<p>Periodontitis is a bacterially induced chronic inflammatory disease that destroys the supporting tissues of teeth. Clinical observations and experimental evidence indicates that there is a genetic influence of risk factors for periodontitis. A specific pattern of IL-1 polymorphisms (known as the composite IL-1 genotype) has been found to influence the severity of chronic periodontitis. The objective of this study was to evaluate the association between the IL-1 gene polymorphisms and the severity of periodontal disease in a selected Xhosa ppopulation of South africa.</p>

<p>Patients who are in end-stage renal disease (ESRD) experience a significantly increased rate of atherosclerotic complications. Inflammation plays a central role in the pathogenesis of these complications. The major acute phase protein, C-reactive protein (CRP) has been found to predict all-cause and cardiovascular mortality in ESRD patients. Many patients in ESRD experience elevated CRP levels without an overt infection. Periodontal diseases in the general population have been associated with both an increased prevalence of atherosclerotic complications and an elevation in serum CRP values. The aim of this present study was to investigate whether periodontal disease is associated with increased systemic inflammation reflected by CRP values, in patients with ESRD on maintenance haemodialysis (HD) or perioneal dialysis (PD).</p>

Mechanical stress has been shown to play a role in bone remodelling during orthodontic tooth movement. Receptor activator of nuclear factor kβ - ligand (RANKL), osteoprotegerin (OPG), monocyte colony stimulating factor (M-CSF) and interleukin 1-β (IL-1β) play key roles in the regulation of bone remodelling, but the role of these cytokines in orthodontic tooth movement is poorly understood. Aim: The aim of this experiment was to examine the response of periodontal ligament (PDL) fibroblasts in monolayer culture to intermittent tensile stress as regards RANKL, OPG, M-CSF and IL-1β production. Methods: Human PDL fibroblasts were dissected from premolars extracted for orthodontic purposes. Explants were seeded out in 1cm wells and grown to confluence in Dulbecco�s modification of Eagle�s medium, containing 10% foetal calf serum and antibiotics, at 37�C in a humidified atmosphere of 5% CO₂/95% air. Upon reaching confluence, the cells were passaged into sequentially larger flasks. Fibroblasts were passaged 6 times. After reaching confluence in T175 flasks, the cells were detached and plated at a cell density of 10⁵/dish in 35mm Bioflex� Plates coated with type 1 collagen. The cells were placed under a continuous uni-axial strain of 12% for 6s of every 90s by a Flexercell FX 4000C[TM] for 0, 12, 24 and 48 hours. Cells were then detached and stored in RNAlater. Quantitative RT-PCR was used to determine the mRNA of the cytokines of interest. Results: Tensile force led to the down regulation of mRNA expression for OPG and IL-1β at 12 and 24 hours respectively, while M-CSF was up-regulated at 6 hours. RANKL was not detected at a significant level for quantification. Conclusion: This osteoclastic-type response indicates the complexity of mechanotransduction in an in vitro setting. Acknowledgments: This research was supported by the New Zealand Dental Research Foundation, the New Zealand Lottery Grants Board and the New Zealand Association of Orthodontists.

Diss. (sammanfattning) Göteborg : Univ., 2007. / Härtill 5 uppsatser.

Thesis (M.D.S.)--University of Adelaide, Dept. of Dentistry, 1984. / Some mounted ill. Includes bibliographical references (leaves 79-101).

Thesis (M.D.S.)--University of Adelaide, 1985. / Some mounted ill. Includes bibliographical references (leaves 191-226).

Thesis (M.D.S.)--University of Adelaide, 1987. / Includes bibliographical references (leaves 157-177).

Thesis (M.D.S.)--University of Adelaide, 1983. / Ill. mounted. Includes bibliographical references (9.1-9.20).

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Thesis (M.D.S. 1979) from the Department of Dental Health, University of Adelaide.