Effects of NSAIDs on beagle crevicular cyclooxygenase metabolites and periodontal bone loss

Abstract

This investigation focuses on the changes in the concentrations of cyclooxygenase (CO) products present within the crevicular fluid in naturally-progressing periodontitis in the beagle and the effects of various non-steroidal anti-inflammatory drugs (NSAIDs) on these metabolite levels and disease progression. Six groups of 5-6 beagles with periodontitis were followed for 6 months to determine the pretreatment rate of radiographic bone loss. At baseline, groups of animals were placed on soft chow to promote disease progression. Groups were treated with either placebo, three different formulations of systemic ibuprofen, systemic naproxen or topical flurbiprofen. During the 6-month treatment phase, crevicular fluid (CF) samples and radiographs were taken at regular intervals. Radioimmunoassay of CF samples from untreated animals demonstrated a steady increase in prostaglandin E2 (PGE2) over baseline values. At 1 month, CF-PGE2 levels increased 2-fold over baseline and, by 6 months, had reached a 5- to 6-fold elevation. Crevicular fluid thromboxane B2 (CF-TxB2) levels rapidly reached a 4- to 5-fold peak over baseline at 1 month and subsequently dropped to a 2-fold elevation for the remainder of the study. The rate of bone loss (BLOSS) in untreated animals increased 38% during the 6-month period, as compared to baseline pretreatment BLOSS rates. Overall, there was a significant depression in the CF levels of both PGE2 and TxB2 in all NSAID-treated groups. All NSAID treatments significantly retarded BLOSS, ranging from 21.0-36.9% of the control BLOSS rate. Furthermore, CO activation represents a major regulatory step in bone destruction and may thereby serve as an important site for pharmacological modulation.

Short-Term effect of COX-2 selective inhibitor as an adjunct for the treatment of periodontal disease: a clinical double-blind study in humans

“…Nevertheless, although PGs levels of the patients were not measured in this experiment, it seems like the present findings are related to the mechanism of the COX-2 inhibition and are supported by previous studies (7)(8)(9)12,16).…”

“…Higher levels of PGE 2 are associated with increased gingival inflammation and alveolar bone loss (1,3,6,7). Therefore, the purpose of this study was to evaluate a selective COX-2 inhibitor derived from phenylpropionic acid, Loxoprofen sodium, as an adjunct for periodontal disease treatment, using probing pocket depth (PD) to verify the inflammation reduction.…”

The effect of inflammatory response modulator agents on gingivitis and periodontitis

“…Offenbacher et al 15 verified higher arachidonic acid byproducts (ciclooxygenase and thromboxane B2) in the groups not under NSAIDs therapy, indicating a positive correlation between these products and a periodontal homeostasis disruption in Beagle dogs.…”

“…Howell et al 6 and Offenbacher et al 15 evaluated different NSAIDs and their different administration forms in the gingival bleeding parameters and rate of bone loss. Offenbacher et al 15 verified higher arachidonic acid byproducts (ciclooxygenase and thromboxane B2) in the groups not under NSAIDs therapy, indicating a positive correlation between these products and a periodontal homeostasis disruption in Beagle dogs.…”

“…Although it is difficult to extrapolate the results of animal studies to humans, it is equally unwise to ignore the many similarities that scientists have demonstrated in these models 13 . Many animal models using NSAIDs of experimental periodontal disease have been proposed throughout the years, such as ligature induced periodontitis 4,14 and periodontitis induced by diet consistence modification [5][6][7]15 . These are the most effective methods to accumulate plaque and induce periodontal disease (Table 1).…”