ORTHODONTIC INSIGHT
Orthodontic movement does not induce
external cervical resorption (ECR)
or
Orthodontic movement does not change gingival color
and volume, and does not induce gingival inflammation
Alberto Consolaro*, Renata B. Consolaro**
Abstract
This study sought to explain, both anatomically and functionally, how the cervical region
of human teeth is structured and organized in order to address the following questions:
1) Why does External Cervical Resorption (ECR) occur in human dentition? 2) Why is
there no ECR in gingivitis and periodontitis? 3) Why ECR can occur after dental trauma
and internal bleaching? 4) Why does orthodontic movement not change the gingival color
and volume during treatment? 5) Why does orthodontic movement not induce ECR although it is common knowledge that the cervical region can undergo much stress? The
existence of sequestered antigens in the dentin, the presence of dentin gaps in the cervical
region of all teeth, the reaction of the junctional epithelium and the gingival distribution
of blood vessels may explain why ECR does not occur, nor do gingival color and volume
change when teeth are orthodontically moved.
Keywords: Tooth resorption. External cervical resorption. Orthodontic treatment. Gingiva.
HOW THE CERVICAL REGION OF THE
TOOTH IS STRUCTURED AND ORGANIZED
On the surface of cervical region of human teeth,
in the area where the enamel borders the cementum,
there is a line known as the cementoenamel junction
(CEJ) (Fig 1). On the circumference of the neck of
all human teeth the CEJ line alternates three types
of relationship between enamel and cementum.3,7 In
some areas of CEJ the cementum covers the enamel
(Fig 4), in others the enamel and cementum meet
edge to edge, but in other regions the enamel and
cementum remain distant from each other, thereby
exposing microscopic dentin gaps or “windows” facing the gingival connective tissue.
How to cite this article: Consolaro A, Consolaro RB. Orthodontic movement
does not induce external cervical resorption (ECR). Dental Press J Orthod. 2011
Nov-Dec;16(6):22-7.
» The authors report no commercial, proprietary, or financial interest in the
products or companies described in this article.
* Head Professor of Pathology, FOB-USP, and postgraduation courses, FORP-USP.
** Professor, FOA-Unesp and Faculdades Adamantinenses Integradas (FAI).
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Consolaro A, Consolaro RB
In the cervical root region, next to the enamel,
it is the connective tissue of the dental follicle,
which gives rise to the connective attachment in
the erupted tooth (Fig 4). Conceptually, the connective attachment in the erupted tooth comprises
the space between the final portion of the enamel
and the initial portion of the alveolar bone crest.
The cementum extends from the final edge
of the cervical enamel and its junctional epithelium. On the cementum surface are the
cementoblasts (Fig 4) nourished by the connective tissue of the dental follicle tissue and
connective attachment. Progressing toward the
apex, the connective tissue and cementoblasts
on the root become part of the periodontal ligament. The average thickness of the cementum
in the cervical third ranges from 16 to 60 µm,
which is equivalent to the thickness of a human
hair. In the apical third, bifurcations and trifurcations range from 150 to 200 µm. The average
thickness of the cementum in a youth aged 20
is 95 µm and at age 60, 215 µm.9
Whatever the relationship between enamel
and cementum in the cervical region, the CEJ
and its components are in direct contact with the
fibrous gingival connective tissue or, more specifically, with its collagen fibers and extracellular
matrix gel interspersed with fibroblasts (Fig 4).
In the CEJ segments, where the dentin gaps are
located, it is "concealed" or protected from exposure to macrophages by the extracellular matrix
gel, which plays this role with great competence.
Having completed its key function of producing enamel, this organ — formed by the outer epithelium, stellate reticulum, stratum intermedium
and ameloblasts — undergoes a sandwich-like restratification and gives rise to the reduced epithelium of the enamel organ. This epithelium is firmly attached to the enamel and receives nutrients
from the peripheral connective tissue. Together,
they form the dental follicle, which generates the
image of the pericoronal space in unerupted teeth.
As a tooth gradually begins to appear in the
mouth, the reduced epithelium of the enamel organ fuses with the oral mucosa and together form
the junctional epithelium. Initially this epithelium has three to four layers, reaching as many
10 to 20 cells of thickness with age. Close to 30
years of age, the junctional epithelium lines the
enamel in its cervical-most portion, but eventually progresses gradually towards the cementum.
The length of the junctional epithelium4 ranges
from 0.25 to 1.35 mm.
