Objectives and background:  This study investigated the expression of key mediators that regulate differentiation of osteoclasts, receptor activator of nuclear factor κB ligand (RANKL), and its natural inhibitor, osteoprotegerin (OPG), in periodontitis. We aimed to compare the levels of the RANKL and OPG in the granulomatous tissue adjacent to areas of alveolar bone loss from patients with periodontitis to that present in tissue from patients without periodontitis. In addition, we aimed to determine the types of cells expressing these factors in these tissues and to demonstrate the expression of the osteoclastic markers, RANK and tartrate-resistant acid phosphatase (TRAP), in periodontitis.



Materials and methods:  Frozen biopsy specimens were analysed using specific monoclonal antibodies and were evaluated by semiquantitative analysis and digital image analysis to compare levels of RANKL and OPG protein expression. Double labelling of frozen sections with antibodies to different cell lineage specific markers was used to determine the types of cells expressing these proteins. In situ hybridization was used to detect cells expressing RANK mRNA.



Results:  Semiquantitative image analysis demonstrated that significantly higher levels of RANKL protein (P < 0.05) were expressed in the periodontitis tissue. Conversely, OPG protein was significantly lower (P < 0.05) in the periodontitis tissues. RANKL protein was associated with lymphocytes and macrophages. OPG protein was associated with endothelial cells in both tissues. Many leukocytes expressing RANK mRNA and TRAP were observed in periodontitis tissues.



Conclusion:  The change in the levels of these key regulators of osteoclast differentiation may play a major role in the bone loss seen in periodontitis.

Receptor activator NF kB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis

Factors regulating osteoclast formation in human tissues adjacent to peri-implant bone loss: expression of receptor activator NFκB, RANK ligand and osteoprotegerin

BACKGROUND: Hypersensitivity drug reactions cause a variety of skin diseases including bullous and pustular eruptions and maculopapular exanthema (MPE). Knowledge of the underlying pathological mechanisms of immune reactions is helpful in understanding diseases imitated by drug allergies. Exanthems are the most frequent form of drug reactions. Recent immunohistological studies of skin lesions, the generation and analysis of drug-specific T -cell lines (TCL) and T-cell clones (TCC) from allergic patients suggest that drug-specific T cells playa major role in these drug-induced skin reactions.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/art.10535

Accelerated nodulosis and vasculitis following etanercept therapy for rheumatoid arthritis

Paired synovial tissue samples were obtained from both clinically uninvolved (CU) and clinically involved (CI) knee joints of eight rheumatoid arthritis (RA) patients. In addition, biopsies were taken from five control subjects. We observed the expression of the chemokines CXCL8, CXCL9, CXCL10, CCL2 and CCL4 in CI and CU joints of RA patients. In particular, CXCL8 protein levels were specifically increased in CI joints compared with CU joints, which was confirmed by immunohistochemistry and in situ hybridization.

/pdf/the-development-of-clinical-signs-of-rheumatoid-synovial-1b3mgpzdxb.pdf

The development of clinical signs of rheumatoid synovial inflammation is associated with increased synthesis of the chemokine CXCL8 (interleukin-8).

E-selectin as a target for drug delivery and molecular imaging.

Objective

To investigate the production of proinflammatory cytokines and expression of cell adhesion molecules in the rheumatoid nodule.



Methods

Cytokine content (tumor necrosis factor α [TNFα], interleukin-1β [IL-1β], and IL-1 receptor antagonist [IL-1Ra]), at the messenger RNA (mRNA) and protein levels, and cell adhesion molecule expression were studied in 16 rheumatoid nodules and 6 synovial membranes.



Results

Macrophages in the rheumatoid nodules contained TNFα, IL-1β, and IL-1Ra mRNA and protein, particularly in perivascular cells of the stroma and in the palisading layer. All cell adhesion molecules studied were expressed in both the rheumatoid nodules and synovial membranes, with increased expression of E-selectin in the rheumatoid nodule compared with the synovial membrane, and with the absence of vascular cell adhesion molecule 1 expression on cells of the palisading layer in the rheumatoid nodule.



Conclusion

The presence of similar proinflammatory cytokines and cell adhesion molecules in the rheumatoid nodule and synovial membrane suggests that similar pathogenic processes result in the chronic inflammation and tissue destruction in these lesions.

Pathogenic mechanisms in the rheumatoid nodule: Comparison of proinflammatory cytokine production and cell adhesion molecule expression in rheumatoid nodules and synovial membranes from the same patient

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Pathogenic mechanisms in the rheumatoid nodule: Comparison of proinflammatory cytokine production and cell adhesion molecule expression in rheumatoid nodules and synovial membranes from the same patient