Osteoporosis future or investigational therapies: Difference between revisions
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Recent advances in the field of bone biology have led to a better understanding of bone cell functions and crosstalk between osteoblasts, osteoclasts, and osteocytes at the molecular level. Research is under way to discover new therapies to reduce the fracture risk in the osteoporotic population. | Recent advances in the field of bone biology have led to a better understanding of bone cell functions and crosstalk between osteoblasts, osteoclasts, and osteocytes at the molecular level. Research is under way to discover new therapies to reduce the fracture risk in the osteoporotic population. | ||
==Future | ==Future or Investigational Therapies== | ||
These include | These include | ||
* New bone anabolic substances such as antibodies directed against the endogenous inhibitors of bone formation sclerostin and dickkopf-1, PTH and PTHrp analogues, and possibly calcilytics | * New bone [[anabolic]] substances such as [[antibodies]] directed against the endogenous inhibitors of bone formation sclerostin and dickkopf-1, PTH and PTHrp analogues, and possibly calcilytics | ||
* New inhibitors of bone resorption such as cathepsin K inhibitors which may suppress osteoclast function without impairing osteoclast viability and thus maintain bone formation by preserving the osteoclast-osteoblast crosstalk, and [[denosumab]]<ref name="pmid22776860">{{cite journal |author=McClung MR, Lewiecki EM, Geller ML, ''et al.'' |title=Effect of denosumab on bone mineral density and biochemical markers of bone turnover: 8-year results of a phase 2 clinical trial |journal=Osteoporos Int |volume= |issue= |pages= |year=2012 |month=July |pmid=22776860 |doi=10.1007/s00198-012-2052-4 |url=}}</ref>, an already widely available antibody against RANKL which inhibits osteoclast formation, function, and survival | * New inhibitors of bone resorption such as cathepsin K inhibitors which may suppress [[osteoclast]] function without impairing osteoclast viability and thus maintain bone formation by preserving the osteoclast-osteoblast crosstalk, and [[denosumab]]<ref name="pmid22776860">{{cite journal |author=McClung MR, Lewiecki EM, Geller ML, ''et al.'' |title=Effect of denosumab on bone mineral density and biochemical markers of bone turnover: 8-year results of a phase 2 clinical trial |journal=Osteoporos Int |volume= |issue= |pages= |year=2012 |month=July |pmid=22776860 |doi=10.1007/s00198-012-2052-4 |url=}}</ref>, an already widely available antibody against RANKL which inhibits osteoclast formation, function, and survival | ||
* Sequential therapies with two or more bone active substances aimed at optimizing the management of bone capital acquired during adolescence and maintained during adulthood in terms of both quantity and quality.<ref name="pmid22815185">{{cite journal |author=Lippuner K |title=The future of osteoporosis treatment - a research update |journal=Swiss Med Wkly |volume=142 |issue= |pages= |year=2012 |pmid=22815185 |doi=10.4414/smw.2012.13624 |url=}}</ref> | * Sequential therapies with two or more bone active substances aimed at optimizing the management of bone capital acquired during adolescence and maintained during adulthood in terms of both quantity and quality.<ref name="pmid22815185">{{cite journal |author=Lippuner K |title=The future of osteoporosis treatment - a research update |journal=Swiss Med Wkly |volume=142 |issue= |pages= |year=2012 |pmid=22815185 |doi=10.4414/smw.2012.13624 |url=}}</ref> | ||
==References== | ==References== | ||
Revision as of 19:44, 27 August 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Raviteja Guddeti, M.B.B.S.[3]
Overview
Recent advances in the field of bone biology have led to a better understanding of bone cell functions and crosstalk between osteoblasts, osteoclasts, and osteocytes at the molecular level. Research is under way to discover new therapies to reduce the fracture risk in the osteoporotic population.
Future or Investigational Therapies
These include
- New bone anabolic substances such as antibodies directed against the endogenous inhibitors of bone formation sclerostin and dickkopf-1, PTH and PTHrp analogues, and possibly calcilytics
- New inhibitors of bone resorption such as cathepsin K inhibitors which may suppress osteoclast function without impairing osteoclast viability and thus maintain bone formation by preserving the osteoclast-osteoblast crosstalk, and denosumab[1], an already widely available antibody against RANKL which inhibits osteoclast formation, function, and survival
- Sequential therapies with two or more bone active substances aimed at optimizing the management of bone capital acquired during adolescence and maintained during adulthood in terms of both quantity and quality.[2]
References
- ↑ McClung MR, Lewiecki EM, Geller ML; et al. (2012). "Effect of denosumab on bone mineral density and biochemical markers of bone turnover: 8-year results of a phase 2 clinical trial". Osteoporos Int. doi:10.1007/s00198-012-2052-4. PMID 22776860. Unknown parameter
|month=ignored (help) - ↑ Lippuner K (2012). "The future of osteoporosis treatment - a research update". Swiss Med Wkly. 142. doi:10.4414/smw.2012.13624. PMID 22815185.