Bone modeling

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Bone Modeling: Biomechanics, Molecular
Mechanisms, and Clinical Perspectives
W. Eugene Roberts, Sarandeep Huja, and Jeffery A. Roberts
Bone modeling is a mechanically mediated adaptive process for changing a
bone’s size, shape, or position. Site specific, anabolic and catabolic modeling
events are manifestations of overload hypertrophy and disuse atrophy, respectively. Catabolic bone modelingat the periodontal ligament (PDL) surface is the
rate-limiting step in tooth movement. In initiating tooth movement, connective
tissue growth factor (CTGF) is expressed in osteoblasts and osteocytes, and
osteopontin (Opn) is expressed by osteoclasts and osteocytes. Undermining
resorption occurs by recruiting osteoclasts to the site of maximal PDL compression and a paravascular osteogenicresponse is initiated in widened areas
of the PDL: (1) preosteoblast formation at 10 hours, (2) peak DNA synthesis at
20 hours, (3) maximum rate of mitosis at 30 hours, and (4) initiation of bone
formation at 48 hours. At other skeletal sites, additional genes have been
linked to mechanical activation of bone: glutamate/aspartate transporter
(GLAST), nitric oxide synthetase (NOS), prostaglandinG/H synthetase (PGHS2), Msx1, and c-fos. An intricate series of endocrine, paracrine, and autocrine
factors has been described. Parathyroid hormone (PTH) enhances expression of
insulin-like growth factor I (IGF-I) and the estrogen receptor beta (ER- ), which
are both modulators of mechanical loading. Transforming growth factor beta
(TGF- ) and the related bone morphogenetic proteins (BMPs) helpcontrol
anabolic modeling. Catabolic modeling is mediated by PGE2, IL-1 , and other
inflammatory cytokines. Osteoclast differentiation and activation is controlled
by genes related to tumor necrosis factor (TNF) and its receptor (TNFR): colony
stimulating factor 1 (CSF-1), osteoprotegerin (OPG), receptor activator of nuclear factor (RANK), and RANK ligand (RANKL). Orthodontic aspects of bonemodeling are reviewed relative to morphology, biomechanics, neurology, molecular control mechanisms, and the periodontal adaptation to loading. Clinical
correlations discussed are orthodontic analgesics, inflammatory cytokines, surgical enhancement of tooth movement, distraction osteogenesis, closure of
atrophic defects, periodontal compromise, traumatized periodontium, and systemic disease.(Semin Orthod 2004;10:123-161.) © 2004 Elsevier Inc. All rights

one is a complex, living tissue that is constantly adapting to metabolic and structural
demands. Because it is a mineralized tissue, all


From the Section of Orthodontics, Department of Oral Facial Development, Indiana University School of Dentistry, Indianapolis, IN; Ohio
State University, School of Dentistry,Department of Orthodontics, Columbus, OH; and Private Practice of Orthodontics, Richmond, IN.
Address correspondence to Dr W. Eugene Roberts, Indiana University School of Dentistry, Department of Oral Facial Development,
1121 West Michigan Street, Indianapolis, IN 46202.
© 2004 Elsevier Inc. All rights reserved.

changes in externalosseous form occur along
vascularized periosteal surfaces via uncoupled
anabolic and catabolic modeling events. Modeling changes the shape, size, and/or position of
bones in response to mechanical loading
and/or wounding. On the other hand, remodeling is turnover of bone that is related to bone
maturation, skeletal maintenance, and mineral
metabolism. There are important distinctionsbetween bone modeling and remodeling that
are relevant to clinical practice (Fig 1). In the
orthodontic literature, the term “bone remodeling” is commonly applied to all bone changes.

Seminars in Orthodontics, Vol 10, No 2 (June), 2004: pp 123-161



Roberts, Huja, and Roberts

Figure 1. Both bone modeling (*) and remodeling
(#) are features of orthodontic tooth movement....
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