Gingiva
Enamel
Vascular dentogingival plexus
Cementoenamel junction
Cervical
root surface
Alveolar
bone
1st
PL
3rd
Alveolar
bone
1) WHy DOES ExTERNAL CERVICAL RESORpTION (ECR) OCCUR IN HUmAN DENTITION?
Some proteins in the dentin are recognized as
antigenic by the immune system because they are
deposited during odontogenesis without direct
contact with the protein memory cells which develop during intrauterine life.1 Thus, the dentin
should be protected from this contact throughout
its life, including in the dentin gaps of the CEJ
present in all teeth.
nd
2
Oral
mucosa
FIGURE 1 - The dentogingival plexus features anastomosis with vessels extending from the periodontal ligament (1st), oral mucosa (2nd)
and alveolar bone (3rd) in the region of the connective attachment next
to the cervical root surface (scheme modified from Glickman4).
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2011 Nov-Dec;16(6):22-7
Orthodontic movement does not induce external cervical resorption (ECR)
Enamel
Gingiva
Cementoenamel
junction
Cervical
root
surface
Alveolar
bone
PL
Oral
mucosa
PL
PL
FIGURE 2 - During orthodontic movement blood supply to the periodontal ligament may be reduced or eliminated without compromising gingival blood
supply, especially in the connective attachment region. Glickman’s modified schemes4 emphasize the osseous and gingival origin of blood vessels in the
cervical region.
a foreign body, they initiate a process through
which foreign proteins are eliminated and, when
these macrophages are present in hard tissues,
bone resorption is the mechanism of choice.1
Before the dentin gaps are exposed to macrophages at the CEJ, with consequent immunological recognition, a direct exposure is required to
occur as a result of the dissolution of the extracellular matrix of connective tissue where these
cells circulate.
The destruction and/or dissolution of the extracellular matrix occur mainly in inflammation:
A defense mechanism typical of connective tissues and dependent on vessels. The mediators and
enzymes that make up the inflammatory exudate
arising from vessels and leukocytes dissolve the
extracellular matrix gel and, at the gingival connective attachment can provide the dentin with
access to the macrophages.
Once the macrophages identify the dentin as
Dental Press J Orthod
2) WHy IS THERE NO ECR IN GINGIVITIS
AND pERIODONTITIS?
When gingival inflammation is induced by
dental bacterial plaque, it promotes epithelial hyperplasia while the junctional epithelium migrates
toward the apical region, placing the CEJ and its
gaps in the gingival sulcus and oral environment,
thereby "protecting" the ECR region. In the oral
environment, macrophages are not capable of recognizing foreign proteins in the dentin and therefore fail to trigger an immune response.
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2011 Nov-Dec;16(6):22-7
Consolaro A, Consolaro RB
Vascular dentogingival plexus
Enamel
Vascular dentogingival plexus
B
1st
2nd
3rd
Vascular dentogingival plexus
Ligamentum vessels
A
C
FIGURE 3 - A) The lace-shaped or net-shaped dentogingival plexus consists of vessels originating from the periodontium (1st), mucosa (2nd) and bone (3rd)
(scheme introduced by Lascala and Moussalli5). B and C highlight the numerous loop-shaped capillaries of dentogingival plexus in rodents, revealed by
scanning electron microscopy performed by Selliseth and Selvig (Source: Newman et al,8 2006).
3) WHy ECR CAN OCCUR AFTER DENTAL
TRAUmA AND INTERNAL bLEACHING?
In dental trauma, inflammation of gingival
connective tissue may occur, but without junctional epithelial hyperplasia. Such is the case in
internal dental bleaching, where hydrogen peroxide leaks into the dentinal tubules that open out
at the junction, causing a local gingival inflammation in the connective tissue, without epithelial hyperplasia. In these two situations, gingival
inflammation dissolves the extracellular matrix,
exposing the dentin in the CEJ gaps. However,
hyperplasia of the junctional epithelium does
not occur, allowing the occurrence of ECR.2
Dental Press J Orthod
4) WHy DOES ORTHODONTIC mOVEmENT
NOT CHANGE GINGIVAL COLOR AND
VOLUmE DURING TREATmENT?
One way to induce inflammation is by obstructing blood vessels, which results in local
cell death. Proteins released by necrotic cells
induce inflammation, as in the gingival connective tissue. Compression of the teeth against
the periodontal ligament and alveolar bone often causes cells death and hyalinization of a
ligament segment. Not only the arterioles and
capillaries, but the veinlets would also be obstructed, along with areas of necrosis, followed
by inflammation.
