Review articles Annals and Essences of Dentistry

10.5368/aedj.2015.7.1.4.2
A REVIEW OF ROOT RESORPTION IN ORTHODONTICS

1 1
Venkatesh Nettam Postgraduate student
2 2
Prasad Mandava Professor and Head
3 3
Gowri Sankar Singaraju Professor
4 4
Vivek Reddy Ganugapanta Senior lecturer

1-4
Department of Orthodontics, Narayana Dental College, Nellore, Andhra Pradesh, India.

ABSTRACT: Root resorption is unavoidable, unwanted and undesirable consequence of the orthodontic tooth movement.
This paper describes the various causes, types and classification of root resorption during orthodontic treatment

KEYWORDS: Orthodontics, Tooth Movement, Root resorption.

INTRODUCTION

Bone is not necessarily the only hard tissue
resorbed during orthodontic tooth movement. Root
resorption involving cementum and dentin can be an
1
unfavourable sequel to orthodontic procedures . Apical
root resorption is one of the most common iatrogenic
problems associated with orthodontic treatment. It is
becoming an increasingly more serious problem from a
2 6
medico legal stand point .
Root shortening as a result of external resorption is a well-
documented possible side effect of orthodontic treatment.
It is irreversible, difficult to predict and can be sufficiently
extensive to cast doubt on the overall benefit to the patient
3
of an otherwise successful orthodontic treatment .Root
resorption is undesirable because it can affect the long-
term viability of the dentition, and reports in the literature
indicate that patients undergoing orthodontic treatment are
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more likely to have severe apical root shortening . Bates
(1856) was the first person to discuss root resorption of
permanent teeth. Ottolengui (1914) related root resorption
directly to orthodontic treatment and mentioned that
Schwarzkopf (1887) demonstrated resorbed roots in
extracted permanent teeth. In 1927 root resorption of
permanent teeth was a subject of major concern to the
orthodontic field. Ketcham, demonstrated with
radiographic evidence, the differences between root shape
before and after orthodontic treatment. This observation
initiated a research on histological, clinical and physiologic
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root resorption occurring during orthodontic treatment .
Periodontal and bone response to normal
function and orthodontic force
Each tooth is attached to and separated from the adjacent
alveolar bone by a heavy collageneous supporting
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structure and the periodontal ligament (PDL) .
The principle cellular elements in the PDL are
undifferentiated mesenchymal cells and their progeny in
the form of fibroblasts and osteoblasts. Remodelling and
recontouring of the bony socket and the cementum of the
root is also constantly being carried out, though on a
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smaller scale, as a response to normal function .
Response to Normal Function : During masticatory
function, the teeth and periodontal structures are
subjected to intermittent heavy forces. When a tooth is
subjected to heavy loads of this type, quick displacement
of the tooth within the PDL space is prevented by the
incompressible tissue fluid. Instead the force is transmitted
to the alveolar bone, which bends in response. Bone
bending in response to normal function generates
piezoelectric currents, which appear to be an important
stimulus to skeletal regeneration and repair. This is the
mechanism by which bony architecture is adapted to
functional demands. When pressure on tooth is applied
for a second, very little of the fluid within the PDL space
gets squeezed out. However, if pressure against a tooth is
maintained, the fluid is rapidly expressed and the tooth
displaces within the PDL space, compressing the ligament
itself against adjacent bone. Although the PDL is
beautifully adapted to resist forces of short duration, it
rapidly loses its adaptive capability as the tissue fluids are
squeezed out of its confined area. Prolonged force, even
of low magnitude, produces a different physiologic
response- remodelling of the adjacent bone. Orthodontic
tooth movement is made possible by the application of
prolonged forces.
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Effects Of Force Magnitude : When light but prolonged
force is applied to a tooth, blood flow through the partially
compressed PDL decreases as soon as fluids are
expressed from the PDL space and the tooth moves in its
socket (i.e. in a few seconds). Within a few hours,

