Links to Exploration step
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Miniplates and mini-implants: bone remodeling as their biological
foundation<xref ref-type="fn" rid="fn01">1</xref>
</title>
<author><name sortKey="Consolaro, Alberto" sort="Consolaro, Alberto" uniqKey="Consolaro A" first="Alberto" last="Consolaro">Alberto Consolaro</name>
<affiliation><nlm:aff id="aff2">Full professor, University of São Paulo (USP), School of Dentistry, Bauru, São Paulo, Brazil and University of São Paulo (USP), School of Dentistry, Ribeirão Preto, São Paulo Brazil</nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">26691966</idno>
<idno type="pmc">4686741</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686741</idno>
<idno type="RBID">PMC:4686741</idno>
<idno type="doi">10.1590/2177-6709.20.6.016-031.oin</idno>
<date when="2015">2015</date>
<idno type="wicri:Area/Pmc/Corpus">000279</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000279</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Miniplates and mini-implants: bone remodeling as their biological
foundation<xref ref-type="fn" rid="fn01">1</xref>
</title>
<author><name sortKey="Consolaro, Alberto" sort="Consolaro, Alberto" uniqKey="Consolaro A" first="Alberto" last="Consolaro">Alberto Consolaro</name>
<affiliation><nlm:aff id="aff2">Full professor, University of São Paulo (USP), School of Dentistry, Bauru, São Paulo, Brazil and University of São Paulo (USP), School of Dentistry, Ribeirão Preto, São Paulo Brazil</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">Dental Press Journal of Orthodontics</title>
<idno type="ISSN">2176-9451</idno>
<idno type="eISSN">2177-6709</idno>
<imprint><date when="2015">2015</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><title>Abstract</title>
<p>The tridimensional network formed by osteocytes controls bone design by coordinating
cell activity on trabecular and cortical bone surfaces, especially osteoblasts and
clasts. Miniplates and mini-implants provide anchorage, allowing all other
orthodontic and orthopedic components, albeit afar, to deform and stimulate the
network of osteocytes to command bone design remodeling upon "functional demand"
established by force and its vectors. By means of transmission of forces, whether
near or distant, based on anchorage provided by miniplates, it is possible to change
the position, shape and size as well as the relationship established between the
bones of the jaws. Understanding bone biology and the continuous remodeling of the
skeleton allows the clinician to perform safe and accurate rehabilitation treatment
of patients, thus increasing the possibilities and types of intervention procedures
to be applied in order to restore patient's esthetics and function.</p>
</div>
</front>
<back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Bakker, Ad" uniqKey="Bakker A">AD Bakker</name>
</author>
<author><name sortKey="Soejima, K" uniqKey="Soejima K">K Soejima</name>
</author>
<author><name sortKey="Klein Nulend, J" uniqKey="Klein Nulend J">J Klein-Nulend</name>
</author>
<author><name sortKey="Burger, Eh" uniqKey="Burger E">EH Burger</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Baron, R" uniqKey="Baron R">R Baron</name>
</author>
<author><name sortKey="Hesse, E" uniqKey="Hesse E">E Hesse</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Bonewald Lynda, F" uniqKey="Bonewald Lynda F">F Bonewald, Lynda</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Bonewald, Lf" uniqKey="Bonewald L">LF Bonewald</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Bonewald, Lf" uniqKey="Bonewald L">LF Bonewald</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Burr, Db" uniqKey="Burr D">DB Burr</name>
</author>
<author><name sortKey="Robling, Ag" uniqKey="Robling A">AG Robling</name>
</author>
<author><name sortKey="Turner, Ch" uniqKey="Turner C">CH Turner</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Crockett, Jc" uniqKey="Crockett J">JC Crockett</name>
</author>
<author><name sortKey="Rogers, Mj" uniqKey="Rogers M">MJ Rogers</name>
</author>
<author><name sortKey="Coxon, Fp" uniqKey="Coxon F">FP Coxon</name>
</author>
<author><name sortKey="Hocking, Lj" uniqKey="Hocking L">LJ Hocking</name>
</author>
<author><name sortKey="Helfrich, Mh" uniqKey="Helfrich M">MH Helfrich</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Ehrlich, Pj" uniqKey="Ehrlich P">PJ Ehrlich</name>
</author>
<author><name sortKey="Noble, Bs" uniqKey="Noble B">BS Noble</name>
</author>
<author><name sortKey="Jessop, Hl" uniqKey="Jessop H">HL Jessop</name>
</author>
<author><name sortKey="Stevens, Hy" uniqKey="Stevens H">HY Stevens</name>
</author>
<author><name sortKey="Mosley, Jr" uniqKey="Mosley J">JR Mosley</name>
</author>
<author><name sortKey="Lanyon, Le" uniqKey="Lanyon L">LE Lanyon</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Feng, Jq" uniqKey="Feng J">JQ Feng</name>
</author>
<author><name sortKey="Ward, Lm" uniqKey="Ward L">LM Ward</name>
</author>
<author><name sortKey="Liu, S" uniqKey="Liu S">S Liu</name>
</author>
<author><name sortKey="Lu, Y" uniqKey="Lu Y">Y Lu</name>
</author>
<author><name sortKey="Xie, Y" uniqKey="Xie Y">Y Xie</name>
</author>
<author><name sortKey="Yuan, B" uniqKey="Yuan B">B Yuan</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Kamioka, H" uniqKey="Kamioka H">H Kamioka</name>
</author>
<author><name sortKey="Honjo, T" uniqKey="Honjo T">T Honjo</name>
</author>
<author><name sortKey="Takano Yamamoto, T" uniqKey="Takano Yamamoto T">T Takano-Yamamoto</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Krstic, Rv" uniqKey="Krstic R">RV Krstic</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Lane, Ne" uniqKey="Lane N">NE Lane</name>
</author>
<author><name sortKey="Yao, W" uniqKey="Yao W">W Yao</name>
</author>
<author><name sortKey="Balooch, M" uniqKey="Balooch M">M Balooch</name>
</author>
<author><name sortKey="Nalla, Rk" uniqKey="Nalla R">RK Nalla</name>
</author>
<author><name sortKey="Balooch, G" uniqKey="Balooch G">G Balooch</name>
</author>
<author><name sortKey="Habelitz, S" uniqKey="Habelitz S">S Habelitz</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Lanyon, Le" uniqKey="Lanyon L">LE Lanyon</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Nakashima, T" uniqKey="Nakashima T">T Nakashima</name>
</author>
<author><name sortKey="Hayashi, M" uniqKey="Hayashi M">M Hayashi</name>
</author>
<author><name sortKey="Fukunaga, T" uniqKey="Fukunaga T">T Fukunaga</name>
</author>
<author><name sortKey="Kurata, K" uniqKey="Kurata K">K Kurata</name>
</author>
<author><name sortKey="Oh Hora, M" uniqKey="Oh Hora M">M Oh-Hora</name>
</author>
<author><name sortKey="Feng, Jq" uniqKey="Feng J">JQ Feng</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Parfitt, Am" uniqKey="Parfitt A">AM Parfitt</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Poole, Ke" uniqKey="Poole K">KE Poole</name>
</author>
<author><name sortKey="Van Bezooijen, Rl" uniqKey="Van Bezooijen R">RL van Bezooijen</name>
</author>
<author><name sortKey="Loveridge, N" uniqKey="Loveridge N">N Loveridge</name>
</author>
<author><name sortKey="Hamersma, H" uniqKey="Hamersma H">H Hamersma</name>
</author>
<author><name sortKey="Papapoulos, Se" uniqKey="Papapoulos S">SE Papapoulos</name>
</author>
<author><name sortKey="Lowik, Cw" uniqKey="Lowik C">CW Löwik</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Raab Cullen, Dm" uniqKey="Raab Cullen D">DM Raab-Cullen</name>
</author>
<author><name sortKey="Thiede, Am" uniqKey="Thiede A">AM Thiede</name>
</author>
<author><name sortKey="Petersen, Dn" uniqKey="Petersen D">DN Petersen</name>
</author>
<author><name sortKey="Kimmel, Db" uniqKey="Kimmel D">DB Kimmel</name>
</author>
<author><name sortKey="Recker, Rr" uniqKey="Recker R">RR Recker</name>
</author>
</analytic>
</biblStruct>
<biblStruct><analytic><author><name sortKey="Skerry, Tm" uniqKey="Skerry T">TM Skerry</name>
</author>
<author><name sortKey="Bitensky, L" uniqKey="Bitensky L">L Bitensky</name>
</author>
<author><name sortKey="Chayen, J" uniqKey="Chayen J">J Chayen</name>
</author>
<author><name sortKey="Lanyon, Le" uniqKey="Lanyon L">LE Lanyon</name>
</author>
</analytic>
</biblStruct>
</listBibl>
</div1>
</back>
</TEI>
<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Dental Press J Orthod</journal-id>
<journal-id journal-id-type="iso-abbrev">Dental Press J Orthod</journal-id>
<journal-id journal-id-type="publisher-id">dpjo</journal-id>
<journal-title-group><journal-title>Dental Press Journal of Orthodontics</journal-title>
</journal-title-group>
<issn pub-type="ppub">2176-9451</issn>
<issn pub-type="epub">2177-6709</issn>
<publisher><publisher-name>Dental Press International</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26691966</article-id>
<article-id pub-id-type="pmc">4686741</article-id>
<article-id pub-id-type="doi">10.1590/2177-6709.20.6.016-031.oin</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Orthodontic Insight</subject>
</subj-group>
</article-categories>
<title-group><article-title>Miniplates and mini-implants: bone remodeling as their biological
