, early menopause, lack of diagnostic facilities, and poor knowledge for bone health, have been contributed towards the high prevalence of osteoporosis based fractures. Bone health can be achieved by creating an environment which includes peak bone mass during adolescence, prevention of bone loss after menopause and maintenance of healthy bone throughout the life cycle. A new medication or treatment for  HYPERLINK "http://www.webmd.com/osteoporosis/default.htm" osteoporosis�is required for the body, which helps to rebuild bone and potentially strengthen the skeleton against�osteoporosis based  HYPERLINK "http://www.webmd.com/a-to-z-guides/understanding-fractures-basic-information" fractures. Though, different drugs are available for the treatment of osteoporosis, but they are devoid of adverse effects, so there is a need to investigate for a safer drug treatment.
REFERENCES
:, diagnosisOsteoporosis
Osteoporosis is the most common metabolic disorder of bone which leads to an increased level of bone fragility & susceptibility to fracture. It is a systemic disorder that affects the entire skeleton & characterized by low bone mass and microartectural deterioration of the skeleton. Osteoporosis is a silent disease with no symptoms until a fracture occurs. The WHO has defined osteoporosis as a condition in which a Bone Mineral Density (BMD) is more than 2.5 standard deviations below the mean of normal, healthy individuals at their peak bone mass.
Bone undergoBone undergoes remodelling at specific sites on the bone surface known as basic multicellular units & is carried out by the osteoclasts (bone resorption cells) & osteoblasts (bone forming cells). The bone remodelling cycle is highly dependent on a delicate balance between regulatory signalling & cellular activity. Loss of capacity to recruit active osteoblasts or deactivate osteoclasts which results in a net bone loss & can lead to the onset of osteoporosis.
Types of osteoporosis:
Type I- Postmenopausal women
Type II- Senile osteoporosis (age related, which is affecting men or women)
Type III- more rare forms of the disease, such as juvenile, pregnancy-related & post-partum osteoporosis.
The Etiology
Bone cell senescence
Lifestyle factors (Primary exercise & nutrition)
Loss of vitamin D metabolism with age
PoorTherefore, poor vitamin D metabolism leads to a decrease in intestinal calcium absorption results in parathyroid hormone signalling to withdraw calcium from the bones. Overtime, this continuous removal of calcium from the bones leads to decreased bone mass & development of osteoporosis.
Treatment
Antiresorptive drugs, which slow the progressive thinning of bone.
Bone forming drugs which helps to rebuild the skeleton, & drugs with a more complex mechanism of action.
Calcium and vitamin D precursors to ensure adequate intake & to ensure maximum effectiveness of the drug therapy.
Osteoporosis & Osteoarthritis
Osteoarthritis is degenerative bone disease which is a form of arthritis, caused by inflammation, breakdown & the eventual loss of cartilage in the joints.
Osteoporosis is porous bone condition, which is characterized by the loss of bone mass which increases the risk of fractures, even spontaneously.
Bone Markers
Serum osteocalcin, bone specific alkaline phosphatase, total alkaline phosphatiase and type I procollagen (C-terminal/ N-terminal) � For bone formation.
Tartrate resistant acid phosphatase (TRAP), type I collagen cross-linked N- (NTX) and C-telopeptide (CTX)- for bone resorption. 
Osteoclasts and Oosteoblasts
Bones are living, active tissues that renew themselves via a process called remodelling. Hormonal cells called �osteoclasts� remove old bone cells from bone tissue, deposit it into the bloodstream for removal and create small holes in the process. Cells called �osteoblasts� then arrive with the �mortar� of calcium, minerals and collagen to fill in the holes. Osteoclasts and osteoblasts are activated by the parathyroid hormone (PTH), which signals osteoclasts to pull calcium from the bones. Calcitonin is the hormone that stimulates osteoblasts to deposit calcium into the bones. Osteoblasts must be able to do their job effectively. Osteoblasts that are exhausted are one of the primary reasonreasons for bone loss.
Steps of bone remodeling:
1- Stimulation of osteoclasts:-. Osteoclasts secrete collagenases and proteinases that solubilize bone matrix, releasing calcium into circulation for physiological functions.
2- Once osteoclasts die, osteoblasts differentiate and lay down new bone matrix (osteoid) at the sites of previous resorption. 
3- Once bone formation is complete, osteoblasts are inactivated and differentiated into osteocytes on the surface of the new bone. 
4- The new bone is then mineralized with hydroxyapatite. The complete mineralization and hardening process takes several months.


Figure No. 1: The diagrammatic representation of different steps of bone remodelling cycle.
