Mkx regulates the orthodontic tooth movement via osteoclast induction
Introduction The periodontal ligament (PDL) plays an important role in orthodontic tooth movement; however, the underlying molecular mechanism remains unclear. We have previously reported that the Mohawk homeobox ( Mkx ), a tendon-specific transcription factor, is expressed in the PDL and regulates...
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Veröffentlicht in: | Journal of bone and mineral metabolism 2021-09, Vol.39 (5), p.780-786 |
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Sprache: | eng |
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Zusammenfassung: | Introduction
The periodontal ligament (PDL) plays an important role in orthodontic tooth movement; however, the underlying molecular mechanism remains unclear. We have previously reported that the Mohawk homeobox (
Mkx
), a tendon-specific transcription factor, is expressed in the PDL and regulates its homeostasis.
Materials and methods
In the present study, we examined the role of
Mkx
in orthodontic tooth movement via bone remodeling induced by mechanical stimulation in
Mkx
-deficient rats, which are widely used as experimental animals for orthodontic force application. Orthodontic tooth movement of the maxillary first molar was performed in 7-week-old male
Mkx
-deficient rats (
n
= 4) and wild-type Wistar rats (
n
= 4) using coil springs for 14 days. Hematoxylin and eosin (H&E) staining and tartrate-resistant acid phosphatase (TRAP) staining were performed to evaluate morphological changes and osteoclasts. Furthermore, changes in the expression of receptor activator nuclear factor-kappa B ligand (RANKL) were demonstrated using immunostaining.
Results
The amount of tooth movement was significantly lower in
Mkx
-deficient rats than in wild-type rats. The number of TRAP-positive cells was suppressed in
Mkx
-deficient rats on the compression side.
Conclusion
Orthodontic tooth movement experiments in
Mkx
-deficient rats suggested that
Mkx
is involved in osteoclast induction at the alveolar bone surface on the compression side. This study reveals the possibility that Mkx plays a mechanosensory role in orthodontic tooth movement by inducing RANKL expression and osteoclastogenesis. |
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ISSN: | 0914-8779 1435-5604 |
DOI: | 10.1007/s00774-021-01233-2 |