foundation<xref ref-type="fn" rid="fn01">1</xref>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Consolaro</surname>
<given-names>Alberto</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<aff id="aff2"><label>2</label>
Full professor, University of São Paulo (USP), School of Dentistry, Bauru, São Paulo, Brazil and University of São Paulo (USP), School of Dentistry, Ribeirão Preto, São Paulo Brazil</aff>
</contrib-group>
<author-notes><corresp id="c01"><bold>Contact address:</bold>
Alberto Consolaro
E-mail:<email>consolaro@uol.com.br</email>
</corresp>
</author-notes>
<pub-date pub-type="epub-ppub"><season>Nov-Dec</season>
<year>2015</year>
</pub-date>
<pmc-comment>Fake ppub date generated by PMC from publisher
pub-date/@pub-type='epub-ppub' </pmc-comment>
<pub-date pub-type="ppub"><season>Nov-Dec</season>
<year>2015</year>
</pub-date>
<volume>20</volume>
<issue>6</issue>
<fpage>16</fpage>
<lpage>31</lpage>
<history><date date-type="received"><day>05</day>
<month>10</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>14</day>
<month>10</month>
<year>2015</year>
</date>
</history>
<permissions><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0"><license-p>This is an open-access article distributed under the terms of the Creative
Commons Attribution License</license-p>
</license>
</permissions>
<abstract><title>Abstract</title>
<p>The tridimensional network formed by osteocytes controls bone design by coordinating
cell activity on trabecular and cortical bone surfaces, especially osteoblasts and
clasts. Miniplates and mini-implants provide anchorage, allowing all other
orthodontic and orthopedic components, albeit afar, to deform and stimulate the
network of osteocytes to command bone design remodeling upon "functional demand"
established by force and its vectors. By means of transmission of forces, whether
near or distant, based on anchorage provided by miniplates, it is possible to change
the position, shape and size as well as the relationship established between the
bones of the jaws. Understanding bone biology and the continuous remodeling of the
skeleton allows the clinician to perform safe and accurate rehabilitation treatment
of patients, thus increasing the possibilities and types of intervention procedures
to be applied in order to restore patient's esthetics and function.</p>
</abstract>
<trans-abstract xml:lang="pt"><title>Resumo</title>
<p>A rede tridimensional formada pelos osteócitos controla o
<italic>design</italic>
ósseo ao coordenar a atividade das células nas superfícies
trabeculares e corticais, especialmente os osteoblastos e os clastos. Miniplacas e
mini-implantes servem de ancoragem para que os demais componentes ortodônticos e
ortopédicos possam - mesmo que à distância - deformar e estimular a rede de
osteócitos a comandar uma remodelação no <italic>design</italic>
de acordo com a
"demanda funcional" criada pela forças aplicadas e seus vetores. Na transmissão
próxima ou longínqua de forças, com base na ancoragem oferecida pela miniplacas,
pode-se mudar a posição, o formato, tamanho e relação entre os ossos maxilares.
Compreender a biologia óssea e a remodelação constante do esqueleto permite atuar com
segurança e precisão nesse tipo de planejamento reabilitador dos pacientes,
aumentando as possibilidades e tipos de intervenção para devolver a estética e função
a eles. </p>
</trans-abstract>
<kwd-group><kwd>Bone remodeling</kwd>
<kwd>Miniplates</kwd>
<kwd>Mini-implants</kwd>
<kwd>Dental implants</kwd>
<kwd>Orthodontic movement</kwd>
</kwd-group>
<counts><fig-count count="22"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="18"></ref-count>
<page-count count="16"></page-count>
</counts>
</article-meta>
</front>
<body><p>Bone growth physically shapes us until adulthood, approximately until 22 to 24 years old.
Continuous cell proliferation and deposition of bone matrix take turns with resorption
sites and moments, which allows us to claim that, during growth, bone modeling also
comprises remodeling phenomena. Changes in shape resulting from growth are associated with
bone remodeling for necessary functional adaptation. After this phase, the bones keep on
changing every day, so as to adapt to functional demands imposed by human activity. This
dynamics and the process of ongoing adaptation are what characterize bone remodeling or
bone turnover.</p>
<p>The human skeleton gives support to soft tissues, enclosing and protecting our organs. The
human skeleton is composed of 206 bones of flawless individual design that allows it to
meet functional demands, in addition to absorbing, producing or transferring force during
movements performed by the body. A newborn might have up to 300 bones, since a number of
bones fuse during childhood and puberty.</p>
<p>In an embryo, each part of the mesenchyme, from which a group of cells will give rise to
osteoblasts and chondroblasts, has a site of bone growth. Cell movement and continuous
deposition of tissue matrix at this site imply the production of forces that add up or act
in opposite directions, thereby resulting in predominant forces also known as vectors or,
to be more specific, bone growth vectors. The mesenchyme is the primary tissue that will
give rise to bone and cartilage, in nuclei or cores, which later on might fuse or remain
independent from each other, with the formation of sutures filled by fibrous connective
tissue.</p>
<sec><title>Tensegrity and mechanotransduction: the language of stimuli that sculpture the
bone!</title>
<p>In the body of animals and vegetables, as well as in objects, natural supporting systems
tend to receive and produce forces throughout their structures. However, in the end,
those forces neutralize each other with a resultant force that equals to zero. Once the
action of those forces, whether originated internal or externally, cease with a
resultant force that equals to zero, the object or anatomical body part will remain as
it were in the first place. This signals to a complete and perfect system of force
distribution, a balance, of which property is named tensegrity. It applies to an
overpass, a palace, the head and other members of the body, for example; but it also
applies to the simplest of things, such as an earthen jar and teeth stably positioned at
the dental arch. Every structure returning to its original shape upon the application of
force is under structural and functional balance; however, should it have its shape
modified by force and be unable to adapt to the new situation (with new tensegrity), it
is natural that it tends to go back to its original shape, so as to establish
balance.</p>
<p>In a set of muscles and tendons, and/or interconnected bones, every time tensegrity
between a cell and its cytoskeleton is broken, cell components will release a number of
mediators with a view to restoring its original shape. For instance, bones will reabsorb
or neoform, vessels will expand, muscles will become sore and tense; all with a view to
restoring tensegrity, since the altered position or shape reestablishes it and
rebalances the system.</p>
<p>A break in the tensegrity of a cell and the release of mediators inducing phenomena
around it, with a view to reestablishing it, is known as mechanotransduction. In other
words, mechanotransduction is a mechanism by which physical mechanical events are
converted into biological cell and tissue events. It is by this means that the organism
receives and absorbs mechanical stimuli and converts them into biological signs and
events.</p>
<p>Surrounding bones, muscles, tendons and tissues form a complex system over which various
types of force act. The chemical mediators released by the cells, as a result of force
application, might cause mineralized tissue to reabsorb in some areas of the skeleton,
while, at other sites, bone neoformation phenomena are induced. Therefore, tensegrity
and mechanotransduction might Figuretively represent tools that daily sculpture the
bones, a phenomenon also known as bone remodeling.</p>
</sec>
<sec><title>Bones, periostea, muscles and primary bones, at the tooth socket and tendon
attachments, form a system of forces</title>
<p>Muscles and tendons are inserted into the bones in order to take us to the wonders of
the world (<xref ref-type="fig" rid="f01">Fig 1</xref>
). The muscles are inserted into
the bones by the periosteum, a thin layer of fibrous connective tissue connected to the
cortical bone, thus forming its surface layers. The tendons have structural proteins
directly fused to the bone, without interposition of the periosteum.</p>
<p><fig id="f01" orientation="portrait" position="float"><label>Figure 1</label>
<caption><title>- Muscles and tendons apply loads over mineralized bone structures which,
with a view to meeting functional demands, have thickness of trabecular and
cortical bones increased while subject to stimuli that characterize the
dynamics of bone remodeling.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf01"></graphic>
</fig>
</p>
<p>It is a very special bone also known as primary bone, which resembles that of an embryo.