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2011 Nov-Dec;16(6):22-7
Orthodontic movement does not induce external cervical resorption (ECR)
E
JE
Conjunctive
insertion
BV
F
Vascular dentogingival plexus
BV
D
C
PL
BV
FB
F
A
B
FIGURE 4 - Net-shaped dentogingival plexus in the cervical dental region of monkeys, more specifically at the site of the cementoenamel junction (larger
arrow). On the root one can see the cementoblasts (small arrows) (E= enamel, JE= junctional epithelium, D= dentin, C= cementum, PL= periodontal ligament, FB= fasciculate bone, BV= blood vessel, F= fibroblast ).
and their venous and lymphatic drainage remain
at normal levels. Gingival color and volume are
not changed during orthodontic movement by
this mechanism or anatomical feature. Neither an
edema develops — due to venous obstruction —
nor does any inflammatory process emerge.
In orthodontic movement, compression of the
vessels occurs in the periodontal ligament and
could potentially influence gingival blood flow,
but this does not occur. It would be natural to expect ischemia would make the gingiva turn whitish, or passive hyperemia would make it violet-red
due to veinlet compression.
In the gingival tissue, more specifically at
the site of the gingival connective attachment,
blood vessels form a lace-like dentogingival
vascular network or plexus with connections
arising from periodontal vascular components.
These connections also originate in the marrow
spaces of the alveolar bone crest and its periosteum, as well as from the vessels of the alveolar mucous membrane via attached gingiva.5,6,8
There are 50 capillaries within every square
millimeter of gingiva5 (Figs 1-4).
The effects of vascular compression of the cervical periodontal tissues and gingival tissues are
offset by anastomosis or by connections from other sources (Fig 2). Blood supply to gingival tissues
Dental Press J Orthod
5) WHy DOES ORTHODONTIC
mOVEmENT NOT INDUCE ExTERNAL
CERVICAL RESORpTION?
In a similar compensatory manner, compression of the periodontal and gingival vessels does
not promote focus areas of necrosis and/or gingival inflammation in the region of the connective
attachment (Fig 2). In the absence of necrosis,
characterized by cell rupture and protein spill,
orthodontic movement does not induce inflammation and dissolution of extracellular matrix in
the gingival connective tissue. The dentin gaps
will not be exposed to macrophages, which in
turn will not perform antigen recognition, nor
present with foreign proteins that might trigger
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2011 Nov-Dec;16(6):22-7
Consolaro A, Consolaro RB
external cervical immune and resorptive responses. This mechanism and anatomical feature does
not induce ECR during orthodontic movement.
On the other hand, damage to the gingiva
caused by dental trauma and internal dental
bleaching cannot be offset by extensive anastomosis: Cellular injury occurs mechanically,
directly and independently of blood supply.
During trauma, cells and vessels are ruptured
by sudden shifts while in tooth bleaching the
toxic effect of hydrogen peroxide occurs independently of local blood supply.
REFERENCES
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FINAL CONSIDERATIONS
1) Dentin comprises proteins, which are considered sequestered antigens and when it is exposed to connective tissues it tends to be resorbed
as a form of elimination by the body.
2) At the cementoenamel junction (CEJ), the
dentin gaps found in all permanent teeth may
expose the dentin whenever inflammation is induced at the connective attachment.
3) Before dentin is exposed at the CEJ, gingivitis and periodontitis reveal a hyperplasia of the
junctional epithelium that covers the gaps, placing
the dentin in the oral environment.
4) In dental trauma and internal bleaching, inflammation of connective gingival tissue does not
promote junctional epithelial hyperplasia and direct exposure of the dentin allows antigen recognition by macrophages.
5) The gingiva receives vessels from the periodontium, bone, periosteum and mucous membrane so that its nutrition and drainage are not
affected, even when the vessels of the periodontal ligament are compressed during orthodontic
movement.
As a result, there is no inflammation at the
connective attachment, nor there is cell death in
the gingiva during orthodontic movement, with
gingival color and volume remaining unchanged,
even if the dentin is exposed at the CEJ gaps,
which is necessary to initiate ECR.
Dental Press J Orthod
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Submitted: October 7, 2011
Revised and accepted: October 11, 2011
Contact address
Alberto Consolaro
E-mail: consolaro@uol.com.br
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