Osteoporosis future or investigational therapies: Difference between revisions
Jump to navigation
Jump to search
(Created page with "{{Osteoporosis}} {{CMG}} __NOTOC__ '''Associate Editor(s)-In-Chief:''' {{CZ}}, Raviteja Guddeti, M.B.B.S.[mailto:rgudetti@perfuse.org] ==Over...") |
No edit summary |
||
| Line 5: | Line 5: | ||
==Overview== | ==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. | 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 investigational therapies== | ==Future 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]], 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]], 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> | ||
Revision as of 18:51, 22 July 2012
|
Osteoporosis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Medical Therapy |
|
Case Studies |
|
Osteoporosis future or investigational therapies On the Web |
|
American Roentgen Ray Society Images of Osteoporosis future or investigational therapies |
|
Osteoporosis future or investigational therapies in the news |
|
Risk calculators and risk factors for Osteoporosis future or investigational therapies |
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 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, 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.[1]
References
- ↑ Lippuner K (2012). "The future of osteoporosis treatment - a research update". Swiss Med Wkly. 142. doi:10.4414/smw.2012.13624. PMID 22815185.