It is known as embryonic bone. Its composition and organization - more cellularized and
less mineralized - render the primary bone more dynamic for renewal and functional
adaptation. </p>
<p>The bone seems to be wrapped up as a gift, since, at the surface, it is covered by a
resistant protective membrane comprising the periosteum - a fibrous connective tissue
made up of cellularized and vascularized layers. There are only two sites where the
outer surface of bones is not covered by the periosteum. The first are the sites where
tendons directly attach via primary bone; whereas the second one is the periodontal
alveolar surface. </p>
<p>At the tooth socket, the periodontal ligament acts as the periosteum and, similarly to
tendons, it attaches directly to the bone by having structural proteins fused to the
primary bone that surrounds it. Primary bone surrounding the tooth socket is also known
as alveolar bone or bundle bone. Primary bone is always fused with structures that do
not cease to transmit forces and require continuous and fast functional adaptation.</p>
<p>The bones also protect vital body parts, such as the brain, heart and lungs, in addition
to containing bone marrow which produces the liquid that gives us life and protection:
the blood. The bones, as the wonderful anatomical pieces that they are, perform a
variety of functions, especially because they act together with a set of cartilage,
tendons, ligaments and joints. </p>
</sec>
<sec><title>Bones have no angles or corners</title>
<p>In the human skeleton, as we observe the shape of bones, how they articulate or relate
to the other parts of the body, we can see that there are no straight angles, corners,
edges or pointy structures: everything is regular, smooth or round. Should bones not be
round, they would wound soft tissues with which they relate at the periphery. Bone
fractures or spurs are extremely painful due to having a pointy configuration. Bones
must be round and smooth. </p>
<p>Pointy edges or straight angles resulting from surgery at operated body cavities and
sites will become round within a few weeks after surgery, since this is the natural and
adaptive configuration of bones in relation to tendons, muscles and other soft
tissues.</p>
<p>The bone crest will always have a stable round cervical end, and whenever it acquires a
curve-like shape, the periosteum gradually disappears to allow the periodontal ligament
tissue to continue. At the inner alveolar bone and periodontal surfaces, the periosteum
is non-existent, with the periodontal ligament performing its functions at the site.</p>
</sec>
<sec><title>Bone dynamism and its ability to adapt</title>
<p>Galileo, in 1638, was the first to suggest that bone shape is directly related to the
forces applied to its structures. However, Julius Wolff, in 1892, was eloquent in
proposing that the bone adapts or responds to forces.<xref rid="B03" ref-type="bibr">3</xref>
</p>
<p>Athletes tend to have bigger, more voluminous and more mineralized bones because their
structure and design are dynamically adapted according to function. Individuals with a
sedentary lifestyle have thinner, less dense and less mineralized bones. At first, we
learn that bones are dry, hard and resistant structures, as depicted by skeletons
displayed at Departments of Anatomy and museums. However, they are in fact malleable,
moldable, adaptable structures that seek to satisfy all functional demands we come up
with. Bones are "moist" and have their surface composed of non-mineralized matrix thin
layers (<xref ref-type="fig" rid="f02">Figs 2</xref>
and <xref ref-type="fig" rid="f03">3</xref>
). They are rich in water, minerals and a number of proteins and growth
factors that most of times are hidden or associated with minerals.</p>
<p><fig id="f02" orientation="portrait" position="float"><label>Figure 2</label>
<caption><title>- Bone structures. The following are highlighted: trabeculae, a thin layer
of osteoid, osteoblasts and especially osteoblasts, which constitute, via
canaliculi and with a number of cytoplasmic extensions, a cell-to-cell network
with mediators and trabecular as well as cortical bones, thus actively
affecting bone remodeling (HE, 25X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf02"></graphic>
</fig>
</p>
<p><fig id="f03" orientation="portrait" position="float"><label>Figure 3</label>
<caption><title>- On the surface, osteoblasts form new bone layers as they are stimulated
by mediators released by local neighboring cells and which travel through the
blood, or by osteocytes travelling through connected canaliculi (HE,
25X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf03"></graphic>
</fig>
</p>
<p>The skeleton is thus an excellent partner, understanding and soft, which erases bruises
and wounds as it remodels itself. The brain and the heart are different, as they are
definite throughout life; they cannot regenerate and are left with permanent marks
whenever injured. </p>
</sec>
<sec><title>THE BONE IS ABLE TO CONTROL ITS SHAPE</title>
<p>A young adult's skeleton undergoes complete renewal every 4-5 years and it is
continuously transformed until the end of life: a 70-year-old man would have an average
of seven complete bone renewals throughout life. </p>
<p>The mineralized structure of bone, both cortical and trabecular, has millions of lacunae
as tiny as cells. Three-dimensionally, these lacunae have a spider-like shape with
dozens of ramifications. They are empty, termed osteoplasts and their function is to
enclose the osteocytes (<xref ref-type="fig" rid="f04">Fig 4</xref>
). </p>
<p><fig id="f04" orientation="portrait" position="float"><label>Figure 4</label>
<caption><title>- Osteocytes and their typical shape, with dozens of extensions forming an
effective network within the mineralized bone matrix. Lacunae where osteocytes
are located are termed osteoplasts.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf04"></graphic>
</fig>
</p>
<p>Osteocytes have between 20 to 50 cytoplasmic extensions randomly distributed by means of
tubules or bone canaliculi throughout the hard bone surface (<xref ref-type="fig" rid="f05">Fig 5</xref>
). Each one of these cells interconnects with other 40 to 50
cells. Imagine several spiders holding hands or making cell-to-cell contact with other
20 to 30 spiders (<xref ref-type="fig" rid="f06">Fig 6</xref>
). </p>
<p><fig id="f05" orientation="portrait" position="float"><label>Figure 5</label>
<caption><title>- Osteocytes within the mineralized matrix, revealing a number of
cytoplasmic extensions inside the intercommunicating canaliculi (HE; A = 25X, B
= 40X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf05"></graphic>
</fig>
</p>
<p><fig id="f06" orientation="portrait" position="float"><label>Figure 6</label>
<caption><title>- Osteocytes were replaced by resin which, after polymerization, formed the
shape of lacunae and canaliculi visible by scanning electron microscopy once
the mineralized portion was completely removed by acids. As evinced, this
network helps us comprehend how sensitive osteocytes in capturing bone
deformation, albeit discreet.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf06"></graphic>
</fig>
</p>
<p>Osteocytes form an interconnecting network within the mineralized bone structure.
