Stimulation of prostaglandin E2 and interleukin-1beta production from old rat periodontal ligament cells subjected to mechanical stress.

Abstract

Although the severity of periodontal disease is known to be affected by the age of the host, the pathological role of aging in periodontal disease, especially that attributable to trauma from occlusion, has not been well characterized. Prostaglandin (PG)E2 and interleukin (IL)-1beta are key mediators involved in periodontal diseases, potent stimulators of bone resorption, and are produced by human periodontal ligament (PDL) cells in response to mechanical stress. To investigate age-related changes in the biosynthetic capacity of PGE2 and IL-1beta in PDL cells, we examined the effects of in vivo aging with mechanical tension on PGE2 and IL-1beta expression by rat PDL cells. PDL cells obtained from the incisors of 6-week (young) and 60-week (old) rats were cultured on flexible-bottomed culture plates. The cells were deformed by causing a 9% or 18% increase in surface area at 6 cycles per minute for 1 to 5 days. We found an approximately twofold increase in PGE2 and IL-1beta production by old PDL cells subjected to mechanical tension compared with that by young cells, although the constitutive levels were similar in both. The expression of cyclooxygenase (COX)-2 and IL-1beta mRNA (messenger ribonucleic acid) was enhanced by mechanical tension as determined by use of reverse transcription-polymerase chain reaction (RT-PCR), whereas COX-1 and IL-1beta-converting enzyme mRNA remained unchanged. It is possible that the large amount of PGE2 and IL-1beta produced by PDL cells from an aged host in response to mechanical force may be positively related to the acceleration of alveolar bone resorption.