Biphasic sutural response is key to palatal expansion

Abstract

IntroductionIt is assumed that transverse force physically open maxillary sutures and induce tensile stress that directly stimulates bone formation. However, orthopedic tensile stress is static, which cannot directly stimulate bone formation. We hypothesize that the anabolic response to transverse forces is indirect, the result of inflammation-induced osteoclast activation followed by a transition into osteogenesis. To test our hypothesis, we evaluated tissue, cellular, and molecular responses in the sutures during maxillary expansion. Materials and methodsSprague-Dawley rats (n = 95) were divided into four groups (n = 5 rats/group/time point, except for the expansion group, which did not have a day 0 sample): untreated control (C), sham (S), expansion (Exp), and expansion with nonsteroidal anti-inflammatory medication (Exp + NSAID). Maxillae were collected 0, 1, 3, 7, 14, and 28 days postexpansion for micro–computed tomography, light microscopy, gene expression, protein, and immunohistochemistry analysis. ResultsCompared with the sham group, the Exp group showed early expression of cytokines in the mid-palatal suture, osteoclast activation, and bone resorption resulting in widening of the suture. Anabolic bone formation was delayed, occurring after this initial catabolic phase. NSAIDs significantly decreased sutural widening, bone formation, and skeletal and dental expansion. During the transition from catabolic to anabolic phase, expression of osteoclast-osteoblast communicator molecules increased significantly. ConclusionTransverse force stimulates two distinct phases in the mid-palatal suture. An early catabolic phase, characterized by inflammation, osteoclast recruitment, and activity, results in bone resorption and sutural widening. Then osteoclasts activate osteoblasts resulting in an anabolic phase, during which the integrity of the skeleton is reestablished.