Whenever forces are applied during movement, deformation is established as a result of
stretching or compression, thus allowing the network to apprehend the changes in shape
while immediately communicating or transferring the new situation to the network of
osteocytes.</p>
<p>In addition to cell-to-cell contact, one of the most effective ways of passing on a
message is to release substances, products or chemical mediators to the inner or outer
surfaces of cells with, for instance, the following biochemically codified information: </p>
<p>... change your current shape, we need or are required to adapt to the new situation,
improve your design. Reabsorb at compression sites, deposit at sites of stretching.</p>
<p>Every day, bone design adapts to function. A clear demonstration of flexibility,
adaptability and will to serve the whole. The ideal, absolute supremacy of the whole
over the parts. </p>
</sec>
<sec><title>THE COMPONENTS</title>
<p>Bone surface cells act as workmen: osteoclasts - or simply clasts - pull walls down or
undo overlays (<xref ref-type="fig" rid="f07">Figs 7</xref>
and <xref ref-type="fig" rid="f08">8</xref>
); osteoblasts build up and reinforce columns and other structures
(<xref ref-type="fig" rid="f03">Figs 3</xref>
and <xref ref-type="fig" rid="f09">9</xref>
). Bone surface cells are controlled by osteocytes; however, not too long
ago, researchers believed they were cells isolated at the farthest of mineralized
matrix: it was a complete mistake!</p>
<p><fig id="f07" orientation="portrait" position="float"><label>Figure 7</label>
<caption><title>- Flow of mononuclear cells towards the bone surface exposed by local
displacement of osteoblasts, resulting from the action of mediators and changes
in local conditions, such as pH reduction due to cellular stress. Note discreet
Howship lacunae, with special attention to osteocytes within the mineralized
bone matrix (HE, 25X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf07"></graphic>
</fig>
</p>
<p><fig id="f08" orientation="portrait" position="float"><label>Figure 8</label>
<caption><title>- Two bone modeling units (BMUs) in Howship lacunae, with special attention
to osteocytes, osteoblasts and macrophages as important components.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf08"></graphic>
</fig>
</p>
<p><fig id="f09" orientation="portrait" position="float"><label>Figure 9</label>
<caption><title>- On periodontal ligament bone surface, bone modeling units (BMUs), as it
occurs in the entire body, continuously renew the bone structures, thus causing
minimal natural tooth movement throughout one's life. Cementoblasts on root
surface, without membrane receptors for bone mediators, do not take part in
bone remodeling (B = Mallory, 25X, C = HE, 25X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf09"></graphic>
</fig>
</p>
<p>Should one's desire be to reinforce the skeleton, it is necessary to deform and stretch
muscles and tendons, so as to deform the bone which has a deflection capacity; thus
stimulating the network of osteocytes to adapt to the design desired by whom planned the
functional demand! </p>
<p>Should osteocytes remain at constant rest or in homeostasis, they have no stimuli to
renew the skeleton and adapt it to one's lifestyle. Bones become increasingly fragile,
less hard and little resistant! The skeleton is an ongoing metamorphosis - a process
also known as bone remodeling or bone turnover. While in children and adolescents the
bones are modeled and remodeled at the same time in order to satisfy development and
growth, adults undergo ongoing bone remodeling.</p>
<p>An adult skeleton has between 1 and 2 million microscopic bone resorption sites. At
every site, bone remodeling occurs in four phases, as follows.</p>
</sec>
<sec><title><bold>Activation:</bold>
precursor cells respond to physical and hormonal signs within
an area of bone surface where they organize as clasts.</title>
</sec>
<sec><title><bold>Resorption:</bold>
after 7 to 15 days, activated clasts open up small, shallow
cavities, or 60-µm Howship lacunae.</title>
<p><bold>Reversion:</bold>
once resorption is complete, clasts activity ceases by means of
removal of stimuli. Within 7 to 14 days, a new thin line of bone matrix is deposited,
with collagen fibers, contrasting with the well-organized, lamellar collagen surface.
This line sets the limit of resorption that ceases with neoformation of bone.</p>
<p><bold>Formation:</bold>
pre-osteoblasts that have been recently required begin to
deposit the new bone matrix. The time required between deposit of immature
non-mineralized bone and mature bone is 21 days. In general, the time required for
filling and return to normality is from 8 to 12 weeks.</p>
</sec>
<sec><title>WHY IS IT SO?</title>
<p>For the organism to have a balanced organization and functioning at varied orders of
magnitude, <italic>calcium ion is key to life:</italic>
it is part, directly or
indirectly, of nearly all biological processes inherent to human life. Generally
speaking, 99% of calcium is found in the bones, whereas only 1% is used for overall
metabolism. In one's organism, calcium is associated with proteins from which it easily
disconnects whenever induced or necessary.</p>
<p>The availability of calcium to cells and tissues must be ensured, since it is related to
maintenance of life. Between meals, the serum levels of calcium mainly come from the
skeleton acting as an active mineral reservoir. Matrix and minerals apposition - by
osteoblasts and osteocytes - as well as bone resorption for disassembly of focal
adhesion and ions release into the blood by clasts primarily aim at reaching maintenance
of serum levels of ions, particularly calcium.</p>
<p>The cells of the <bold>four parathyroid glands</bold>
(positioned on the side of the
thyroid, in the trachea) capture the reduction in serum levels of calcium and release
<bold>parathormone</bold>
directly into the blood, the main mediator inducing clastic
activity. Once parathormone has been distributed and begins to rapidly interact with the
other body cells via membrane receptors - especially osteoblasts that control the clasts
- it establishes resorptive activities for ions release from the bones and return to
normality of the serum levels (<xref ref-type="fig" rid="f10">Figs 10</xref>
and <xref ref-type="fig" rid="f11">11</xref>
).</p>
<p><bold>Vitamin D3</bold>
- which molecularly is not considered a vitamin, but a hormone -
plays a major role in this process, as it increases calcium absorption in the intestinal
mucosa while also being an important stimulator of osteoclastogenesis, or the maturation
of new clasts.</p>
<p>Within a few minutes or hours, this resorptive activity might increase significantly the
serum level of calcium, which is detected by C cells, also called parafollicular cells
in the thyroid, producers of <bold>calcitonin.</bold>
Calcitonin release into the blood
inhibits bone resorption in other skeletal cells, thus contributing to the prevalence of
bone apposition phenomena while distributing mineral ions throughout the bone matrix.
<bold>Estrogens</bold>
also contribute to this reversion from resorption to
predominant bone apposition (<xref ref-type="fig" rid="f10">Figs 10</xref>
and <xref ref-type="fig" rid="f11">11</xref>
).</p>
<p><fig id="f10" orientation="portrait" position="float"><label>Figure 10</label>
<caption><title>- At the bone environment, there are mediators intrinsic to bone modeling
units. They speed up or inhibit bone remodeling according to stimuli extrinsic
to these units, and are represented by bone remodeling local and systemic
mediators. A few mediators stimulate osteoblasts, osteocytes and other local
cells to release RANKL which, in turn, stimulates clastic activity. Other
mediators, however, stimulate the production of osteoprotegerin, or OPG, which
reduces the effect of RANKL by connecting to the molecules and preventing them
to interact with clastic membrane receptors or RANKL.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf10"></graphic>
</fig>
</p>
<p><fig id="f11" orientation="portrait" position="float"><label>Figure 11</label>
<caption><title>- Various bone modeling units and their clasts in their respective Howship
lacunae, and a network of osteocytes associated with the resorptive phenomenon,
potentially releasing mediators and directly affecting local bone remodeling
(HE, 25X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf11"></graphic>
</fig>
</p>
<p>This dynamics of continuous apposition and resorption, for maintenance of ion balance in
the body, allows the bone to adapt significantly to a number of daily functional
demands. These are the reasons why an analysis of bone structure and composition allows
one to determine the modern individual lifestyle and skeletal as well as muscular
functional patterns, as the bone adapts and renews itself at every stage of life! </p>
</sec>
<sec><title>LOCAL BONE REMODELING: HOW DOES IT OCCUR?</title>
<p>In specific areas, adaptation of bone shape and volume are rendered necessary and occur
regularly. Whenever forces are applied to a specific area, osteoblasts, osteocytes and
other cells, such as vascular endothelial cells, at blood vessel walls, and neural
threads as well as neighboring connective tissue fibroblasts cells, will locally deform. </p>
<p>Cell deformation affects the spatial configuration of the cytoskeletons responsible for
the original shape of each cell. In general, the shape of cells is stable, steady and
typical of each one of the 206 types of cells found in the human body. Cell deformation
represents a break in tensegrity: the cell is subject to stress, in other words,
cellular metabolism increases and so does the amount of mediators released to the outer
surface of cells where extracellular matrix is located. Cytokines and growth factors
induce local phenomena in order to have tensegrity restored or to create new tensegrity
or local balance. These phenomena include local bone resorption or neoformation,
provided that the environment where deformation occurs be central or peripheral bone
tissue.</p>
<p>In short, it is reasonable to claim that bone remodeling occurs as a whole; however, at
specific areas, if necessary, specific remodeling might occur, particularly if the
number of local mediators, such as cytokines and growth factors, increase significantly
within a specific region. Orthodontic and/or orthopedic movement is a good example of
