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Omosh
Conservative Dentistry
Royal Medical Services
079 565 25 27
Abstract
A correct diagnosis and an understanding of the
aetiology and dynamics of the processes involved in
tooth resorption is critical to effective management.
Tooth resorptions can be classified as: (1) trauma
induced; (2) infection induced; or (3) hyperplastic
invasive. Some transient trauma induced resorptions
require no treatment but must be carefully
monitored to check that there are no complicating
issues such as infection. In cases of trauma induced
replacement resorption, a multidisciplinary approach
is usually necessary to ensure an optimal long-term
solution. Infection induced tooth resorptions require
the removal of the invading micro-organisms by
endodontic therapy including intra-canal medication
which can also facilitate repair of the resorbed tooth
structure. The hyperplastic invasive tooth resorptions
pose considerable challenges in management due to
the complexity and aggressive nature of the
resorptive process. With careful case selection and
complete inactivation of resorptive tissue successful
management can be achieved.
Key words: Tooth resorption, endodontics, dental
trauma, hyperplastic tooth resorptions.
INTRODUCTION
Dental clinicians can be faced with difficult diagnostic
and treatment decisions with respect to tooth resorption.
Tooth resorption in the primary and permanent dentition
has been extensively studied and the complex processes
involved in the removal of the organic and inorganic
components of tooth structure by clastic cells continue
to evolve through basic research (for reviews see
Pierce,1 Dreyer et al.,2 Davidovitch et al.3). Knowledge
gained from experimental studies and observations of
histopathological material has provided a sound basis
for the diagnosis and treatment of many tooth
resorptive processes.4,5
The aim of this paper is to simplify for general dental
practitioners the diagnosis and clinical management of
tooth resorption by focusing on those resorptions
which do not and those which do require treatment,
and to identify other resorptions where combined or
alternative treatment is indicated. Emphasis will be
placed on preventive measures to control resorption,
*Clinical Professor, Endodontic Teaching Group, School of Dentistry,
Faculty of Health Sciences, The University of Adelaide, South
Australia.
Australian Dental Journal Endodontic Supplement 2007;52:1.
b
c
b
d
c
Fig 4a. Radiograph showing evidence of intrusion of the maxillary
right central incisor of an eight year old female. The intruded tooth
was surgically repositioned within 30 minutes of the injury.
Fig 4b. Radiograph taken 18 days after surgical repositioning of the
intruded central incisor.
Fig 4c. Six months later a slight change in root contour is evident
on the mesial aspect of the repositioned tooth (arrow) indicative of
trauma induced surface resorption.
f
Fig 5a. Labial view of a maxillary right central incisor which had
been palatally luxated and repositioned 1 month earlier showing
slight coronal discolouration.
Fig 5b. The palatal view reveals more extensive discolouration in
the traumatized maxillary right central incisor.
Fig 5c. Radiograph taken 1 month after the luxation injury shows
evidence of transient apical internal resorption (arrow)
Fig 5d. One year later there has been total restitution of tooth
colour.
Fig 5e. Palatal view showing colour reversal.
Fig 5f. Radiograph taken 1 year after the original trauma shows
resolution of the apical internal resorption and no other signs of
periradicular pathosis.
a
Fig 8a. Labial appearance of an
11 year old female showing the
maxillary right central incisor in
infra-occlusion as a result of
trauma induced replacement
resorption.
Fig 8b. Radiograph of Fig 8a
showing the image of the
replacement of tooth structure
by bone which characterizes
trauma induced replacement
resorption.
e
d
g
Fig 10a. Labial appearance of an ankylosed maxillary left central
incisor in a 13 year old female. The tooth had been intruded at
age 8.
Fig 10b. Radiographically the maxillary left central incisor shows a
discernable periodontal ligament image over the majority of the
root surface but in one region it appears to be lacking (arrow).
Fig 10c. Labial appearance after intentional replantation into an
extruded position. After careful extraction of the tooth, Emdogain
was applied to the conditioned root surface prior to replantation.
Fig 10d. Radiograph of repositioned tooth 3 months after treatment
which included root canal preparation and the placement of a
Ledermix paste intra-canal dressing.
Fig 10e. Radiograph taken after root filling 6 months following
repositioning and Emdogain application. Slight extruded AH26 is
present periapically.
Fig 10f. Eleven-year follow-up shows the tooth had continued
normal eruption and the gingival contour is symmetrical.
Fig 10g. A radiograph taken at the 11-year follow-up shows no sign
of ongoing resorption. The slight amount of AH26 sealer
periapically appears to have been well tolerated.
a
b
Fig 14a. A further example of infection induced radicular
inflammatory root resorption which was treated endodontically
including the use of sonication.
