osteoprotegerin and Bacterial-Infections

One of the most distinct features of middle ear cholesteatoma is bone destruction. Aetiology of cholesteatoma is thought to be multifactorial. Endotoxins produced by bacteria are thought to initiate the inflammation process in the middle ear leading to cholesteatoma. There are physiological differences in bone metabolism between men and women. The aim of our study was the immunohistochemical evaluation of the contents of two key components of the OPG/RANK/RANKL triad-RANKL and OPG in cholesteatoma, to analyse if there are any differences between the sexes and to evaluate the bacteria species isolated from cholesteatoma just before surgical treatment and to evaluate their plausible influence on the expression of OPG and RANKL in cholesteatoma. Twenty-one adult patients with acquired cholesteatoma who underwent surgery were analysed. There were no statistically significant differences in the expression of both regulators of osteoclastogenesis between the sexes. In 38.1 % patients cholesteatoma was not infected, whereas in 61.9 % patients various bacterial infections or mycosis were found. The most frequently isolated species was Pseudomonas aeruginosa (14.29 % infections) followed by Staphylococcus aureus (9.52 % infections). There were no statistically significant differences in expression of both OPG and RANKL between uninfected and infected cholesteatomas.

Topics: Adult; Bacterial Infections; Bone and Bones; Cholesteatoma; Female; Gene Expression Regulation, Bacterial; Humans; Immunohistochemistry; Inflammation; Male; Middle Aged; Osteoclasts; Osteogenesis; Osteoprotegerin; Pilot Projects; Pseudomonas aeruginosa; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Staphylococcus aureus

Raised levels of pro-inflammatory, pro-resorptive cytokines during pulmonary infection may contribute to osteoporosis in cystic fibrosis (CF). We assessed osteoclast number and activity during infective exacerbations and examined their relationship to serum inflammatory cytokines and bone turnover markers.. Serum samples from 24 adults with CF were obtained before, during and after treatment of infection. Osteoclastic cells were generated from peripheral blood mononuclear cells and their number and activity assessed. Serum osteocalcin, type 1 collagen cross-linked N-telopeptide (NTx), interleukin-6 (IL-6), tumour necrosis factor alpha (TNFalpha), receptor activator of NFkB ligand (RANKL) and osteoprotegerin (OPG) were measured.. Osteoclast number and activity were increased at the start of exacerbation and decreased with antibiotic therapy. Significant correlations were demonstrated between osteoclast formation and serum TNFalpha, OPG, osteocalcin and NTx and between osteoclast activity and serum IL-6 and NTx.. The systemic response to infection is associated with increased bone resorptive activity in patients with CF.

Topics: Adult; Bacterial Infections; Bone Remodeling; Cell Count; Collagen Type I; Cystic Fibrosis; Cytokines; Female; Humans; Inflammation Mediators; Interleukin-6; Male; Osteocalcin; Osteoclasts; Osteoprotegerin; Peptides; Pseudomonas aeruginosa; Pseudomonas Infections; Severity of Illness Index; Tumor Necrosis Factor-alpha; Young Adult

Nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) plays an important role in host defense, as well as in inflammation-induced tissue lesions. Here we evaluated the role of NO in bone loss in bacterial infection-induced apical periodontitis by using iNOS-deficient mice (iNOS(-/-)). The iNOS(-/-) mice developed greater inflammatory cell recruitment and osteolytic lesions than WT mice. Moreover, tartrate-resistant acid-phosphatase-positive (TRAP(+)) osteoclasts were significantly more numerous in iNOS(-/-) mice. Furthermore, the increased bone resorption in iNOS(-/-) mice also correlated with the increased expression of receptor activator NF-kappaB (RANK), stromal-cell-derived factor-1 alpha (SDF-1 alpha/CXCL12), and reduced expression of osteoprotegerin (OPG). These results show that NO deficiency was associated with an imbalance of bone-resorption-modulating factors, leading to severe infection-stimulated bone loss.

Topics: Acid Phosphatase; Actinomycosis; Alveolar Bone Loss; Animals; Bacterial Infections; Bacteroidaceae Infections; Biomarkers; Cell Count; Cell Movement; Chemokine CXCL12; Dental Pulp Exposure; Isoenzymes; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Nitric Oxide; Nitric Oxide Synthase Type II; Osteoclasts; Osteolysis; Osteoprotegerin; Periapical Periodontitis; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Tartrate-Resistant Acid Phosphatase