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2016 ; 57
(3
): 161-74
Nephropedia Template TP
gab.com Text
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English Wikipedia
The cast of clasts: catabolism and vascular invasion during bone growth, repair,
and disease by osteoclasts, chondroclasts, and septoclasts
#MMPMID26818783
Odgren PR
; Witwicka H
; Reyes-Gutierrez P
Connect Tissue Res
2016[May]; 57
(3
): 161-74
PMID26818783
show ga
Three named cell types degrade and remove skeletal tissues during growth, repair,
or disease: osteoclasts, chondroclasts, and septoclasts. A fourth type, unnamed
and less understood, removes nonmineralized cartilage during development of
secondary ossification centers. "Osteoclasts," best known and studied, are
polykaryons formed by fusion of monocyte precursors under the influence of colony
stimulating factor 1 (CSF)-1 (M-CSF) and RANKL. They resorb bone during growth,
remodeling, repair, and disease. "Chondroclasts," originally described as highly
similar in cytological detail to osteoclasts, reside on and degrade mineralized
cartilage. They may be identical to osteoclasts since to date there are no
distinguishing markers for them. Because osteoclasts also consume cartilage cores
along with bone during growth, the term "chondroclast" might best be reserved for
cells attached only to cartilage. "Septoclasts" are less studied and appreciated.
They are mononuclear perivascular cells rich in cathepsin B. They extend a
cytoplasmic projection with a ruffled membrane and degrade the last transverse
septum of hypertrophic cartilage in the growth plate, permitting capillaries to
bud into it. To do this, antiangiogenic signals in cartilage must give way to
vascular trophic factors, mainly vascular endothelial growth factor (VEGF). The
final cell type excavates cartilage canals for vascular invasion of articular
cartilage during development of secondary ossification centers. The "clasts" are
considered in the context of fracture repair and diseases such as arthritis and
tumor metastasis. Many observations support an essential role for hypertrophic
chondrocytes in recruiting septoclasts and osteoclasts/chondroclasts by supplying
VEGF and RANKL. The intimate relationship between blood vessels and skeletal
turnover and repair is also examined.