Fig 14b. Radiograph taken after obturation of the root canal with
gutta percha and AH26 using a vertically condensed heated gutta
percha technique.
b
a
a
Fig 13a. Radiograph of a maxillary right central incisor showing
infection induced internal radicular inflammatory resorption.
Arrow indicates the likely presence of a large interconnecting
accessory canal.
Fig 13b. Radiograph of a maxillary right central incisor showing an
infection induced radicular internal inflammatory resorption. Arrow
indicates the likely presence of an accessory canal.
Australian Dental Journal Endodontic Supplement 2007;52:1.
c
d
Fig 18a. Mandibular left first premolar of a 30 year old male
showing an infection induced communicating internal-external
inflammatory root resorption and a related periradicular
inflammatory lesion.
Fig 18b. Radiograph showing evidence of good healing following
the preparation of the root canal system and long-term dressing
with a calcium hydroxide paste.
Fig 18c. Radiograph following filling of the root canal system with
gutta percha and AH26 and the placement of a crown.
Fig 18d. A 35-year follow-up radiograph shows continuing
periradicular health and no evidence of further resorption.
b
b
c
d
c
Fig 19a. Radiograph of a maxillary right central incisor of a 39 year
old female showing an extensive infection induced communicating
internal-external inflammatory root resorption.
Fig 19b. Radiograph taken at the time of filling the root canal with
gutta percha and AH26, 5 months after treatment of the resorptive
lesion by the topical application of trichloracetic acid followed by
dressing with calcium hydroxide. There is radiographic evidence of
hard tissue deposits within the resorptive defect.
Fig 19c. Radiograph taken 13 years after scaffolding therapy
showing extensive hard tissue deposition within the resorptive
lesion.
b
Fig 21a. Hyperplastic invasive coronal resorption in the maxillary
right central incisor of an 11 year old male, the resorption being
apparently associated with an area of hypomineralization of the
crown.
Fig 21b. Radiograph of the maxillary right central incisor showing
an extensive irregular radiolucency indicative of hyperplastic
invasive coronal resorption.
Fig 24a. The maxillary right central incisor of a 21 year old woman
shows a pink discolouration on the labial aspect of the crown. The
tooth had been traumatized 9 years earlier.
Fig 24b. A radiograph of the maxillary right central incisor reveals
an irregular radiolucency overlying the root canal with no obvious
extensions into the root canal. This invasive cervical resorptive
lesion is classified as Class 2.
Fig 24c. After a protective application of glycerol to adjacent soft
tissue, a rubber dam "cuff" has been placed for protection and
isolation. This has been supplemented with a glycerol impregnated
cotton roll placed in the labial sulcus.
Fig 24d. Trichloracetic acid on a small cotton pellet is applied to the
resorptive defect with slowly increasing pressure, so that the
resorptive tissue within the cavity undergoes coagulation necrosis.
Fig 24e. The appearance of the tissue within the resorptive defect
following the application of trichloracetic acid indicates tissue
necrosis. The adjacent whitened gingival tissues indicate a limited
zone of coagulation necrosis.
Fig 24f. Following curettage of the avascular tissue from the
resorption cavity, the glistening dentinal base of the cavity is
revealed. The incisal margin of the cavity has been smoothed with
high-speed bur under water spray.
Fig 24g. A glass-ionomer restoration has been placed in the cavity,
and its surface has been protected with a light-activated unfilled
bonded resin.
Fig 24h. Clinical appearance of the tooth 5 years postoperatively.
The original glass-ionomer cement has been faced with a resin
composite restoration.
Fig 24i. A 5 year follow-up radiograph of the maxillary right
central incisor shows no evidence of periapical pathosis or extension
of the treated resorptive lesion.
Reproduced from Heithersay GS, Quintessence Int 1999;30:96-110,
courtesy Quintessence International.
Table 1.
Management
Trauma induced
Surface
Transient apical internal
Pressure
Orthodontic
Replacement
Infection induced
Internal inflammatory
External inflammatory
Hyperplastic
Invasive cervical
CONCLUSION
An alternative classification of dental resorptions
based on aetiological groups has been used to define
dental resorption and then to apply management to
each group and sub-groups. The groups are: (1) trauma
induced dental resorption; (2) infection induced dental
resorption; and (3) hyperplastic invasive dental
resorptions. The diagnosis of dental resorptions and an
understanding of the underlying pathosis within each
group is critical to clinical management. A summary of
the groups and sub-groups of dental resorptions and
their management is shown in Table 1.
ACKNOWLEDGEMENTS
The author wishes to acknowledge Quintessence
International for their permission to reproduce figures
from his original publications. Professor Sven Lindskog
and Dr John McNamara also kindly allowed the
reproduction of some of their research and clinical
material. In addition, he wishes to acknowledge the
assistance of Dr William Kahler and Dr Khashnary
Nassery in the preparation of this paper.
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