Osteoblasts are derived from mesenchymal stem cell. The Wingless-type (Wnt) pathway recognised as having a major role in the regulation of bone formation. It is a protein signalling pathway for osteoblasts). It inhibits adipocytes differentiation and promotes osteoblast cell lineages by controlling proliferation, maturation, and terminal differentiation. It has Low density lipoprotein receptor related protein (LRP) 5 & 6 as co-receptors to the frizzled receptors. It shows some of the transcription factors involved (the bone morphogenetic protein 2 & 7, beta-catenin, Runx2, osterix & nuclear factor of activated T-cells (NFAT). When osteoblasts have done their job, they may become incorporated into the bone matrix as osteocytes, may transform into living cells on the bone surface or may undergo death/apoptosis/necrosis. Sclerostin, a protein secreted by osteocytes, binds to co-receptors LRP5/6 and inhibits their association with Wnt pathway, thus acting as an inhibitor of this pathway. Dickkopf1 (DKK1) is another negative regulator of the Wnt signaling pathway that acts by directly binding to LRP5 and LRP6. Osteoblasts synthesize RANKL (receptor activator of NF-Kappa B ligand) which is necessary for osteoclasts formation and function. But osteoprotegerin (OPG) is its decoy receptor.  Ratio of RANKL/OPG is used to predict the induction or suppression of osteoclastogenesis, the decreased ratio represents induction of osteoclastogenesis and vice-versa.
  
Diagnosis of osteoporosis: Computed tomography, X-ray & dual energy X-ray absorptiometry images are used in cross-sectional & longitudinal studies in osteoporosis. Fracture Risk Assessment Tool (FRAX), an absolute risk assessment tool, with BMD testing based on age and fracture probability using predetermined assessment thresholds.
Animal models: The suitable animal model used for the treatment of osteopororsisosteoporosis is ovariectomized rats (OVX), by making use of this model we can quantify the drug levels in the desired part of the body. The findings will be assessed on the basis of animal weight, morphology of target bone, and histochemical localization of alkaline phosphatase (ALP) (an osteoblastic marker) and tartrate-resistant acid phosphatase (TRAP).�The osteoclastic activity will be confirmed by TRAP staining, and the bone formation is assessed by ALP staining in the target bone sections. The color intensity of TRAP and ALP enzymes from the images will be evaluated by image analysis software developed locally.
Drugs used in the treatment offor osteoporosis
1. Bisphosphonates e.g. Alendronate
2. Teriparatide and parathyroid hormone
3. Raloxifene (Selective estrogen receptor modulator)
4. Calcitonin
5. Strontium Ranelate
6. Hormone Replacement Therapy (HRT)
7. Calcium and vitamin D
8. Denosumab

1. Bisphosphonates (BP): alendronate, ibandronate, etiodronate, zoledronic acid and risedronate
Bisphosphonates have phosphonate groups linked by phosphoether bonds., Tthis arrangement makes BP stable & resistant to biological degradation. They are called bisphosphonates because thaythey have two phosphonate groups (PO(PO (OH)2). They inhibit the osteoporosis by encouraging osteoclasts to undergo apoptosis, or cell death, by slowing bone loss.
They appear to stimulate transiently the proliferation of preosteoblast cells and to increase their differentiation., theyThey may increase the production of antiresorptive protein osteoprotegerin by osteoblasts. As a class bisphosphonates are hydrophilic. Nitrogen containing bisphosphonates i.e.,alendronate  are more potent than the non-nitrogen containing bisphosphonates i.e. etiodronate, by their ability to suppress osteoclast activity (as measured by biochemical markers of bone turnover). 
Negative charge on the phosphate group of the bisphosphonate nucleus gave these compounds a high affinity for the surface of bone. After binding to mineralized bone surface, thay are taken up by the osteoclasts during bone resorption. They inhibit the enzyme farnesyl pyrophosphate synthetase. With this loss of protein prenylation, osteoclasts become unable to resorb bone and ultimately die.
Mechanism of Action: 
Bisphosphonats Aact on bone metabolism by binding and blocking the enzyme farnesyl pyrophosphate synthase (FPPS) in the HMG-CoA reductase pathway (also known as mevalonate pathway). As a result, protein prenyalation is inhibited. It causes lipid modification of many proteins found in osteoclast i.e., Ras, Rho and Rac (which play a central role in the regulation of core osteoclasts cellular activity including stress fiberfibre assembly, membrane ruffling and survival is inhibited, ultimately leading to osteoclast apoptosis. 
Alendronate is the second generation derivative of bisphosphonates, which localizes preferentially on bone resorption surfaces by binding to the exposed calcium phosphate bone mineral. OsteoclastOsteoclasts attach to these surfaces by a tight seal enclosing a space into which they secrete acid & dissolve the mineral. During this process, the bisphosphonates are released and can reach local concentration in high micromolecular range.
