The results of the present study suggest that MCP-1 and RANTES could play key roles in both activation and recruitment of inflammatory and immune cells in periodontal environment of G-AgP patients. In conclusion, these CC chemokines may be considered in the biological mechanism underlying the pathogenesis and progression of G-AgP.

These data indicate that combination of SDD with non-surgical therapy improves clinical parameters of periodontal disease and increases GCF TGF-beta1 levels together with a decrease in prevalence of residual pockets in patients with severe, generalized chronic periodontitis. Increased GCF TGF-beta1 levels following SDD therapy might suggest a novell pleiotrophic mechanism for tetracyclines to inhibit connective tissue breakdown.

No abstract

Nimesulides, relatively selective COX-2 inhibitors, may have additional inhibitory effects on GT PGF2alpha levels in the first week following non-surgical periodontal treatment. However, nimesulide has an insignificant effect on reducing PGE2 levels in gingival tissue. The determination of GT levels of COX-1 and COX-2 enzymes as well as PGE2 and PGF2alpha in long-term studies may provide further support for the adjunctive use of selective COX-2 inhibitors in treatment of chronic periodontitis.

No abstract

The results of the present study indicate that LTB4 is likely to be an important mediator in regulating inflammatory responses in the human periodontal tissues. This lipid mediator may play an important role in the pathophysiology of periodontal disease.

The results of the present study indicate that PAF is likely to be an important mediator in regulating inflammatory responses in the human periodontal tissues. To our knowledge, this is the first report investigating PAF levels in GCF and GT in specific periodontal diseases. We believe that this potent phospholipid mediator may need to be considered in the pathogenesis of periodontal diseases.

The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-α (TNF-α) and plateletactivating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirtythree of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-α and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.