Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26065002
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Immunol+Res
2015 ; 2015
(ä): 615486
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Mechanisms of Bone Resorption in Periodontitis
#MMPMID26065002
Hienz SA
; Paliwal S
; Ivanovski S
J Immunol Res
2015[]; 2015
(ä): 615486
PMID26065002
show ga
Alveolar bone loss is a hallmark of periodontitis progression and its prevention
is a key clinical challenge in periodontal disease treatment. Bone destruction is
mediated by the host immune and inflammatory response to the microbial challenge.
However, the mechanisms by which the local immune response against
periodontopathic bacteria disturbs the homeostatic balance of bone formation and
resorption in favour of bone loss remain to be established. The osteoclast, the
principal bone resorptive cell, differentiates from monocyte/macrophage
precursors under the regulation of the critical cytokines macrophage
colony-stimulating factor, RANK ligand, and osteoprotegerin. TNF-?, IL-1, and
PGE2 also promote osteoclast activity, particularly in states of inflammatory
osteolysis such as those found in periodontitis. The pathogenic processes of
destructive inflammatory periodontal diseases are instigated by subgingival
plaque microflora and factors such as lipopolysaccharides derived from specific
pathogens. These are propagated by host inflammatory and immune cell influences,
and the activation of T and B cells initiates the adaptive immune response via
regulation of the Th1-Th2-Th17 regulatory axis. In summary, Th1-type T
lymphocytes, B cell macrophages, and neutrophils promote bone loss through
upregulated production of proinflammatory mediators and activation of the RANK-L
expression pathways.
free
free
free