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resulting change in the chemical environment produces a
different pattern of cellular activity. Animal experiments
indicate that increased levels of cyclic adenosine
monophosphate (AMP), the “second messenger” appear
after about 4 hours of sustained pressure. If removable
appliances are worn less than 4 to 6 hours per day, it will
produce no orthodontic effects.
Experiments have shown that prostaglandin and
interleukin –1 beta levels increase within the PDL within a
short time after the application of pressure, and it now
seems clear that prostaglandin E is an important mediator
of the cellular response. Changes in cell shape probably
play a role. There is some evidence that prostaglandins
are released when cells are mechanically deformed. Since
drugs of various types can affect both prostaglandin levels
and other potential chemical messengers, it is clear that
pharmacologic modification of the response to orthodontic
force is more than just a theoretic possibility.
Prostaglandin E has the interesting property of stimulating
both osteoclastic and osteoblastic activity, making it
particularly suitable as a mediator of tooth movement. If
parathyroid hormone is injected, osteoclasts can be
induced in only a few hours, but the response is much
slower when mechanical deformation of the PDL is the
stimulus. The course of the events is different if the
sustained force against the tooth is great enough to totally
occlude blood vessels and cut off the blood supply to an
area within the PDL, When this happens, rather than cells
within the compressed area of the PDL being stimulated to
develop into osteoclasts, a sterile necrosis starts within the
compressed area. Because of its histological appearance
as the cells disappear; an avascular area in the PDL
traditionally has been referred to as hyalinized. When this
happens, remodeling of bone bordering the necrotic area
of the PDL must be accomplished by cells derived from
adjacent undamaged areas. After a delay of several days,
cellular elements begin to invade the necrotic (hyalinized)
area. More importantly, osteoclasts appear within the
adjacent bone marrow spaces and begin an attack on the
underside of the bone immediately adjacent to the necrotic
PDL area. This process is appropriately described as
undermining resorption, since the attack is from the
underside of the lamina dura. When hyalinization and
undermining resorption occur, an unwanted delay in tooth
movement results. This is caused first by a delay in
stimulating differentiation of cells within the marrow
spaces, and second because considerable thickness of
bone must be removed from the underside before any
tooth movement can take place. The PDL response is
determined not by force alone, but by force per unit area,
or pressure. The different time course of tooth movement
when frontal resorption is compared with undermining
resorption is shown in diagram(Fig 1).
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Effects On Root Structures:Thomas M. Graber has
mentioned that according to Rygh and his co-workers,
cementum adjacent to hyalinised (necrotic) areas of the
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Annals and Essences of Dentistry
PDL is marked by the contact and the clast cells attack
this marked cementum when the PDL area is repaired.
This observation helps explain why heavy continuous
orthodontic force can lead to severe root resorption.
PROCESS OF ROOT RESORPTION
Resorption of deciduous roots during permanent
tooth eruption is a necessary process that eventually
results in the exfoliation of the deciduous tooth in
anticipation of the arrival of its permanent successor.
However, root resorption that occurs in permanent teeth is
an unwanted process and is considered pathologic (Bates
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1856) . The publications of Wehrbein et al made
substantial contributions to the research concerning OIIRR
in humans. These authors discussed different grades of
root resorption in detail, mainly in terms of the close
proximity of the root to the cortical nonmetaplastic bones,
as well as other pathologic phenomena such as
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dehiscence and fenestrations .
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The Cellular Process
