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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Mol+Pain
2016 ; 12
(ä): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Preventing painful age-related bone fractures: Anti-sclerostin therapy builds
cortical bone and increases the proliferation of osteogenic cells in the
periosteum of the geriatric mouse femur
#MMPMID27837171
Thompson ML
; Chartier SR
; Mitchell SA
; Mantyh PW
Mol Pain
2016[]; 12
(ä): ä PMID27837171
show ga
Age-related bone fractures are usually painful and have highly negative effects
on a geriatric patient's functional status, quality of life, and survival.
Currently, there are few analgesic therapies that fully control bone fracture
pain in the elderly without significant unwanted side effects. However, another
way of controlling age-related fracture pain would be to preemptively administer
an osteo-anabolic agent to geriatric patients with high risk of fracture, so as
to build new cortical bone and prevent the fracture from occurring. A major
question, however, is whether an osteo-anabolic agent can stimulate the
proliferation of osteogenic cells and build significant amounts of new cortical
bone in light of the decreased number and responsiveness of osteogenic cells in
aging bone. To explore this question, geriatric and young mice, 20 and 4 months
old, respectively, received either vehicle or a monoclonal antibody that
sequesters sclerostin (anti-sclerostin) for 28 days. From days 21 to 28, animals
also received sustained administration of the thymidine analog, bromodeoxyuridine
(BrdU), which labels the DNA of dividing cells. Animals were then euthanized at
day 28 and the femurs were examined for cortical bone formation, bone mineral
density, and newly borne BrdU+ cells in the periosteum which is a tissue that is
pivotally involved in the formation of new cortical bone. In both the geriatric
and young mice, anti-sclerostin induced a significant increase in the thickness
of the cortical bone, bone mineral density, and the proliferation of newly borne
BrdU+ cells in the periosteum. These results suggest that even in geriatric
animals, anti-sclerostin therapy can build new cortical bone and increase the
proliferation of osteogenic cells and thus reduce the likelihood of painful
age-related bone fractures.
|*Aging
[MESH]
|*Pain/etiology/pathology/prevention & control
[MESH]
|Adaptor Proteins, Signal Transducing
[MESH]
|Analysis of Variance
[MESH]
|Animals
[MESH]
|Antibodies/*therapeutic use
[MESH]
|Bone Density
[MESH]
|Bromodeoxyuridine/metabolism
[MESH]
|Cell Proliferation/*physiology
[MESH]
|Cortical Bone/*pathology
[MESH]
|Fractures, Bone/*complications
[MESH]
|Glycoproteins/immunology/metabolism
[MESH]
|Intercellular Signaling Peptides and Proteins
[MESH]