therapeutically intended induced local bone remodeling.</p>
</sec>
<sec><title>ANCHORAGE: LIMITS AND POSSIBILITIES</title>
<p>In the maxilla and the mandible (<xref ref-type="fig" rid="f09">Fig 9</xref>
), as in any
other bone, processes and general design, including volume, shape and other minor
details, are determined by functional demand. The alveolar process gives support to
teeth without which there is no reason that justifies the existence of this bone
protuberance. In edentulous patients, there is a tendency towards atrophy, causing the
alveolar process to disappear completely. </p>
<p>The <bold>use of osseointegrated implants</bold>
soon after tooth loss contributes at
least to reduce alveolar bone loss. Masticatory load over osseointegrated implants is
transmitted to neighboring bone tissues; thus, the structure tends to remain unchanged,
since there is continuous functional demand.</p>
<p><bold>Teeth move naturally throughout life</bold>
and follow the vectors initially
provided by modeling and then remodeling at adulthood. The balance of muscle and soft
tissue forces acting over teeth added to masticatory load associated with alveolar bone
support determine more or less stability of teeth into the dental arch. Dental crowding
is considered an imbalance of this system and it is found, in most people, as some sort
of oral aging.</p>
<p>Initially, <bold>induced tooth movement</bold>
guides natural movement and, many times,
induces forces intentionally directed towards speeding up bone remodeling in one of the
root surfaces, so that a new position of teeth is achieved. </p>
<p>On the compression side, periodontal ligament cells release several mediators of
cellular stress, thus stimulating bone cells to rapidly reabsorb on the periodontal
surface of the alveolar bone (<xref ref-type="fig" rid="f13">Figs 13</xref>
and<xref ref-type="fig" rid="f14">14</xref>
). In areas where the periodontal ligament is
stretched out, bone apposition phenomena are predominant, since mediators of cellular
stress are found in smaller amounts, thus inducing apposition phenomena.</p>
<p><fig id="f12" orientation="portrait" position="float"><label>Figure 12</label>
<caption><title>- Diagram illustrating the function and organization of a bone modeling
unit. Each BMU is controlled by osteoblasts and secondarily by macrophages via
RANKL mediators. At the active or brush border, acids and enzymes are released
by an effective sealing zone formed by molecular fusion between membrane and
bone proteins. Note the relationship established with osteocytes.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf12"></graphic>
</fig>
</p>
<p><fig id="f13" orientation="portrait" position="float"><label>Figure 13</label>
<caption><title>- The bone crest periodontal surface of a tooth subject to induced tooth
movement reveals areas without osteoblasts, in addition to stress and
inflammation of ligament (asterisks) at the periphery. Subsequently, bone
modeling units, or BMUs, settle down and begin the process of bone resorption.
In B, note the BMU components in function, with clasts and mononuclear cells
located at the periphery while representing osteoblasts and macrophages (A and
B = HE, 10 and 40X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf13"></graphic>
</fig>
</p>
<p><fig id="f14" orientation="portrait" position="float"><label>Figure 14</label>
<caption><title>- Stimuli or aggressive agents frequently found in the bone and teeth
subject to force application. They are responsible for releasing mediators key
to the biological process of bone remodeling.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf14"></graphic>
</fig>
</p>
<p><bold>Induced tooth movement</bold>
is a therapeutically and esthetically intended
biological phenomenon; however, it <bold>has its limitations</bold>
. These limitations
are associated not only with the speed in which movement occurs in time, but also with
the harmonious extent of movement involving the whole set of teeth.<italic>For patients
with time and extent restraints for induced tooth movement, orthodontists usually opt
for orthognathic surgery.</italic>
</p>
<p>Due to absence of periodontal ligament and natural tooth movement, osseointegrated
implants present with more stability. Including osseointegrated implants as anchorage
points in rehabilitation treatment planning performed with mechanics associated with
miniplates is a perfectly feasible option, particularly from a biological and physical
perspective. Anchorage forces, albeit substantial, are much less significant than those
forces produced by daily mastication.</p>
</sec>
<sec><title>ANCHORAGE: boosting possibilities and the role of Orthodontics in oral
rehabilitation</title>
<p>One of the factors responsible for increasing orthodontic treatment time and reducing
the potential for certain types of tooth movement extension was lack of anchorage.
Initially, mini-implants were introduced with promises of absolute anchorage, but later
on they presented with limitations on supporting heavy loads, in other words, anchorage
proved to be not as absolute. They aid in the resolution of many cases, most of them
requiring additional anchorage beyond that offered by teeth; however, they also have
their limitations.</p>
<p>A few cases of extensive movement, thought to be impossible for many decades, required
significant reshaping of the maxilla and mandible. There remained cases which, despite
anchorage offered by mini-implants, could not be solved. In some cases, orthognathic
surgery itself was not the ideal solution, under any circumstances. </p>
<p>More complex cases, particularly in terms of esthetics and function, require a
combination of Orthodontics with other clinical specialties for patient's complete
rehabilitation. Nevertheless, these cases present with high risks of yielding
unsatisfactory outcomes. The limitations of results are usually attributed to technical,
physiological and anatomical reasons, such as impaired mechanical possibilities due to
lack of anchorage.</p>
<p>The use of miniplates is a great opportunity for anchorage and offers new solutions of
maxillary orthodontic as well as orthopedic mechanics, as it allows force to act with
greater intensity and to a greater extent, reaching almost the entire extension of the
maxilla and mandible. </p>
<p><italic>Under no circumstances, the orthodontic and orthopedic use of miniplates
replaces or imply changing orthognathic surgery treatment planning.</italic>
It
solely implies that the possibilities of success in more complex cases, in which all
therapeutic actors must be used in synergy, are improved. Miniplates are not indicated
and do not solve all cases, which also applies to orthognathic surgery. </p>
<p>The sculptor, such as the surgeon, uses the marble or wood before him to make sculptures
as planned, making his art real based on what had been envisioned! Moving teeth and
changing the shape of bones on the basis of anchorage and active forces, thanks to the
dynamics of bone remodeling, might be compared to the art of a ceramic sculptor, the
artist of clay (<xref ref-type="fig" rid="f18">Fig 18</xref>
). Taking advantage of a
malleable material, fingers, hands and tools - such as forces exerted by bones - the
artist creates new shapes and produces new details, so as to achieve the final design.
There are two ways by means of which final outcomes can be achieved: the beauty and
function of art as part of human imagination. <bold>To the surgeon, the art of carving;
to the orthodontist, the art of modeling: beauty shall benefit human beings!</bold>
</p>
<p><fig id="f15" orientation="portrait" position="float"><label>Figure 15</label>
<caption><title>- Cells with cytoskeleton proteins evinced by immunofluorescence, and
diagram in B. Proteins, in red and green, reveal the structure that maintains
cell shape and which provides the cell with mobility, whenever necessary.
Cytoskeleton proteins are connected with integrins within the cell membrane and
with the nuclear membrane at the center (in blue).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf15"></graphic>
</fig>
</p>
<p><fig id="f16" orientation="portrait" position="float"><label>Figure 16</label>
<caption><title>- Diagram illustrating how osteocytes actively participate in bone
remodeling as mechanotransductors. Deformation of the network of osteocytes
induces mechanical stress. RANKL local levels are raised, with a higher number
of active clasts and greater release of sclerostin by osteocytes. Once the
response to stimulus is adequate, there is a reduction in the number and
activity of clasts, and a reduction in sclerostin levels by osteocytes.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf16"></graphic>
</fig>
</p>
<p><fig id="f17" orientation="portrait" position="float"><label>Figure 17</label>
<caption><title>- The periosteum, within the area corresponding to induced tooth movement
(arrow in B), receives mechanical stimuli also provided by mediators released
by osteocytes subject to deformation and acting as mechanotransductors by
reacting with deposition of new bone layers on the cortical surface (arrows in
C), thus changing the shape, volume and size of the jaws, in addition to
affecting teeth positioning (HE; 25X).</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf17"></graphic>
</fig>
</p>
<p><fig id="f18" orientation="portrait" position="float"><label>Figure 18</label>
<caption><title>- Clay modeling is performed with force application intended to adapt the
material to the design planned by the artist. It is analogy to the application
of forces by means of mini-implants and miniplates on the tridimensional
network of osteocytes which will cause the bone structure to adapt, thus
determining a new shape and tensegrity for the modified structure.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf18"></graphic>
</fig>
</p>
<p>Understanding the function of miniplates in orthodontic and orthopedic treatment
planning requires mastering the concepts of bone biology within the context of bone
remodeling. Drawing analogies might render understanding faster and applicable.</p>
</sec>
<sec><title>MINIPLATES AND MINI-IMPLANTS "ACT" OVER OSTEOCYTES!</title>
<p>The bone is composed of more than 50% of organic matter, including water. This suggests
that the bone is highly malleable and deforms when subject to compression or stretching.