The ability of bisphosphonates (BPs) to inhibit apoptosis in osteocytes appears to be mediated through the opening of connexin 3 hemichannels and subsequent activation of extracellular signal-regulated kinases (ERKs).
Zoledronic acid which is the third generation derivative of bisphosphinatebisphosphonates, is the only BP that has been developed exclusively for i.v. but not for oral use, which has led to an attractive once-yearly regimen in the treatment for osteoporosis.
Fastest onset of action among the bisphosphonates on all types of fracture, a rapid effect appears for vertebral fractures and not for reduction of hip and nonvertebral fractures.





Table No.1: The different drugs of class bisphosphonatebisphosphonates with its respective potencies.

2. Teriparatide and parathyroid hormone:
It is a 34-amino acid polypeptide produced by recombinant DNA technique, which represents the biologically active part of human parathyroid hormone. Teriparatide treatment alone was more expensive and produced a smaller increase in Quality-adjusted life-year (QALYs) than alendronate. quality-adjusted life-year (QALY). It is given by subcutaneous injection to the patient once a day.
3. Raloxifene (Selective estrogen receptor modulator, SERM):
It is the only marketed SERM. It prevents bone loss and is indicated for the prevention and treatment of vertebral fractures in postmenopausal women. Post hoc analysis showed a significant reduction of non-vertebral fractures.
4. Calcitonin:
Calcitonin is a good option in subjects with back pain because of its analgesic effect.

5. Strontium Ranelate:
Marketed and registered for the treatment of postmenopausal osteoporosis. 
Dose:-2 gm sachet once daily by mouth. Strontium ranelate is not given to the patient with a history of thrombophlebitis.
6. Hormone Replacement Therapy (HRT):
7. Calcium and vitamin D:
8. Denosumab:
Denosumab fully inhibits teriparatide-induced bone resorption at approved doses.  This property of denosumab is distinct from that of alendronate and likely contributes to the efficacy of combination denosumab and teriparatide therapy. Significantly greater treatment adherence was observed=. for s.c. administration of denosumab every 6 months than for oral alendronate once weekly. 
Table No. 2: The comparison of different types of drugs which are used for osteoporosis with its route of administration, adverse effects & indications.DrugPMOGIO (Men & Women)MO

EstrogenAlendronate PO
PMO: Postmenopausal osteoporosis, GIO: Glucorticoid Induced Osteoporosis, or MO: Male osteoporosis.
Contraindications:
1. sSevere renal failure,  hypocalcemia, hypersensitivity, pregnancy.
2. Caution in patients with Gastroesophageal reflux disease (GERD) or peptic ulcer disease.
3. Contraindication in Barrett�s esophagus and inability to sit upright for 30-60 minutes.
4. Venous thromboembolism (VTE) past or present, liver failure, moderate or severe renal failure, patients with coronary heart disease: increased risk of stroke or death.
5. Severe renal or liver impairment, metabolic bone disease, previous radiation therapy involving the skeleton, hypercalcemia, elevation of Alkaline phosphatase                                                     (ALP), bone metastases, skeletal malignancies.
provide A new medication for  HYPERLINK "http://www.webmd.com/osteoporosis/default.htm" osteoporosis�prompts the body to rebuild bone and could potentially strengthen the skeleton against� HYPERLINK "http://www.webmd.com/a-to-z-guides/understanding-fractures-basic-information" fractures. Though, different drugs are available on the treatment of osteoporosis, they are devoid of adverse effects and need to be investigated more for to have safer drug treatment available.