The studies in mice and rats conducted by Brudvik
and Rygh confirmed that Orthodontically Induced
Inflammatory Root resorption (OIIR) is a part of the
hyaline zone elimination process. The first cells to be
involved in this necrotic tissue removal are cells that are
negative for tartrate resistance acid phosphatase (TRAP)
and that have no ruffled borders. These are Macrophage-
like cells, which are most probably activated by signals
coming from the sterile necrotic tissue, the result of the
orthodontic force application. As described by Brudvik and
Rygh, the initial elimination process takes place at the
periphery of the hyaline zone, where blood supply to the
periodontal ligament exists is even increased. During
removal of the hyaline zone, the nearby outer surface of
the root, which consists of the cementoblast layer covering
the cementoid, can be damaged, thus exposing the
underlying highly dense mineralized cementum. It is
possible that the orthodontic pressure itself directly
damages the outer root surface layers in such a way that
there is a need for their removal as well. The resorption
process continues until no hyaline tissue is present and/or
the force level decreases. The extent of root resorption
was increased only when force reactivation was performed
at the peak presence of osteoclast count in the involved
region (day 4). Idiopathic root resorption is most frequently
found at the apex followed by mesial, buccal, distal and
lingual surfaces. Small differences were noted between
right and left sides, or between mandibular and maxillary
teeth. More resorption areas were seen on molars since
their total surface area is greater than that of other teeth.
Factors affecting root resorption
Naphtali Brezniak, Atalia Wasserstein (1993) have
described the following factors responsible for root
resorption.
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Review articles Annals and Essences of Dentistry
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I) BIOLOGIC FACTORS: NAPHTALI BREZNIAK ET AL have published three types
1) Individual susceptibility of external root resorption originally given by Andreasen:-
2) Genetics
3) Systemic factors i)Surface resorption: - Surface resorption is a self-limiting
4) Nutrition process, usually involving small outlining areas followed
5) Chronologic Age by spontaneous repair from adjacent intact parts of the
6) Dental age periodontal ligament.Root resorption after orthodontic
7) Gender treatment is surface resorption.
8) The presence of root resorption before
orthodontic treatment ii) Inflammatory resorption: In inflammatory resorption,
9) Habits initially root resorption occurs up to dentinal tubules of an
10) Tooth structure infected necrotic pulpal tissue or an infected leukocyte
11) Previously traumatized teeth zone.There are two types of inflammatory resorption.
12) Endodontically Treated Teeth
13) Alveolar bone density a) Transient inflammatory resorption
14) Types of malocclusion It occurs when the stimulation to the damage is
15) Specific tooth vulnerability to root resorption minimal and for a short period. This defect is
usually undetected radiographically and is repaired
II) MECHANICAL FACTORS by a cementum-like tissue.
1) Orthodontic appliances: -
A. Fixed versus removable b) Progressive inflammatory resorption
B. Begg versus edgewise When stimulation for damage is for longer period,
C.Magnets ankylosis occurs. Ankylosis is the result of an
D.Inter maxillary elastics extensive necrosis of the periodontal ligament with
2) Extraction versus nonextraction formation of bone into a denuded area of the root
3) Serial extractions surface. Since the tooth becomes a part of the
4) Other appliances bone, normal remodeling process will gradually
5) Types of orthodontic tooth movement lead to a complete destruction of the tooth by the
6) Orthodontic force bone.
7) Continuous versus intermittent force
8) Jiggling and occlusal trauma iii) Replacement resorption: - In replacement resorption,
9) The extent of tooth movement bone replaces the resorbed tooth material that leads to
III) BIOLOGIC AND MECHANICAL FACTORS:- ankylosis.Replacement resorption is rarely seen during or
after orthodontic treatment.
1) Treatment duration
2) Relapse
3) Root resorption after appliance removal
IV) OTHER CONSIDERATIONS:-
1) Teeth vitality.
2)Loss of crestal bone and tooth stability