The intercellular network of osteocytes is immediately altered (<xref ref-type="fig" rid="f04">Figs 4</xref>
to <xref ref-type="fig" rid="f06">6</xref>
), thus affecting
the tridimensional pattern of each osteocyte cytoskeleton (<xref ref-type="fig" rid="f15">Fig 15</xref>
). </p>
<p>The inner shape of osteocytes is determined by another network that resembles the
tridimensional network of osteocytes itself, but formed by interconnected proteins. This
network is known as cytoskeleton (<xref ref-type="fig" rid="f15">Fig 15</xref>
) in which
loss of balance in shape stability implies cellular stress characterized by an increase
in metabolism and secretion of chemical mediators which will induce a number of
phenomena, regardless of which, with a view to restoring physical and metabolic
stability (<xref ref-type="fig" rid="f14">Fig 14</xref>
).</p>
<p>In other words, bone deformation increases metabolism and message exchange among
osteocytes by means of mediators release, as well as among osteocytes, osteoblasts and
clasts on trabecular and cortical bone surfaces (<xref ref-type="fig" rid="f11">Figs
11</xref>
, <xref ref-type="fig" rid="f12">12</xref>
and <xref ref-type="fig" rid="f13">13</xref>
).</p>
<p>Bone deformation caused by compression and stress raises the production of RANKL
mediators and osteocyte-derived sclerostin, while also enhancing the mechanisms of
resorption by clasts (<xref ref-type="fig" rid="f16">Fig 16</xref>
). On the other hand,
reduced functional demand, under mild stimuli, leads to a decrease in the release of
these mediators by osteocytes, thus causing bone neoformation phenomena by osteoblasts
to predominate (<xref ref-type="fig" rid="f16">Fig 16</xref>
). </p>
<p>Osteocytes biochemically control bone cell activity on structural surfaces, signaling
where resorption and apposition of bone layers should take place in order to adapt bone
shape, design or anatomical profile to the functional demand that represents the
deformity (<xref ref-type="fig" rid="f17">Fig 17</xref>
). </p>
<p>The role osteocytes play in bone biology was practically ignored for decades. Analysis
of leading-edge studies on bone homeostasis reveals that the role played by osteocytes
is key to understanding metabolical bone diseases and bone remodeling and repair
processes. <italic>Osteocytes account for 90 to 95% of bone cells.</italic>
</p>
<p>The forces applied at <bold>induced tooth movement</bold>
minimally deform the teeth;
instead, they deform - to a greater extent - the alveolar processes externally (<xref ref-type="fig" rid="f17">Fig 17</xref>
) as well as the basal bones of the jaws.
<italic>Orthodontic movement does not affect the inner part of the tooth socket only,
but it also affects the size, thickness as well as shape of trabeculae found in
neighboring bones and the outer surface of their cortical bones, thus establishing or
changing itself into layers of bone juxtaposed by the underlying periosteum.</italic>
On the basis of osteoplasts, osteocytes, acting as architects, control all the workers
juxtaposed on inner and outer bone surfaces (<xref ref-type="fig" rid="f17">Fig
17</xref>
).</p>
<p>The <bold>use of osseointegrated implants</bold>
does not only imply in a still and
inactive abutment screwed to the bone structure, only. Its function, performed via
loading, affects the surrounding areas and, albeit afar, the neighboring trabecular bone
and its underlying cortical bone. Continuous remodeling takes place directly - and on a
daily basis - in areas surrounding it, and the bone is readjusted every minute to all
necessary and functional demands.</p>
<p><bold>Orthopedic appliances,</bold>
with their plates, shields and other devices, back
up changes based on the following grounds of bone pathophysiology understanding: the
tridimensional network of osteocytes that controls bone shape. Changes in this network
of osteocytes implies in changes in bone shape and repositioning of structures involved,
namely: teeth, muscles and tendons. The dynamism offered by bone remodeling implies in
continuous adjustment of the body to functional demands.</p>
<p>The <bold>use of mini-implants</bold>
increased the potential for appliance treatment
planning towards a more effective biomechanics in tooth repositioning, with outstanding
outcomes usually restricted to a small area of the maxilla where they could be used as
anchorage sites.</p>
<p><bold>Tooth movement</bold>
performed by means of conventional <bold>orthodontic
appliance,</bold>
regardless of the type of bracket, might be compared to forces
transmitted by the reins placed on the head of a horse controlled by a horseman who
directly affects command of what is ahead of him. The head and the body immediately move
around him. The horseman on the horse might be compared to the bracket bonded to the
anchorage tooth (<xref ref-type="fig" rid="f19">Fig 19</xref>
).</p>
<p><fig id="f19" orientation="portrait" position="float"><label>Figure 19</label>
<caption><title>- Tooth movement performed by means of conventional orthodontic appliance,
regardless of the type of bracket, might be compared to forces transmitted by
the reins placed on the head of a horse controlled by a horseman who directly
affects command of what is ahead of him. The head and the body immediately move
around him. The horseman on the horse might be compared to the bracket bonded
to the anchorage tooth.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf19"></graphic>
</fig>
</p>
<p>The <bold>use of mini-implants</bold>
might be compared to a cart or a small carriage
where the coachman, with the reins placed on the animal or a couple of animals
side-by-side, controls the forces applied to the animals' mouths, restraining them and
inducing right, left or forward movements. The reins would be the wires; whereas the
devices in the animal's mouth would be the brackets. The coachman might be compared to
the mini-implant. Thus, the cart changes and operates according to the forces applied
and the needs of the coachman. </p>
<p><bold>Miniplates</bold>
correspond to larger carriages, with two to three pairs of
animals, used for grandiose events and journeys at old English imperial times (<xref ref-type="fig" rid="f20">Fig 20</xref>
). The reins - or wires - must be well
calibrated and secured to the animals' mouth. The coachman must be properly trained to
excellence, and the carriage must be stable enough to ensure passengers' safety
throughout the desired path. The coachman knows exactly what to expect from each couple
of animals. The first, on the front, leads the others in harmony by the forces exerted
by the reins placed on the beautiful carriage.</p>
<p><fig id="f20" orientation="portrait" position="float"><label>Figure 20</label>
<caption><title>- Analogy: Miniplates correspond to larger carriages, with various animals.
The reins or wires must be well calibrated and secured, the coachman must be
properly and the carriage must be stable. Miniplates can control, albeit afar,
the shape of the network of osteocytes in the bone that gives support to
anterior incisors and canines, in addition to influencing midline position and
relationship.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf20"></graphic>
</fig>
</p>
<p><fig id="f21" orientation="portrait" position="float"><label>Figure 21</label>
<caption><title>- Miniplates offer anchorage to a number of elastics and devices, which
allows the shape of the maxilla and mandible to be remodeled and have their
relationship with all other anatomical structures to be changed. This example
of miniplates clinical use allows the analogy with reins to be applied.
Clinical case granted by Dr. Ertty Silva.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf21"></graphic>
</fig>
</p>
<p><fig id="f22" orientation="portrait" position="float"><label>Figure 22</label>
<caption><title>- Miniplates provide greater anchorage, as they are secured to a wider base
with two to three screws fixed in thicker bone areas where ordinary bone
remodeling tends to occurs slowly when compared to other areas, as depicted by
the images. Clinical case granted by Dr. Ertty Silva.</title>
</caption>
<graphic xlink:href="2176-9451-dpjo-20-06-00016-gf22"></graphic>
</fig>
</p>
<p>Similarly to a majestic carriage, miniplates can control, albeit afar, the shape of the
network of osteocytes in the bone that gives support to anterior incisors and canines.
