Orthodontic tooth movement is achieved by the remodeling of periodontal ligament (PDL) and alveolar bone in response to mechanical loading and is believed to be mediated by several host mediators, such as cytokines. By means of real-time polymerase chain reaction (PCR), we studied the pattern of expression of mRNA encoding several pro- and anti-inflammatory cytokines in relation to several extracellular matrix and bone remodeling markers, in tension (T) and compression (C) sides of the PDL of human teeth subjected to rapid maxillary expansion. The PDL of normal teeth was used as a control. The results showed that both T and C sides exhibited significantly higher expression of all targets when compared with controls, except for type I collagen (COL-I) and tissue inhibitor of metalloproteinase-1 (TIMP-1) on the C side. Comparing C and T sides, the C side exhibited higher expression of tumor necrosis factor-alpha (TNF-alpha), receptor activator of nuclear factor-kappaB ligand (RANKL), and matrix metalloproteinase-1 (MMP-1), whereas the T side presented higher expression of interleukin-10 (IL-10), TIMP-1, COL-I, osteoprotegerin (OPG), and osteocalcin (OCN). The expression of transforming growth factor-beta (TGF-beta) was similar in both C and T sides. Our data demonstrate a differential expression of pro- and anti-inflammatory cytokines in compressed and stretched PDL during orthodontic tooth movement.
RANKL and OPG are expressed in apical periodontitis, suggesting a role for these molecules during lesion development. However, the profiles of RANKL/OPG expression in periapical lesions remain unknown. In this study we investigated the patterns of RANKL and OPG mRNA expression by RealTime-PCR in human periapical granulomas (N=44), and compared them with sites presenting characteristic bone resorpting activity: healthy (n=14) and orthodontically stretched and compressed periodontal ligament (n=26), healthy gingiva (n=24), chronic gingivitis (n=32) and chronic periodontitis (n=34) samples. Both RANKL and OPG mRNA expression was higher in periapical granulomas when compared to healthy periodontal ligament. Distinct patterns of RANKL and OPG expression ratio were found in the granulomas and in different physiological and pathological conditions with characteristic bone resorption activity potentially being an indicative of the stable or progressive nature of the lesions. Lesions with radiographic image smaller than 5mm demonstrated higher RANKL/OPG expression than images greater than 5mm. Periapical granulomas presented heterogeneous patterns of RANKL and OPG expression, ranging from samples with RANKL/OPG ratio similar to that seen in sites with minimal or absent bone resorption, until samples with RANKL/ OPG expression pattern comparable with active bone resorption sites.
Inflammatory cytokines contribute to periapical tissue destruction. Their activity is potentially regulated by SOCS (suppressors of cytokine signaling), which downregulate signal transduction as part of an inhibitory feedback loop. We investigated the expression of the cytokines TNF-α, IL-10 and RANKL, and SOCS-1, -2 and -3 by Real Time-PCR in 57 periapical granulomas and 38 healthy periapical tissues. Periapical granulomas exhibited significant higher SOCS-1, -2 and -3, TNF-α, IL-10 and RANKL mRNA levels when compared to healthy controls. Significant positive correlations were found between SOCS1 and IL-10, and between SOCS3 and IL-10. Significant inverse correlations were observed between SOCS1 and TNF-α, SOCS1 and RANKL, and SOCS3 and TNF-α. Increased SOCS-1, -2 and -3 mRNA levels in periapical granulomas may be related to the downregulation of inflammatory cytokines in these lesions; therefore, SOCS molecules may have a role in the dynamics of periapical granulomas development.
During orthodontic tooth movement (OTM), alveolar bone is resorbed by osteoclasts in compression sites (CS) and is deposited by osteoblasts in tension sites (TS). The aim of this study was to develop a standardized OTM protocol in mice and to investigate the expression of bone resorption and deposition markers in CS and TS. An orthodontic appliance was placed in C57BL6/J mice. To define the ideal orthodontic force, the molars of the mice were subjected to forces of 0.1N, 0.25 N, 0.35 N and 0.5 N. The expression of mediators that are involved in bone remodeling at CS and TS was analyzed using a Real-Time PCR. The data revealed that a force of 0.35 N promoted optimal OTM and osteoclast recruitment without root resorption. The levels of TNF-α, RANKL, MMP13 and OPG were all altered in CS and TS. Whereas TNF-α and Cathepsin K exhibited elevated levels in CS, RUNX2 and OCN levels were higher in TS. Our results suggest that 0.35 N is the ideal force for OTM in mice and has no side effects. Moreover, the expression of bone remodeling markers differed between the compression and the tension areas, potentially explaining the distinct cellular migration and differentiation patterns in each of these sites.
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