Histochemical examination of cathepsin K, MMP1 and MMP2 in compressed periodontal ligament during orthodontic tooth movement in periostin deficient mice

Abstract

The purpose of this study was to investigate immunolocalization of collagenolytic enzymes including cathepsin K, matrix metalloproteinase (MMP) 1 and 2 in the compressed periodontal ligament (PDL) during orthodontic tooth movement using a periostin deficient (Pn-/-) mouse model. Twelve-week-old male mice homozygous for the disrupted periostin gene and their wild type (WT) littermates were used in these experiments. The tooth movement was performed according to Waldo's method, in which elastic bands of 0.5 mm thickness were inserted between the first and second upper molars of mice under anesthesia. At 1 and 3 days after orthodontic force application, mice were fixed with transcardial perfusion of 4 % paraformaldehyde in 0.1 M phosphate buffer (pH 7.4), and the first molars and peripheral alveolar bones were extracted for histochemical analyses. Compared with WT mice, immunolocalization of cathepsin K, MMP1 and MMP2 was significantly decreased at 1 and 3 days after orthodontic tooth movement in the compressed PDL of Pn-/- mice, although MMP1-reactivity and MMP2-reactivity decreased at different amounts. Very little cathepsin K-immunoreactivity was observed in the assessed regions of Pn-/- mice, both before and after orthodontic force application. Furthermore, Pn-/- mice showed a much wider residual PDL than WT mice. Taken together, we concluded that periostin plays an essential role in the function of collagenolytic enzymes like cathepsin K, MMP1 and MMP2 in the compressed PDL after orthodontic force application.

Altered distribution of HMGB1 in the periodontal ligament of periostin-deficient mice subjected to Waldo’s orthodontic tooth movement

“…Our previous study demonstrated that periostin plays an essential role in the function of collagenolytic enzymes such as cathepsin K, MMP1 and MMP2 in the compressed PDL after orthodontic force application. This aided the degradation of collagen fibers and facilitating orthodontic force-induced tooth movement, while deficiency of periostin inhibited the elimination of collagen fibers and obstructed the corresponding tooth movement (Lv et al 2014b). In this study, we obtained similar results showing that both groups exhibited extensive formation of cell-free hyaline zones at the PDL of the compression side and the PDL at this side was less compressed in Pn-/-mice than in WT mice.…”

“…Specially, Wolf et al (2013c) reported the peak expression of HMGB1 in periodontal ligament cells following 3 days of mechanical loading. Furthermore, our previous study showed the fully formed cell free hyaline zones in PDL of the compression side at day 3 after the application of mechanical stress using Waldo's method (Lv et al 2014b). There is no significant difference between the mesial and distal PDL surrounding the root (e).…”

Expression of HMGB1 in the periodontal tissue subjected to orthodontic force application by Waldo’s method in mice

“…Only the hyalinized tissue at the compression side be eliminated by macrophages can osteoclasts be recruited and formed here to perform bone resorption which makes further orthodontic tooth movement possible (Kurol and Owman-Moll 1998). Otherwise, further tooth movement would be obstructed if the secretion of matrix degradation-associated enzymes such as cathepsin K, MMP1 and MMP2 by macrophages or osteoclasts is disturbed, just as reported by our previous study (Lv et al 2014).…”

Periostin is required for matricellular localization of CCN3 in periodontal ligament of mice

“…Previously we reported that the expression of cathepsin K, matrix metalloproteinase 1 (MMP1), and MMP2 was significantly decreased in the periodontal ligament of periostin −/− mice compared with that in their wildtype counterparts (Lv et al 2014), suggesting that periostin was required for the expression of these enzymes. CCN3 has been demonstrated to play roles in the expression of MMPs (Laurent et al 2003;Benini et al 2005;Lin et al 2005;Fukunaga-Kalabis et al 2008;Tzeng et al 2011;Kular et al 2012).…”