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  • Title: The effect of aspirin on gingival crevicular fluid levels of inflammatory and anti-inflammatory mediators in patients with gingivitis.
    Author: Kim DM, Koszeghy KL, Badovinac RL, Kawai T, Hosokawa I, Howell TH, Karimbux NY.
    Journal: J Periodontol; 2007 Aug; 78(8):1620-6. PubMed ID: 17668982.
    Abstract:
    BACKGROUND: Inflammatory and anti-inflammatory mediators may play a significant role in patients with gingivitis. The purpose of this study was to assess the short-term effects of the systemic administration of two different concentrations of aspirin (81 and 325 mg/day, by mouth) on clinical periodontal parameters and gingival crevicular fluid (GCF) levels of 15-epi-lipoxin A4 (15-epi-LXA4), lipoxin A4, leukotriene B4 (LTB4), prostaglandin E2 (PGE2), and interleukin (IL)-6 and -1beta in a sample of naturally occurring gingivitis patients. METHODS: At day 0, after initial screening for entry, baseline periodontal parameters, including bleeding on probing (BOP), periodontal probing depths (PDs), and plaque index (PI) were measured, and GCF was sampled from 12 intrasulcular sites with filter paper strips for the measurement of six types of inflammatory and anti-inflammatory mediators using competitive enzyme immunoassay and enzyme-linked immunosorbent assay (prevalues). Forty-seven subjects were assigned randomly to one of three treatment groups: placebo (15 subjects); aspirin, 81 mg (16 subjects); and aspirin, 325 mg (16 subjects) once daily. On day 7, subjects were recalled for the measurement of periodontal parameters and collection of GCF samples for the measurement of six types of mediators (postvalues). RESULTS: Changes in inflammatory and anti-inflammatory mediator levels were not statistically significant for any of the three treatment groups. However, when pre- and postvalues were compared in the subjects receiving aspirin, 325 mg, there was a negative trend in the relationship between 15-epi-LXA4 and PGE2, whereas the relationship between LTB4 and PGE2 was not as strong. This might indicate that the subjects responding to aspirin-mediated PGE2 suppression effects produced higher 15-epi-LXA4 in GCF than non-responders. No statistically significant differences in PD and PI between pre- and postvalues were found for any of the three treatment groups. However, the results demonstrated a significant increase in BOP when aspirin, 325 mg was compared to placebo (P <0.001) and aspirin, 81 mg (P = 0.001). CONCLUSIONS: Aspirin can have an affect on BOP in naturally occurring gingivitis patients. Although most of the inflammatory mediators did not show significantly detectable changes after aspirin treatment for 7 days, the trend of aspirin-associated increases of 15-epi-LXA4 implied that this recently discovered aspirin-dependent eicosanoid may be associated with the increased incidence of BOP observed in the subjects who received aspirin therapy.
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