They can, therefore, affect the position and midline relationship between the maxilla
and the mandible. </p>
<p>In other words: anchorage offered by miniplates allows force to be exerted so intensely,
so as to be transmitted further. This property enhances orthodontic, orthopedic and
rehabilitation treatment outcomes with implications for esthetics and function that are
restored to the patient. Miniplates might allow a broader remodeling of the maxilla and
mandible than the limited remodeling resulting from the use of brackets and
mini-implants. </p>
</sec>
<sec><title>CARE AND LIMITS ON THE USE OF MINIPLATES AND MINI-IMPLANTS</title>
<p><bold>Area contamination.</bold>
A possible drawback of miniplates is the continuous
communication between the inner environment and the oral environment by means of the
miniplate external loop. Patient's guidance/awareness about oral hygiene, in addition to
technical care during miniplate placement, is key to avoid this type of problem.
Patients must be informed on a number of oral antisepsis protocols to be performed while
the miniplates are in function.</p>
<p>Microbial biofilm and bacteria build-up on miniplates might trigger inflammatory
processes with exudate formation and the potential need for miniplate removal.
Nevertheless, it is worth noting that patient's compliance and awareness is compulsory
when deciding whether to use miniplates or not. </p>
<p>Importantly, due to the opening offered by miniplates, patients must be healthy, since
uncontrolled systemic diseases, such as uncontrolled diabetes mellitus, long-term use of
corticosteroids, immunosuppression and anemia, might cause the area to be contaminated
more often.</p>
<p><bold>Unthread screws and/or miniplate.</bold>
Incidents that might occur with all
procedures. The chances are reduced by properly selecting the area of insertion,
technical elements and the technique to be used. </p>
<p><bold>Sinus problems.</bold>
Should the maxillary/sinus cortical bone be perforated by
fixation screws faced towards the maxillary sinus, chronic as well as local maxillary
sinusitis might occur, especially considering the length and diameter of screws. </p>
<p>In general, cases of sinus diseases are subclinical and asymptomatic, tending to
disappear within a few days. However, the following might originate at these sites: 1)
sinus polyps represented by isolated areas of swelling in the sinus mucosa; or 2) cyst
of maxillary sinus mucosa represented by isolated lumps filled with mucus at the
submucosa. Both cases, sinus polyps and cyst of maxillary sinus mucosa, are asymptomatic
and require no treatment, since they disappear completely within a few weeks or days
without further consequences.</p>
<p><bold>Tooth roots perforations or gliding.</bold>
Tooth roots are occasionally
accidently damaged. In cases of mini-implant gliding, removal implies root surface
repair within a few weeks, with cement neoformation and reinsertion of periodontal
collagen fibers. </p>
<p>Root perforation caused by previous drilling requires pulp vitality to be assessed
because, in the event of pulp space damage, aseptic pulp necrosis might be achieved,
with the need for endodontic treatment. Should perforation not have reached the pulp
space, mini-implant removal implies repair with cement and reinsertion of periodontal
collagen fibers within a few weeks or months. Normality will be restored without the
need for endodontic treatment.</p>
</sec>
<sec><title>FINAL CONSIDERATIONS</title>
<p>Osteocytes form a tridimensional network that controls bone design, coordinating cell
activity on trabecular and cortical bone surfaces, especially osteoblasts and clasts. </p>
<p>Miniplates and mini-implants are used for support or anchorage, so as to allow all other
orthodontic and orthopedic components, albeit afar, to deform and stimulate the network
of osteocytes to command bone design remodeling on "functional demand" created by force
and its vectors. In the transmission of forces, whether near or distant, based on
anchorage offered by miniplates, it is possible to change the position, shape, size and
relationship established between the bones of the jaws. </p>
<p>There is a potential for accidents and incidents in all technical procedures; however,
safety and prevention reduce their frequency, which does not refrain these procedures
from being employed. We must understand bone biology and continuous skeletal remodeling
in order to perform patient's safe and accurate rehabilitation treatment while raising
the possibilities of intervention with a view to restoring patient's esthetics and
function.</p>
</sec>
</body>
<back><fn-group><fn fn-type="other" id="fn02"><label>»</label>
<p> The author reports no commercial, proprietary or financial interest in the products
or companies described in this article.</p>
</fn>
<fn fn-type="other" id="fn01"><label>1</label>
<p> This is the third out of a series of versions about bone remodeling, adapted to
several specialties or different situations, such as Oral Rehabilitation,
Orthodontics, Clinics, Orthodontic Research, Cosmetic Dentistry, Endodontics and Oral
and Maxillofacial Surgery, in which the core text is repeated.</p>
</fn>
</fn-group>
<ref-list><title>REFERENCES</title>
<ref id="B01"><label>1</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bakker</surname>
<given-names>AD</given-names>
</name>
<name><surname>Soejima</surname>
<given-names>K</given-names>
</name>
<name><surname>Klein-Nulend</surname>
<given-names>J</given-names>
</name>
<name><surname>Burger</surname>
<given-names>EH</given-names>
</name>
</person-group>
<article-title>The production of nitric oxide and prostaglandin E(2) by primary bone
cells is shear stress dependent</article-title>
<source>J Biomech</source>
<year>2001</year>
<volume>34</volume>
<issue>5</issue>
<fpage>671</fpage>
<lpage>677</lpage>
<pub-id pub-id-type="pmid">11311708</pub-id>
</element-citation>
</ref>
<ref id="B02"><label>2</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Baron</surname>
<given-names>R</given-names>
</name>
<name><surname>Hesse</surname>
<given-names>E</given-names>
</name>
</person-group>
<article-title>Update on bone anabolics in osteoporosis treatment: rationale, current
status, and perspectives</article-title>
<source>J Clin Endocrinol Metab</source>
<year>2012</year>
<volume>97</volume>
<issue>2</issue>
<fpage>311</fpage>
<lpage>325</lpage>
<pub-id pub-id-type="pmid">22238383</pub-id>
</element-citation>
</ref>
<ref id="B03"><label>3</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bonewald, Lynda</surname>
<given-names>F</given-names>
</name>
</person-group>
<article-title>Mechanosensation and transduction in osteocytes</article-title>
<source>Bonekey Osteovision</source>
<year>2006</year>
<volume>3</volume>
<issue>10</issue>
<fpage>7</fpage>
<lpage>15</lpage>
<pub-id pub-id-type="pmid">17415409</pub-id>
</element-citation>
</ref>
<ref id="B04"><label>4</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bonewald</surname>
<given-names>LF</given-names>
</name>
</person-group>
<article-title>Osteocytes as multifunctional cells</article-title>
<source>J Musculoskelet Neuronal Interact</source>
<year>2006</year>
<volume>6</volume>
<issue>4</issue>
<fpage>331</fpage>
<lpage>333</lpage>
<pub-id pub-id-type="pmid">17185811</pub-id>
</element-citation>
</ref>
<ref id="B05"><label>5</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bonewald</surname>
<given-names>LF</given-names>
</name>
</person-group>
<article-title>The amazing osteocyte</article-title>
<source>J Bone Miner Res</source>
<year>2011</year>
<volume>26</volume>
<issue>2</issue>
<fpage>229</fpage>
<lpage>238</lpage>
<pub-id pub-id-type="pmid">21254230</pub-id>
</element-citation>
</ref>
<ref id="B06"><label>6</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Burr</surname>
<given-names>DB</given-names>
</name>
<name><surname>Robling</surname>
<given-names>AG</given-names>
</name>
<name><surname>Turner</surname>
<given-names>CH</given-names>
</name>
</person-group>
<article-title>Effects of biomechanical stress on bones in animals</article-title>
<source>Bone</source>
<year>2002</year>
<volume>30</volume>
<issue>5</issue>
<fpage>781</fpage>
<lpage>786</lpage>
<pub-id pub-id-type="pmid">11996920</pub-id>
</element-citation>
</ref>
<ref id="B07"><label>7</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Crockett</surname>
<given-names>JC</given-names>
</name>
<name><surname>Rogers</surname>
