Mechanisms of alveolar bone destruction in periodontitis

Inhibitory Effect of Panduratin A on c-Jun N-Terminal Kinase and Activator Protein-1 Signaling Involved in Porphyromonas gingivalis Supernatant-Stimulated Matrix Metalloproteinase-9 Expression in Human Oral Epidermoid Cells

“…P. gingivalis has virulence factors like gingipains, lipopolysaccharides, and fimbriae, and activates several MMPs including MMP-9 in various periodontal cell lines. 2,28,29) Our results confirm that P. gingivalis supernatant up-regulated MMP-9 secretion, protein, and gene expression ( Fig. 2A), suggesting that P. gingivalis supernatant may be involved in the progress of periodontitis through the production of MMP-9 in KB cells.…”

“…These bacteria trigger periodontal host cells to release inflammatory mediators including cytokines such as interleukin 1b (IL-1b), tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), matrix metalloproteinases (MMPs), chemokines, and prostaglandins. 1,2) The initial synthesis of these mediators combats the noxious effects of the pathogens, however their excess expression promotes chronic inflammatory responses. Among MMP groups, MMP-9 (a 92-kDa gelatinase B) is thought to be a key enzyme for degrading type IV collagen and specifically regulating basement membrane remodeling during periodontitis progression.…”

Osteogenesis and angiogenesis: The potential for engineering bone

“…A number of factors have been found to have a prominent effect on the pathology of the vasculature and skeleton, including Osteoprotegerin (OPG), which inhibits Receptor Activator of NF-˜B Ligand (RANKL) induced osteoclastogenic bone resorption (Bucay et al, 1998). Transgenic mice over expressing OPG display a marked increase in bone density (osteopetrosis) with very few active osteoclasts (Simonet et al, 1997). Additionally, mice deficient in OPG exhibit an osteoporotic phenotype characterised by a decrease in bone density, severe trabecular and cortical porosity and high incidence of fractures.…”

“…Disruption of the normal bone vasculature can result in skeletal problems such as osteopetrosis (Aharinejad et al, 1995;Aharinejad et al, 1999), metastatic bone disease (Taichman et al, 2002) and inflammatory bone loss in rheumatoid arthritis and periodontal disease Walsh and Mapp, 1998;Schwartz et al, 2000). Thus, we are now beginning to understand the intimate relationship between the vasculature and bone, and the important role played in maintaining bone homeostasis, offering the possibility of novel new approaches to solving the problems of fracture healing, particularly in delayed and non-union pathologies.…”

Histone deacetylases (HDAC) in physiological and pathological bone remodelling

“…In pathological bone loss, there is an uncoupling of bone formation and resorptive processes leading to excessive bone loss. While diseases such as osteoporosis, periodontitis, RA and multiple myeloma are characterised by enhanced osteoclast resorption there are also reports of reduced osteoblast bone formation [60][61][62]. For this reason, osteoblasts have been targeted with anabolic agents including parathyroid hormone (PTH), bone morphogenetic proteins (BMPs), as well as sclerostin neutralising antibody, in order to stimulate bone formation [63].…”