REFERENCES:









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(��?��bD<EndNote><Cite><Author>Baron R</Author><Year>2007</Year><RecNum>27</RecNum><record><rec-number>27</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">27</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Baron R,</author><author>Rawadi G,</author></authors></contributors><titles><title>Targeting the Wnt/beta-catenin pathway to regulate bone formation in the adult skeleton</title><secondary-title>Endocrinology.</secondary-title></titles><periodical><full-title>Endocrinology.</full-title></periodical><pages>2635-43</pages><volume>148</volume><number>6</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Bone Morphogenetic Proteins)</keyword><keyword>0 (DKK1 protein, human)</keyword><keyword>0 (Genetic Markers)</keyword><keyword>0 (Intercellular Signaling Peptides and Proteins)</keyword><keyword>0 (LDL-Receptor Related Proteins)</keyword><keyword>0 (LRP5 protein, human)</keyword><keyword>0 (LRP6 protein, human)</keyword><keyword>0 (Low Density Lipoprotein Receptor-Related Protein-5)</keyword><keyword>0 (Low Density Lipoprotein Receptor-Related Protein-6)</keyword><keyword>0 (Lrp5 protein, mouse)</keyword><keyword>0 (Lrp6 protein, mouse)</keyword><keyword>0 (Receptors, LDL)</keyword><keyword>0 (SOST protein, human)</keyword><keyword>0 (Wnt Proteins)</keyword><keyword>0 (beta Catenin)</keyword><keyword>EC 2.7.11.1 (glycogen synthase kinase 3 beta)</keyword><keyword>EC 2.7.11.26 (Glycogen Synthase Kinase 3)</keyword><keyword>Adult</keyword><keyword>Animals</keyword><keyword>Bone Density Conservation Agents/chemical synthesis/therapeutic use</keyword><keyword>Bone Diseases/drug therapy/genetics</keyword><keyword>Bone Morphogenetic Proteins/physiology</keyword><keyword>Bone and Bones/metabolism/*physiology</keyword><keyword>Drug Design</keyword><keyword>Genetic Markers/physiology</keyword><keyword>Glycogen Synthase Kinase 3/physiology</keyword><keyword>Humans</keyword><keyword>Intercellular Signaling Peptides and Proteins/physiology</keyword><keyword>LDL-Receptor Related Proteins/chemistry/metabolism/physiology</keyword><keyword>Low Density Lipoprotein Receptor-Related Protein-5</keyword><keyword>Low Density Lipoprotein Receptor-Related Protein-6</keyword><keyword>Models, Biological</keyword><keyword>Osteogenesis/*genetics</keyword><keyword>Receptors, LDL/chemistry/metabolism/physiology</keyword><keyword>Signal Transduction/genetics/physiology</keyword><keyword>Wnt Proteins/antagonists &amp; inhibitors/genetics/metabolism/*physiology</keyword><keyword>beta Catenin/genetics/*physiology</keyword></keywords><dates><year>2007</year></dates><isbn>0013-7227 (Print)&#xD;0013-7227 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Raisz LG</Author><Year>2005</Year><RecNum>3</RecNum><record><rec-number>3</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">3</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Raisz LG,</author></authors></contributors><titles><title>Pathogenesis of osteoporosis: concepts, conflicts, and prospects</title><secondary-title>J Clin Invest.</secondary-title></titles><periodical><full-title>J Clin Invest.</full-title></periodical><pages>3318-25.</pages><volume>115</volume><number>12</number><keywords><keyword>0 (Estrogens)</keyword><keyword>0 (Glycoproteins)</keyword><keyword>0 (Hormones)</keyword><keyword>0 (Leptin)</keyword><keyword>0 (Ligands)</keyword><keyword>0 (NF-kappa B)</keyword><keyword>0 (Osteoprotegerin)</keyword><keyword>0 (Parathyroid Hormone)</keyword><keyword>0 (Prostaglandins)</keyword><keyword>0 (Receptors, Cytoplasmic and Nuclear)</keyword><keyword>0 (Receptors, Tumor Necrosis Factor)</keyword><keyword>0 (TNFRSF11B protein, human)</keyword><keyword>0 (Tnfrsf11b protein, mouse)</keyword><keyword>1406-16-2 (Vitamin D)</keyword><keyword>31C4KY9ESH (Nitric Oxide)</keyword><keyword>9007-34-5 (Collagen)</keyword><keyword>SY7Q814VUP (Calcium)</keyword><keyword>Animals</keyword><keyword>Bone Density</keyword><keyword>Bone Remodeling</keyword><keyword>Bone and Bones/metabolism</keyword><keyword>Calcium/metabolism</keyword><keyword>Cell Differentiation</keyword><keyword>Collagen/metabolism</keyword><keyword>Estrogens/*metabolism</keyword><keyword>Fractures, Bone</keyword><keyword>Glycoproteins/metabolism</keyword><keyword>Hematopoietic Stem Cells/cytology</keyword><keyword>Hormones/metabolism</keyword><keyword>Humans</keyword><keyword>Leptin/metabolism</keyword><keyword>Ligands</keyword><keyword>Mice</keyword><keyword>Models, Biological</keyword><keyword>NF-kappa