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An apparatus was developed to apply positive or negative hydrostatic pressure dynamically to periodontal ligament (PDL) cells in vitro. The objective of this investigation was to construct this apparatus and to determine its effects on PDL cells. Human PDL cells were collected from freshly extracted premolars. At the sixth passage, the cells were mechanically stimulated by this apparatus at different magnitudes of continuous positive or negative hydrostatic pressures (PHP or NHP, respectively). The application of PHP between 0.3 and 30 gm/cm2 significantly enhanced prostaglandin E (PGE) production and intracellular cyclic AMP (cAMP) of the cells. In contrast, perturbation by NHP significantly decreased PGE production and intracellular level of cAMP. Proliferation rate increased significantly at 24 and 48 hours due to stimulation of these cells with -30 gm/cm2 of NHP. Challenging these cells with +30 gm/cm2 of PHP significantly decreased the proliferation rate of these cells at 24 and 48 hours. Stimulation by PHP between +30 to +600 gm/cm2 increased cell length and width and appeared to increase surface area attachment to the bottom of the culture dishes. In contrast, NHP (between -30 and -600 gm/cm2) decreased these dimensions and appeared to reduce the surface area of attachment. These results indicate that this type of mechanical perturbation of PDL cells produces physiologic responses and is not detrimental to their vitality.

Studies have shown that patients undergoing orthodontic tooth movement can experience varying degrees of discomfort. The objective of this study was to determine whether nonsteroidal antiinflammatory agents, such as aspirin or ibuprofen, which inhibit prostaglandin synthesis through acetylation and inactivation of the enzyme cyclooxygenase, can suppress orthodontic discomfort by inhibiting the inflammatory response normally observed after orthodontic adjustments. A total of 77 patients were included in a double-blind, randomized, parallel, placebo-controlled, single-dose, analgesic efficacy evaluation of ibuprofen and aspirin. Patients were divided into three groups. Group A received one dose of the drug ibuprofen (400 mg), group B received aspirin (650 mg), and group C received a placebo (beta-lactose). The level of discomfort was assessed using a visual analogue scale at 2, 6, and 24 hours and 2, 3, and 7 days after the insertion of either orthodontic separators or an initial arch wire. A repeated measures analysis of variance and post hoc studentized range statistics showed that the placebo group had significantly more discomfort than either the ibuprofen or the aspirin group at all the time intervals tested. In addition, ibuprofen produced significantly less discomfort than aspirin at the 6 and 24-hour and 2-day time phase after separator placement; and 2 and 6 hours and 2, 3, and 7 days after arch wire placement. These results support a recommendation for ibuprofen as a preferred analgesic in the treatment of discomfort because of postorthodontic adjustments.

Cytokines are local mediators released by cells of the immune system in response to stimulation by a variety of agents. These polypeptides may interact directly or indirectly with bone cells. The objectives of this study were (1) to localize prostaglandin E (PGE) and the cytokine interleukin-1 beta (IL-1 beta) in the periodontal ligament after the application of mechanical force to teeth in vivo and (2) to determine the effects of mechanical stress or IL-1 beta (or the two in combination) on PGE synthesis and bone resorption by fibroblasts in the human periodontal ligament (PDL). In 24 female cats, one maxillary canine was tipped distally by 80 gm force for 12 hours, 24 hours, or 7 days. PGE and IL-1 beta were localized immunohistochemically in serial jaw sections, and semiquantitation of cellular-staining intensity was done by microphotometry. Unstressed periodontal ligament cells stained mildly for PGE and IL-1 beta, but the staining intensity increased significantly in sites of tension. Human periodontal ligament fibroblasts were preincubated with mechanical stress and/or IL-1 beta in the presence or absence of indomethacin for 1 hour. Then the media were replaced by BGJb (Fitton-Jackson modification) medium (GIBCO), and incubation was continued for 4, 8, or 24 hours in conditioned media. PGE concentrations in conditioned media were determined by radioimmunoassay, and bone-resorbing activity in conditioned media was assessed by 45Ca release from prelabeled neonatal mouse calvaria. The conditioned media derived from cells stimulated by mechanical stress plus IL-1 beta caused significantly more bone resorption than the conditioned media obtained from cells that had been treated by each factor alone. The addition of indomethacin did not inhibit bone resorption completely. These results demonstrate that periodontal ligament cells respond to mechanical stress by increased production of PGE, and that IL-1 beta enhances this response.