Interleukin-1 beta and tumor necrosis factor-alpha production by human monocytes cultured with L-thyroxine and thyrocalcitonin: relation to severe root shortening.

The objectives of this study were to determine whether L-thyroxine (T4) and thyrocalcitonin (TCA) influence monocyte production of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) and to examine IL-1 beta and TNF-alpha production in monocytes from a group of orthodontic patients with severe root shortening. Human monocytes were incubated with varying concentrations of T4 and TCA for 24 hours, and IL-1 beta and TNF-alpha levels were measured by ELISA. At a concentration of 0.1 microgram/ml, T4 and TCA induced significantly more IL-1 beta than untreated controls, and T4 induced more IL-1 beta than TCA. Neither hormone induced significant TNF-alpha release, conversely, TCA had an inhibitory effect on unstimulated monocyte release of TNF-alpha. TCA was also shown to inhibit, but not reverse, the activational effect of lipopolysaccharide on monocyte TNF-alpha release. T4 and TCA concentrations as low as 0.1 pg/ml caused monocytes to release significant amounts of IL-1 beta. The highest concentration of T4 tested (1.0 microgram/ml) induced significantly less IL-1 beta production than lower concentrations. T4- and TCA-treated monocytes bound more labeled IL-1 beta than untreated controls, which suggests that these hormones increase IL-1 receptor expression. There was a wide range of unstimulated and stimulated IL-1 beta and TNF-alpha production by root resorption subject monocytes with no significant differences between resorption and nonresorption group means. This data suggest that patient monocytes did not differ from control monocytes in regard to these cytokine parameters, and therefore in vitro IL-1 beta and TNF-alpha levels could not distinguish resorption subjects.