B/metabolism</keyword><keyword>Neurons/metabolism</keyword><keyword>Nitric Oxide/metabolism</keyword><keyword>Osteoblasts/cytology</keyword><keyword>Osteoporosis/metabolism/pathology/*physiopathology</keyword><keyword>Osteoporosis, Postmenopausal/pathology</keyword><keyword>Osteoprotegerin</keyword><keyword>Parathyroid Hormone/metabolism</keyword><keyword>Prostaglandins/metabolism</keyword><keyword>Receptors, Cytoplasmic and Nuclear/metabolism</keyword><keyword>Receptors, Tumor Necrosis Factor/metabolism</keyword><keyword>Vitamin D/metabolism</keyword><keyword>Vitamin D Deficiency/metabolism</keyword></keywords><dates><year>2005</year></dates><isbn>0021-9738 (Print)&#xD;0021-9738 (Linking)</isbn><urls></urls></record></Cite></EndNote>F
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Possible role in pathogenesis of senile osteoporosis</title><secondary-title>J Clin Invest.</secondary-title></titles><periodical><full-title>J Clin Invest.</full-title></periodical><pages>1668-72.</pages><volume>73</volume><number>6</number><keywords><keyword>0 (Parathyroid Hormone)</keyword><keyword>0 (Phosphates)</keyword><keyword>1406-16-2 (Vitamin D)</keyword><keyword>E0399OZS9N (Cyclic AMP)</keyword><keyword>EC 3.1.3.1 (Alkaline Phosphatase)</keyword><keyword>FXC9231JVH (Calcitriol)</keyword><keyword>P6YZ13C99Q (Calcifediol)</keyword><keyword>SY7Q814VUP (Calcium)</keyword><keyword>Aged</keyword><keyword>*Aging</keyword><keyword>Alkaline Phosphatase/blood</keyword><keyword>Calcifediol/blood</keyword><keyword>Calcitriol/blood</keyword><keyword>Calcium/blood</keyword><keyword>Cyclic AMP/urine</keyword><keyword>Female</keyword><keyword>Glomerular Filtration Rate</keyword><keyword>Humans</keyword><keyword>Osteoporosis/etiology/*physiopathology</keyword><keyword>Parathyroid Hormone/blood</keyword><keyword>Phosphates/blood</keyword><keyword>Vitamin D/*metabolism</keyword></keywords><dates><year>1984</year></dates><isbn>0021-9738 (Print)&#xD;0021-9738 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Khadilkar AV</Author><Year>2015</Year><RecNum>10</RecNum><record><rec-number>10</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">10</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Khadilkar AV,</author><author>Mandlik RM,</author></authors></contributors><titles><title>Epidemiology and treatment of osteoporosis in women: an Indian perspective</title><secondary-title>Int J Womens Health.</secondary-title></titles><periodical><full-title>Int J Womens Health.</full-title></periodical><pages>841-50 </pages><volume>7</volume><dates><year>2015</year></dates><orig-pub>Indian perspective&#xD;epidemiology&#xD;osteoporosis&#xD;treatment</orig-pub><isbn>1179-1411 (Electronic)&#xD;1179-1411 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Ardakani FE</Author><Year>2009</Year><RecNum>30</RecNum><record><rec-number>30</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">30</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Ardakani FE,</author><author>Mirmohamadi SJ,</author></authors></contributors><titles><title>Osteoporosis and oral bone resorption: a review</title><secondary-title>J Maxillofac Oral Surg.</secondary-title></titles><periodical><full-title>J Maxillofac Oral Surg.</full-title></periodical><pages>121-6</pages><volume>8</volume><number>2</number><dates><year>2009</year></dates><orig-pub>Bone resorption&#xD;Oral Bone&#xD;Osteoporosis</orig-pub><isbn>0972-8279 (Print)&#xD;0972-8270 (Linking)</isbn><urls></urls></record></Cite></EndNote>�D<EndNote><Cite><Author>Windahl SH</Author><Year>2001</Year><RecNum>42</RecNum><record><rec-number>42</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">42</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Windahl SH,</author><author>Hollberg K,</author><author>Vidal O,</author><author>Gustafsson JA,</author><author>Ohlsson C,</author><author>Andersson G,</author></authors></contributors><titles><title>Female estrogen receptor beta-/- mice are partially protected against age-related trabecular bone loss</title><secondary-title>J Bone Miner Res.</secondary-title></titles><periodical><full-title>J Bone Miner Res.