CLASSIFICATION OF ROOT RESORPTION

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ACCORDING TO SHAFER, HINE AND LEVY ,
resorption of root occurs in many circumstances other
than the normal process associated with shedding of
deciduous teeth. Resorption of root may occur either on
the external surface or internal surface of the root. Root
resorption is mainly of two types

1.External root resorption:- This resorption mainly

occurs as a result of a tissue reaction in the periodontal or
pericoronal tissues. Following are the few conditions: -
a. Periapical inflammation Fig. 1.Diagrammatic representation of the time
b. Reimplantation of teeth course of tooth movement with
c. Tumors or cysts frontal resorption vs. undermining resorption.
d. Excessive mechanical or occlusal forces
e. Impaction of teeth
f. Idiopathic

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1 2 3 4
Fig 2:- Grading scale for apical root resorption.
2. Internal resorption: -
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According to Shafer, Hine and Levy internal
resorption mainly arises from inflammatory
hyperplasia of pulp. This begins centrally within the
tooth. The cause of the pulpal inflammation and
subsequent resorption of the root. David N.
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Ramingtonet al in 1989 described the following
grading scale for apical root resorption as shown in
Fig 2.
Grade-0: Normal apical contour, same length as
- pretreatment.
Grade-1: Apical irregularity, same length as
- pretreatment.
Grade-2: Apical root resorption of less than 2mm.
- restored to its original width.
Grade-3: Apical root resorption more than 2mm,
- less than one third of original root
length.
Grade-4: Apical root resorption more than one
- third of original root length
REPAIR PROCESS OF ROOT RESORPTION
According to the appearance of these incremental lines,
histologicaly the repair process is divided into following
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phases
1) Early lag phase: -In this phase no cementum
apposition was seen which can be explained by the
dissipation of residual forces and the replacement of
clastic cell population by blastic cell population.
2) Incipient phase (First 14 days): - This phase implies a
transitional stage from no apposition (lag phase) to active
deposition stages of repair cementum. In this phase, first
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Annals and Essences of Dentistry
incremental line is seen which is characterized by a slim
deposit of cellular cementum with a deficient width in
comparison with the sound width of all consecutive
incremental lines.
3) Peak phase (14 to 28 days): - This phase is seen with
successive first and second incremental lines because of
spurt in matrix formation as defined by an increase in
width. This phase is also characterized by initial
incorporation of periodontal fiber bundle into intrinsic
cementum matrix.
4) Steady phase (42 to 56 days): - This phase included
rest of the incremental lines which were of equal width,
indicating a steady deposit phase of mix fibrillar
cementum.
5) Retreating phase (70 days): - This phase was seen
during relapse period (after removal of retention
appliance). In this phase only first and second incremental
lines were seen. This phase may be attributed to the
conversion of the former pressure site of active treatment
period into the tension side of the relapse period as a
consequence of appliance removal. This conversion led to
an increase in osteogenesis on the new tension site along
with a decrease in cementogenesis.
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Naphtali Brezniak and Atlia Wasserstein have mentioned
that according to Henry and Weinmann, repair can be
classified as,
1) Anatomic repair: - In this type of repair the root
surface gets restored to its original contour.
2) Functional repair: - In this type of repair, a thin
layer of repair cementum covers the exposed
dentine, resulting in a deficient root outline. In
both types, the periodontal ligament (PDL) was
DIAGNOSTIC AIDS
According to Naphtali Brezniak and Atalia
9 ,
Wasserstein (1993) radiographs are commonly used as a
diagnostic aid for investigating root resorption. Following
are the various radiographic techniques used as
diagnostic aids for assessing root resorption:
1) Periapical bisecting angle.
2) Periapical paralleling.
3) Orthopantomogram.
4) Cephalogram.
5) Lamiogram.
6) Computed tomography.
A biochemical assay could potentially offer advantages of
1) sensitivity, 2) non-invasiveness, 3) No radiation
exposure, 4) information on the stage of resorptive activity
and Severity, 5) possibly identifying at-risk individuals, 6)
reducing the time between clinical onset and Usual
clinical diagnosis and prognosis, 7) predicting subsequent
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Review articles
clinical course and diagnosis 8) implementing alterations
in therapy, 9) assessment of the actual response to
13
treatment alterations. Balducciet al. (2006) explored the
presence of dentine sialoprotein (DSP),dentine
phosphoprotein (DPP), and dentine matrix protein-1
(DMP-1) in the GCF, concluded that the use of DSP and
DPP as biomarkers were suitable alternatives for
monitoring root resorption during orthodontic tooth
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movement . RANKL and osteoprotegerin (OPG) in
periodontal tissues are important determinants for the
regulation of bone remodelling as well as root resorption
during orthodontic tooth movement.
Zhang et al demonstrated that compressive force
stimulates gene expression in the IL-17 and IL-17 (IL-17R)
in MC3T3-E1 cells, and also results in the induction of
15
osteoclastogenesis. Immunoreactivities for interleukin-6
and interleukin -17 were detected in gingival crevicular
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fluid of subjects with severe root resorption. Hayashi et al
demonstrated that heavy orthodontic force induced
expression of Th17, IL-17 and IL-17R in rat root resorbed
tissue on day7. Therefore, IL-17 and Th17 cells may
15
aggravate the process of OIIRR.
CONCLUSION
In post-orthodontic treatment, all permanent teeth
may show microscopic root resorption that is clinically
insignificant and radiographically undetected. Root
resorption of permanent teeth is a probable consequence
of orthodontic force and active tooth movement. The
incidence of reported root resorption during orthodontic
treatment varies widely among investigators. Most studies
agree that the root resorption process ceases once the
active treatment is terminated. The question if there is any
ideal (optimal) force to move teeth without root resorption
and whether root resorption is predictable remains
unanswered.
References
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Corresponding Author
Venkatesh Nettam
Post Graduate Student,
Department of Orthodontics, Narayana
Dental College, Nellore, Andhra
Pradesh, India.
Ph no. 9493223512
e-mail: venkateshnettam@gmail.com
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