Osteozyten: Schaltzentralen der kieferorthopädischen Zahnbewegung

Zusammenfassung

Die kieferorthopädische Zahnbewegung nutzt mechanische Kräfte um zelluläre und molekulare Ereignisse einzuleiten, die letztlich zur Knochenresorption an der Druck- und zur Knochenneubildung an der Zugseite der Alveolenwand führen. Osteozyten wirken dabei als Sensoren für mechanische Kräfte, und steuern die jeweiligen Effektorzellen, nämlich die Osteoklasten und die Osteoblasten. Diese kurze Übersicht diskutiert die Rolle der Osteozyten im Rahmen der kieferorthopädischen Zahnbewegung – die durch die Apoptose von Osteozyten bedingte Osteoklastogenese und die durch die Produktion von Sklerostin durch Osteozyten gestreute Osteoblastogenese.

Abstract

Orthodontic tooth movement uses mechanical forces to initiate cellular and molecular events that ultimately lead to bone resorption and bone formation on the pressure and tension site of the alveolar bone, respectively. Osteocytes have turned out to be sensors of the mechanical forces controlling the respective effector cells, namely osteoclasts and osteoblasts. This short review discusses the role of osteocytes in the context of orthodontic tooth movement – the osteocyte apoptosis-related osteoclastogenesis and the osteocyte-produced sclerostin-related osteoblastogenesis, respectively.

Schlüsselwörter

Osteozyten - Zahnbewegung

Key words

osteocytes - tooth movement

• Literatur

• 1 Reitan K. The initial tissue reaction incident to orthodontic tooth movement as related to the influence of function; an experimental histologic study on animal and human material. Acta Odontol Scand Suppl 1951; 6: 1-240
• 2 Rygh P. Hyalinization of the periodontal ligament incident to orthodontic tooth movement. Nor Tannlaegeforen Tid 1974; 84: 352-357
• 3 Krishnan V, Davidovitch Z. On a path to unfolding the biological mechanisms of orthodontic tooth movement. J Dent Res. 2009; 88: 597-608
• 4 Hamaya M, Mizoguchi I, Sakakura Y. et al. Cell death of osteocytes occurs in rat alveolar bone during experimental tooth movement. Calcif Tissue Int. 2002; 70: 117-126
• 5 Bonewald LF. The amazing osteocyte. J Bone Miner Res. 2011; 26: 229-238
• 6 Plotkin LI, Bellido T. Osteocytic signalling pathways as therapeutic targets for bone fragility. Nat Rev Endocrinol 2016; 12: 593-605
• 7 Dallas SL, Prideaux M, Bonewald LF. The osteocyte: an endocrine cell… and more. Endocr Rev. 2013; 34: 658-690
• 8 Zhao N, Foster BL, Bonewald LF. The Cementocyte-An Osteocyte Relative?. J Dent Res 2016; 95: 734-741
• 9 Murshid SA. The role of osteocytes during experimental orthodontic tooth movement: A review. Arch Oral Biol. 2016; 73: 25-33
• 10 Tatsumi S, Ishii K, Amizuka N. et al. Targeted ablation of osteocytes induces osteoporosis with defective mechanotransduction. Cell Metab. 2007; 5: 464-475
• 11 Verborgt O, Gibson GJ, Schaffler MB. Loss of osteocyte integrity in association with microdamage and bone remodeling after fatigue in vivo. J Bone Miner Res. 2000; 15: 60-67
• 12 Burger EH, Klein-Nulend J, Smit TH. Strain-derived canalicular fluid flow regulates osteoclast activity in a remodelling osteon – a proposal. J Biomech. 2003; 36: 1453-1459
• 13 Verna C, Dalstra M, Lee TC. et al. Microcracks in the alveolar bone following orthodontic tooth movement: a morphological and morphometric study. Eur J Orthod. 2004; 26: 459-467
• 14 Verna C, Dalstra M, Lee TC. et al. Microdamage in porcine alveolar bone due to functional and orthodontic loading. Eur J Morphol. 2005; 42: 3-11
• 15 Sakai Y, Balam TA, Kuroda S. et al. CTGF and apoptosis in mouse osteocytes induced by tooth movement. J Dent Res. 2009; 88: 345-350
• 16 Nakashima T, Hayashi M, Fukunaga T. et al. Evidence for osteocyte regulation of bone homeostasis through RANKL expression. Nat Med 2011; 17: 1231-1234
• 17 Xiong J, Onal M, Jilka RL. et al. Matrix-embedded cells control osteoclast formation. Nat Med 2011; 17: 1235-1241
• 18 Kogianni G, Mann V, Noble BS. Apoptotic bodies convey activity capable of initiating osteoclastogenesis and localized bone destruction. J Bone Miner Res. 2008; 23: 915-927
• 19 Winkler DG, Sutherland MK, Geoghegan JC. et al. Osteocyte control of bone formation via sclerostin, a novel BMP antagonist. EMBO J. 2003; 22: 6267-6276
• 20 van Bezooijen RL, Roelen BA, Visser A. et al. Sclerostin is an osteocyte-expressed negative regulator of bone formation, but not a classical BMP antagonist. J Exp Med. 2004; 199: 805-814
• 21 Balemans W, Van Den Ende J, Freire Paes-Alves A. et al. Localization of the gene for sclerosteosis to the van Buchem disease-gene region on chromosome 17q12-q21. Am J Hum Genet. 1999; 64: 1661-1669
• 22 Li X, Ominsky MS, Niu QT. et al. Targeted deletion of the sclerostin gene in mice results in increased bone formation and bone strength. J Bone Miner Res. 2008; 23: 860-869
• 23 Kuchler U, Schwarze UY, Dobsak T. et al. Dental and periodontal phenotype in sclerostin knockout mice. Int J Oral Sci 2014; 6: 70-76
• 24 Robling AG, Niziolek PJ, Baldridge LA. et al. Mechanical stimulation of bone in vivo reduces osteocyte expression of Sost/sclerostin. J Biol Chem. 2008; 283: 5866-5875
• 25 Frost HM. A 2003 update of bone physiology and Wolff’s Law for clinicians. Angle Orthod. 2004; 74: 3-15
• 26 Nishiyama Y, Matsumoto T, Lee JW. et al. Changes in the spatial distribution of sclerostin in the osteocytic lacuno-canalicular system in alveolar bone due to orthodontic forces, as detected on multimodal confocal fluorescence imaging analyses. Arch Oral Biol. 2015; 60: 45-54
• 27 Morse A, McDonald MM, Kelly NH. et al. Mechanical load increases in bone formation via a sclerostin-independent pathway. J Bone Miner Res. 2014; 29: 2456-2467
• 28 Cosman F, Crittenden DB, Adachi JD et al. Romosozumab Treatment in Postmenopausal Women with Osteoporosis. N Engl J Med. 2016 Epub ahead of print