</full-title></periodical><pages>1388-98</pages><volume>16</volume><number>8</number><keywords><keyword>0 (Collagen Type I)</keyword><keyword>0 (Cross-Linking Reagents)</keyword><keyword>0 (Estrogen Receptor alpha)</keyword><keyword>0 (Estrogen Receptor beta)</keyword><keyword>0 (Peptides)</keyword><keyword>0 (RNA, Messenger)</keyword><keyword>0 (Receptors, Estrogen)</keyword><keyword>0 (collagen type I trimeric cross-linked peptide)</keyword><keyword>104982-03-8 (Osteocalcin)</keyword><keyword>4TI98Z838E (Estradiol)</keyword><keyword>67763-96-6 (Insulin-Like Growth Factor I)</keyword><keyword>9007-34-5 (Collagen)</keyword><keyword>Animals</keyword><keyword>Body Weight</keyword><keyword>Bone Density</keyword><keyword>Collagen/blood</keyword><keyword>Collagen Type I</keyword><keyword>Cross-Linking Reagents</keyword><keyword>Disease Models, Animal</keyword><keyword>Estradiol/blood</keyword><keyword>Estrogen Receptor alpha</keyword><keyword>Estrogen Receptor beta</keyword><keyword>Female</keyword><keyword>Femur/metabolism/pathology</keyword><keyword>Gene Expression</keyword><keyword>Insulin-Like Growth Factor I/analysis</keyword><keyword>Male</keyword><keyword>Mice</keyword><keyword>Mice, Knockout</keyword><keyword>Osteoblasts/metabolism</keyword><keyword>Osteocalcin/blood</keyword><keyword>Osteoclasts/metabolism</keyword><keyword>Osteoporosis/*metabolism/pathology/prevention &amp; 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dosage</keyword><keyword>Delayed-Action Preparations</keyword><keyword>Drug Administration Schedule</keyword><keyword>Etidronic Acid/administration &amp; dosage/*analogs &amp; derivatives</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Osteoporosis, Postmenopausal/*drug therapy</keyword><keyword>Patient Compliance</keyword><keyword>Risedronate Sodium</keyword></keywords><dates><year>2008</year></dates><isbn>1176-9092 (Print)&#xD;1176-9092 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Geusens</Author><Year>2001</Year><RecNum>45</RecNum><record><rec-number>45</rec-number><foreign-keys><key app="EN" db-id="psta9xsv2fv2dhextr0vwzrkap59rvtp9dx2">45</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Geusens, P.,</author><author>McClung, M.,</author></authors></contributors><titles><title>Review of risedronate in the treatment of osteoporosis</title><secondary-title>Expert Opin Pharmacother.</secondary-title></titles><periodical><full-title>Expert Opin Pharmacother.</full-title></periodical><pages>2011-25</pages><volume>2</volume><number>12</number><keywords><keyword>M2F465ROXU (Etidronic Acid)</keyword><keyword>OFG5EXG60L (Risedronate Sodium)</keyword><keyword>Clinical Trials, Phase III as Topic</keyword><keyword>Etidronic Acid/*administration &amp; dosage/adverse effects/*analogs &amp;</keyword><keyword>derivatives/chemistry/pharmacokinetics/pharmacology/*therapeutic use</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Osteoporosis/*drug therapy</keyword><keyword>Osteoporosis, Postmenopausal/drug therapy</keyword><keyword>Risedronate Sodium</keyword><keyword>Spinal Fractures/prevention &amp; control</keyword></keywords><dates><year>2001</year></dates><isbn>1465-6566 (Print)&#xD;1465-6566 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Siris</Author><Year>1998</Year><RecNum>46</RecNum><record><rec-number>46</rec-number><foreign-keys><key app="EN" db-id="psta9xsv2fv2dhextr0vwzrkap59rvtp9dx2">46</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Siris, ES.,</author><author>Chines, AA.,</author><author>Altman, RD.,</author><author>Brown, JP.,</author><author>Johnston, CC Jr.,</author><author>Lang, R.,</author><author>McClung, MR.,</author><author>Mallette, LE.,</author><author>Miller, PD.,</author><author>Ryan, WG.,</author><author>Singer, FR.,</author><author>Tucci, JR.,</author><author>Eusebio, RA.,</author><author>Bekker, PJ.,</author></authors></contributors><titles><title>Risedronate in the treatment of Paget&apos;s disease of bone: an open label, multicenter study</title><secondary-title>J Bone Miner Res.</secondary-title></titles><periodical><full-title>J Bone Miner Res.