<given-names>MJ</given-names>
</name>
<name><surname>Coxon</surname>
<given-names>FP</given-names>
</name>
<name><surname>Hocking</surname>
<given-names>LJ</given-names>
</name>
<name><surname>Helfrich</surname>
<given-names>MH</given-names>
</name>
</person-group>
<article-title>Bone remodelling at a glance</article-title>
<source>J Cell Sci</source>
<year>2011</year>
<volume>124</volume>
<issue>7</issue>
<fpage>991</fpage>
<lpage>998</lpage>
<pub-id pub-id-type="pmid">21402872</pub-id>
</element-citation>
</ref>
<ref id="B08"><label>8</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ehrlich</surname>
<given-names>PJ</given-names>
</name>
<name><surname>Noble</surname>
<given-names>BS</given-names>
</name>
<name><surname>Jessop</surname>
<given-names>HL</given-names>
</name>
<name><surname>Stevens</surname>
<given-names>HY</given-names>
</name>
<name><surname>Mosley</surname>
<given-names>JR</given-names>
</name>
<name><surname>Lanyon</surname>
<given-names>LE</given-names>
</name>
</person-group>
<article-title>The effect of in vivo mechanical loading on estrogen receptor alpha
expression in rat ulnar osteocytes</article-title>
<source>J Bone Miner Res</source>
<year>2002</year>
<volume>17</volume>
<issue>9</issue>
<fpage>1646</fpage>
<lpage>1655</lpage>
<pub-id pub-id-type="pmid">12211435</pub-id>
</element-citation>
</ref>
<ref id="B09"><label>9</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Feng</surname>
<given-names>JQ</given-names>
</name>
<name><surname>Ward</surname>
<given-names>LM</given-names>
</name>
<name><surname>Liu</surname>
<given-names>S</given-names>
</name>
<name><surname>Lu</surname>
<given-names>Y</given-names>
</name>
<name><surname>Xie</surname>
<given-names>Y</given-names>
</name>
<name><surname>Yuan</surname>
<given-names>B</given-names>
</name>
</person-group>
<article-title>Loss of DMP1 causes rickets and osteomalacia and identifies a role for
osteocytes in mineral metabolism</article-title>
<source>Nat Genet</source>
<year>2006</year>
<volume>38</volume>
<issue>11</issue>
<fpage>1310</fpage>
<lpage>1315</lpage>
<pub-id pub-id-type="pmid">17033621</pub-id>
</element-citation>
</ref>
<ref id="B10"><label>10</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kamioka</surname>
<given-names>H</given-names>
</name>
<name><surname>Honjo</surname>
<given-names>T</given-names>
</name>
<name><surname>Takano-Yamamoto</surname>
<given-names>T</given-names>
</name>
</person-group>
<article-title>A three-dimensional distribution of osteocyte processes revealed by
the combination of confocal laser scanning microscopy and differential
interference contrast microscopy</article-title>
<source>Bone</source>
<year>2001</year>
<volume>28</volume>
<issue>2</issue>
<fpage>145</fpage>
<lpage>149</lpage>
<pub-id pub-id-type="pmid">11182371</pub-id>
</element-citation>
</ref>
<ref id="B11"><label>11</label>
<element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Krstic</surname>
<given-names>RV</given-names>
</name>
</person-group>
<source>Human microscopic anatomy</source>
<publisher-loc>Berlin</publisher-loc>
<publisher-name>Springer-Verlag</publisher-name>
<year>1994</year>
</element-citation>
</ref>
<ref id="B12"><label>12</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lane</surname>
<given-names>NE</given-names>
</name>
<name><surname>Yao</surname>
<given-names>W</given-names>
</name>
<name><surname>Balooch</surname>
<given-names>M</given-names>
</name>
<name><surname>Nalla</surname>
<given-names>RK</given-names>
</name>
<name><surname>Balooch</surname>
<given-names>G</given-names>
</name>
<name><surname>Habelitz</surname>
<given-names>S</given-names>
</name>
</person-group>
<article-title>Glucocorticoid-treated mice have localized changes in trabecular bone
material properties and osteocyte lacunar size that are not observed in
placebo-treated or estrogen-deficiente mice</article-title>
<source>J Bone Miner Res</source>
<year>2006</year>
<volume>21</volume>
<issue>3</issue>
<fpage>466</fpage>
<lpage>476</lpage>
<pub-id pub-id-type="pmid">16491295</pub-id>
</element-citation>
</ref>
<ref id="B13"><label>13</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lanyon</surname>
<given-names>LE</given-names>
</name>
</person-group>
<article-title>Osteocytes, strain detection, bone modeling and
remodeling</article-title>
<source>Calcif Tissue Int</source>
<year>1993</year>
<volume>53</volume>
<issue>1</issue>
<fpage>S102</fpage>
<lpage>S106</lpage>
<pub-id pub-id-type="pmid">8275362</pub-id>
</element-citation>
</ref>
<ref id="B14"><label>14</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Nakashima</surname>
<given-names>T</given-names>
</name>
<name><surname>Hayashi</surname>
<given-names>M</given-names>
</name>
<name><surname>Fukunaga</surname>
<given-names>T</given-names>
</name>
<name><surname>Kurata</surname>
<given-names>K</given-names>
</name>
<name><surname>Oh-Hora</surname>
<given-names>M</given-names>
</name>
<name><surname>Feng</surname>
<given-names>JQ</given-names>
</name>
</person-group>
<article-title>Evidence for osteocyte regulation of bone homeostasis through RANKL
expression</article-title>
<source>Nat Med</source>
<year>2011</year>
<volume>17</volume>
<issue>10</issue>
<fpage>1231</fpage>
<lpage>1234</lpage>
<pub-id pub-id-type="pmid">21909105</pub-id>
</element-citation>
</ref>
<ref id="B15"><label>15</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Parfitt</surname>
<given-names>AM</given-names>
</name>
</person-group>
<article-title>The cellular basis of bone turnover and bone loss: a rebuttal of the
osteocytic resorption--bone flow theory</article-title>
<source>Clin Orthop Relat Res</source>
<year>1977</year>
<issue>127</issue>
<fpage>236</fpage>
<lpage>247</lpage>
<pub-id pub-id-type="pmid">912987</pub-id>
</element-citation>
</ref>
<ref id="B16"><label>16</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Poole</surname>
<given-names>KE</given-names>
</name>
<name><surname>van Bezooijen</surname>
<given-names>RL</given-names>
</name>
<name><surname>Loveridge</surname>
<given-names>N</given-names>
</name>
<name><surname>Hamersma</surname>
<given-names>H</given-names>
</name>
<name><surname>Papapoulos</surname>
<given-names>SE</given-names>
</name>
<name><surname>Löwik</surname>
<given-names>CW</given-names>
</name>
</person-group>
<article-title>Sclerostin is a delayed secreted product of osteocytes that inhibits
bone formation</article-title>
<source>FASEB J</source>
<year>2005</year>
<volume>19</volume>
<issue>13</issue>
<fpage>1842</fpage>
<lpage>1844</lpage>
<pub-id pub-id-type="pmid">16123173</pub-id>
</element-citation>
</ref>
<ref id="B17"><label>17</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Raab-Cullen</surname>
<given-names>DM</given-names>
</name>
<name><surname>Thiede</surname>
<given-names>AM</given-names>
</name>
<name><surname>Petersen</surname>
<given-names>DN</given-names>
</name>
<name><surname>Kimmel</surname>
<given-names>DB</given-names>
</name>
<name><surname>Recker</surname>
<given-names>RR</given-names>
</name>
</person-group>
<article-title>Mechanical loading stimulates rapid changes in periosteal gene
expression</article-title>
<source>Calcif Tissue Int</source>
<year>1994</year>
<volume>55</volume>
<issue>6</issue>
<fpage>473</fpage>
<lpage>478</lpage>
<pub-id pub-id-type="pmid">7895187</pub-id>
</element-citation>
</ref>
<ref id="B18"><label>18</label>
<element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Skerry</surname>
<given-names>TM</given-names>
</name>
<name><surname>Bitensky</surname>
<given-names>L</given-names>
</name>
<name><surname>Chayen</surname>
<given-names>J</given-names>
</name>
<name><surname>Lanyon</surname>
<given-names>LE</given-names>
</name>
</person-group>
<article-title>Early strain-related changes in enzyme activity in osteocytes
following bone loading in vivo</article-title>
<source>J Bone Miner Res</source>
<year>1989</year>
<volume>4</volume>
<issue>5</issue>
<fpage>783</fpage>
<lpage>788</lpage>
<pub-id pub-id-type="pmid">2816520</pub-id>
</element-citation>
</ref>
</ref-list>
</back>
</pmc>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/EdenteV2/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000279 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 000279 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Santé |area= EdenteV2 |flux= Pmc |étape= Corpus |type= RBID |clé= |texte= }}
![]() | This area was generated with Dilib version V0.6.32. | ![]() |