</full-title></periodical><pages>1032-8</pages><volume>13</volume><number>6</number><keywords><keyword>0 (Biomarkers)</keyword><keyword>0 (Calcium Channel Blockers)</keyword><keyword>0 (Capsules)</keyword><keyword>0 (Delayed-Action Preparations)</keyword><keyword>9000-70-8 (Gelatin)</keyword><keyword>EC 3.1.3.1 (Alkaline Phosphatase)</keyword><keyword>M2F465ROXU (Etidronic Acid)</keyword><keyword>OFG5EXG60L (Risedronate Sodium)</keyword><keyword>Administration, Oral</keyword><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Aged, 80 and over</keyword><keyword>Alkaline Phosphatase/blood</keyword><keyword>Biomarkers/blood/urine</keyword><keyword>Calcium Channel Blockers/administration &amp; dosage/*therapeutic use</keyword><keyword>Capsules</keyword><keyword>Delayed-Action Preparations/administration &amp; dosage/therapeutic use</keyword><keyword>Etidronic Acid/administration &amp; dosage/*analogs &amp; derivatives/therapeutic use</keyword><keyword>Female</keyword><keyword>Gelatin</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Osteitis Deformans/blood/*drug therapy/urine</keyword><keyword>Risedronate Sodium</keyword></keywords><dates><year>1998</year></dates><isbn>0884-0431 (Print)&#xD;0884-0431 (Linking)</isbn><urls></urls></record></Cite></EndNote>,D<EndNote><Cite><Author>Procter &amp; Gamble Pharmaceuticals  Inc.</Author><Year>2004</Year><RecNum>143</RecNum><record><rec-number>143</rec-number><foreign-keys><key app='EN' db-id='wrrwztps82zperewsevpvpph0a0r2rfwpp00'>143</key></foreign-keys><ref-type name='Web Page'>12</ref-type><contributors><authors><author>Procter &amp; Gamble Pharmaceuticals  Inc.,</author></authors></contributors><titles><title><style face='normal' font='default' size='100%'>Actonel</style><style face='superscript' font='default' size='100%'>®</style></title></titles><volume>2016</volume><number>Sept, 8</number><dates><year>2004</year></dates><urls><related-urls><url>http://www.accessdata.fda.gov/drugsatfda_docs/label/2005/020835s018lbl.pdf</url></related-urls></urls><custom1>2004</custom1></record></Cite><Cite><Author>Moro-Alvarez</Author><Year>2008</Year><RecNum>44</RecNum><record><rec-number>44</rec-number><foreign-keys><key app="EN" db-id="psta9xsv2fv2dhextr0vwzrkap59rvtp9dx2">44</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Moro-Alvarez, MJ.,</author><author>Diaz-Curiel, M.,</author></authors></contributors><titles><title>Risedronate once monthly: a potential new regimen for the treatment of postmenopausal osteoporosis</title><secondary-title>Clin Interv Aging.</secondary-title></titles><periodical><full-title>Clin Interv Aging.</full-title></periodical><pages>227-32</pages><volume>3</volume><number>2</number><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>0 (Delayed-Action Preparations)</keyword><keyword>M2F465ROXU (Etidronic Acid)</keyword><keyword>OFG5EXG60L (Risedronate Sodium)</keyword><keyword>Bone Density</keyword><keyword>Bone Density Conservation Agents/*administration &amp; dosage</keyword><keyword>Delayed-Action Preparations</keyword><keyword>Drug Administration Schedule</keyword><keyword>Etidronic Acid/administration &amp; dosage/*analogs &amp; derivatives</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Osteoporosis, Postmenopausal/*drug therapy</keyword><keyword>Patient Compliance</keyword><keyword>Risedronate Sodium</keyword></keywords><dates><year>2008</year></dates><isbn>1176-9092 (Print)&#xD;1176-9092 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Geusens</Author><Year>2001</Year><RecNum>45</RecNum><record><rec-number>45</rec-number><foreign-keys><key app="EN" db-id="psta9xsv2fv2dhextr0vwzrkap59rvtp9dx2">45</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Geusens, P.,</author><author>McClung, M.,</author></authors></contributors><titles><title>Review of risedronate in the treatment of osteoporosis</title><secondary-title>Expert Opin Pharmacother.</secondary-title></titles><periodical><full-title>Expert Opin Pharmacother.</full-title></periodical><pages>2011-25</pages><volume>2</volume><number>12</number><keywords><keyword>M2F465ROXU (Etidronic Acid)</keyword><keyword>OFG5EXG60L (Risedronate Sodium)</keyword><keyword>Clinical Trials, Phase III as Topic</keyword><keyword>Etidronic Acid/*administration &amp; dosage/adverse effects/*analogs &amp;</keyword><keyword>derivatives/chemistry/pharmacokinetics/pharmacology/*therapeutic use</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Osteoporosis/*drug therapy</keyword><keyword>Osteoporosis, Postmenopausal/drug therapy</keyword><keyword>Risedronate Sodium</keyword><keyword>Spinal Fractures/prevention &amp; control</keyword></keywords><dates><year>2001</year></dates><isbn>1465-6566 (Print)&#xD;1465-6566 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Siris</Author><Year>1998</Year><RecNum>46</RecNum><record><rec-number>46</rec-number><foreign-keys><key app="EN" db-id="psta9xsv2fv2dhextr0vwzrkap59rvtp9dx2">46</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Siris, ES.,</author><author>Chines, AA.,</author><author>Altman, RD.,</author><author>Brown, JP.,</author><author>Johnston, CC Jr.,</author><author>Lang, R.,</author><author>McClung, MR.,</author><author>Mallette, LE.,</author><author>Miller, PD.,</author><author>Ryan, WG.,</author><author>Singer, FR.,</author><author>Tucci, JR.,</author><author>Eusebio, RA.,</author><author>Bekker, PJ.,</author></authors></contributors><titles><title>Risedronate in the treatment of Paget&apos;s disease of bone: an open label, multicenter study</title><secondary-title>J Bone Miner Res.</secondary-title></titles><periodical><full-title>J Bone Miner Res.</full-title></periodical><pages>1032-8</pages><volume>13</volume><number>6</number><keywords><keyword>0 (Biomarkers)</keyword><keyword>0 (Calcium Channel Blockers)</keyword><keyword>0 (Capsules)</keyword><keyword>0 (Delayed-Action Preparations)</keyword><keyword>9000-70-8 (Gelatin)</keyword><keyword>EC 3.1.3.1 (Alkaline Phosphatase)</keyword><keyword>M2F465ROXU (Etidronic Acid)</keyword><keyword>OFG5EXG60L (Risedronate Sodium)</keyword><keyword>Administration, Oral</keyword><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Aged, 80 and over</keyword><keyword>Alkaline Phosphatase/blood</keyword><keyword>Biomarkers/blood/urine</keyword><keyword>Calcium Channel Blockers/administration &amp; dosage/*therapeutic use</keyword><keyword>Capsules</keyword><keyword>Delayed-Action Preparations/administration &amp; dosage/therapeutic use</keyword><keyword>Etidronic Acid/administration &amp; dosage/*analogs &amp; derivatives/therapeutic use</keyword><keyword>Female</keyword><keyword>Gelatin</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Osteitis Deformans/blood/*drug therapy/urine</keyword><keyword>Risedronate Sodium</keyword></keywords><dates><year>1998</year></dates><isbn>0884-0431 (Print)&#xD;0884-0431 (Linking)</isbn><urls></urls></record></Cite></EndNote>�
D<EndNote><Cite><Author>Sethi BK</Author><Year>2008</Year><RecNum>34</RecNum><record><rec-number>34</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">34</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Sethi BK,</author><author>Chadha M,</author><author>Modi KD,</author><author>Kumar KM,</author><author>Mehrotra R,</author><author>Sriram U,</author></authors></contributors><titles><title>Efficacy of teriparatide in increasing bone mineral density in postmenopausal women with osteoporosis--an Indian experience</title><secondary-title>J Assoc Physicians India.</secondary-title></titles><periodical><full-title>J Assoc Physicians India.</full-title></periodical><pages>418-24.</pages><volume>56</volume><keywords><keyword>0 (Bone Density Conservation Agents)</keyword><keyword>10T9CSU89I (Teriparatide)</keyword><keyword>1406-16-2 (Vitamin D)</keyword><keyword>SY7Q814VUP (Calcium)</keyword><keyword>Aged</keyword><keyword>*Bone Density</keyword><keyword>Bone Density Conservation Agents/*administration &amp; dosage</keyword><keyword>Bone Resorption</keyword><keyword>Calcium/administration &amp; dosage</keyword><keyword>Double-Blind Method</keyword><keyword>Female</keyword><keyword>Follow-Up Studies</keyword><keyword>Humans</keyword><keyword>Injections, Subcutaneous</keyword><keyword>Middle Aged</keyword><keyword>Osteogenesis</keyword><keyword>Osteoporosis, Postmenopausal/*drug therapy/*physiopathology</keyword><keyword>Prospective Studies</keyword><keyword>Teriparatide/*administration &amp; dosage</keyword><keyword>Treatment Outcome</keyword><keyword>Vitamin D/administration &amp; dosage</keyword></keywords><dates><year>2008</year></dates><isbn>0004-5772 (Print)&#xD;0004-5772 (Linking)</isbn><urls></urls></record></Cite><Cite><Author>Drake MT</Author><Year>2015</Year><RecNum>37</RecNum><record><rec-number>37</rec-number><foreign-keys><key app="EN" db-id="tdra5r0vppfsfrexvskp2rf7zw0fwwexfx9s">37</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Drake MT,</author><author>Clarke BL,</author><author>Lewiecki EM,</author></authors></contributors><titles><title>The Pathophysiology and Treatment of Osteoporosis</title><secondary-title>Clin Ther</secondary-title></titles><periodical><full-title>Clin Ther</full-title></periodical><pages>1837-50</pages><volume>37</volume><number>8</number><dates><year>2015</year></dates><orig-pub>aging&#xD;bisphosphonate&#xD;bone&#xD;bone mineral density&#xD;menopause&#xD;osteoporosis</orig-pub><isbn>1879-114X (Electronic)&#xD;0149-2918 (Linking)</isbn><urls></urls></record></Cite></EndNote>�$$If�!vh#v�#v�#v#vn:V�l��
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