endodontic point of view

1. ROOT RESORPTION
-V.NIVEDHA

2. CONTENTS:
 History
 Introduction
 Physiological resorption
 Etiology(pathological)
 Classification
 Internal resorption
 Pathogenesis
 Histopathology
 Mediators of internal resorption
 Clinical and raadiographic features
 Inflammatory internal resorption
 Treatment line

3. CONTENTS
 Replacement resorption
 External root resorption
 Transient apical breakdown
 Cervical resorption
 Resorptive pattern
 External replacement resorption and ankylosis
 Chronic action of mechanical trauma
 Resorption associated with systemic diseases
 Referrences

4. HISTORY:
 As early as 1829, Bell recognized the presence of both external and
internal “absorptive” defects.
 Sir John Tomes made a remarkable and meaningful observation when he
encountered a case of “absorption” in permanent teeth. He discussed his
case in his text, A System ofDental Surgery in 1859 .
 A further delineation of the process of absorption and repair can be seen in from
Tomes and Nowell in 1906 , depicting drawings of the hollowed out lacuna due to
dentinoclastic action followed by the deposition of new cementum.
 Dr. John P. Buckley used both absorption and resorption . Becks and Marshall met
the challenge of the terminology head on with their 1922 publication Resorption
or Absorption?.

5.  Sadly, resorption was viewed as both a disease and an etiology. Stalwart authors
during this time period, such as Prinz, Grossman, Coolidge, Healey, Sommer,
Ostrander and Crowley did not address the issue of resorption, or gave it mere lip
service in their widely accepted publications.
 Even Ingle in 1965 only alluded to idiopathic types of resorption, both internal and
external.
 However, in 1963 Penick provided guidelines for the clinical management of root
resorption and in 1973 the America Association of Endodontists chose to define
resorption, root resorption, internal and external resorption finally bringing to the
forefront this malady and its challenges.
 In 1974 Frank addressed more thoroughly apical and internal resorption, especially
in the clinical management of such.
 Possibly the first full-fledged treatise on resorption and its detailed management
was presented in a chapter on Root Resorption by Chivian in 1976 .

6. INTRODUCTION:
 Resorption is the combination of physiological or pathological factors leading to the
loss of enamel, dentin, cementum, and the alveolar bone by the action of polynuclear
giant cells.
 These cells, depending on tissue resorbed by them are called osteoclasts,
cementoclasts or dentinoclasts.
 Resorption is a physiological process only in milk teeth in the period preceding the
teeth replacement.
 Pathological process however occur in both the deciduous and permanent dentition .
 Root cementum from the side of periodontium is coated with osseomucoid
(precementum) and cementoblasts that protect it from resorption. A similar protective
role in the dentine plays odontoblasts layer and predentin.
 Damage to these layers and the appearance of local inflammation predisposes to the
occurrence of resorption

7. If resorption is left untreated it eventually leads to tooth loss.

8. PHYSIOLOGICAL RESORPTION:
 The osteoclast plays a key role in the shedding of primary teeth (physiologic
resorption).
 At a certain stage in the development of a permanent successor and the eruption
process, the coronal part of the follicle induces a rim of osteoclasts that over a
couple of years resorb the roots of the primary predecessor and the adjacent bone.
 In the case of the ectopic position of a permanent tooth germ, nonphysiologic
root resorption may affect adjacent permanent teeth.
If the ectopic eruption path changes to a normal path, or
if the canine is removed, the resorption process of the
lateral incisor will be arrested and the pulp should
survive. Consequently, root canal treatment of such
teeth is definitely not indicated.
An example of lateral root resorption on a maxillary lateral
incisor from the ectopic eruption of the adjacent canine.

9. ETIOLOGY: (PATHOLOGICAL)
 LOCAL FACTORS
 1. Sharp injuries
 2. Chronic injuries
 3. Microtrauma eg. related to the
profession (eg. trumpeter, seamstress),
crack a tooth crown
 4. Damage of periodontium after teeth
replantation
 5. Malocclusion
 6. Improper habits
 7. Too much force in orthodontic treatment
 8. Teeth whitening
 9. Biological treatment with calcium
hydroxide
 10.Delayed or irregular eruption of
permanent teeth
 11. The pressure of the tumor or cyst
 12. Iatrogenic action, e.g. thermal pulp
damage
 13.Dental abnormalities, e.g. invaginated
teeth
 14. Periodontitis, incorrect execution of
periodontal treatment (scaling, rootplaning)
 SYSTEMIC FACTORS
 1. Hormonal disorders, e.g. hyperthyroidism
 and hypoparathyroidism
 2. Hypertension
 3. Atherosclerosis
 4. Paget’s disease
 5. Papillon-Lefevre syndrome
 6. Stevens-Johnson syndrome
 7. Hepatic impairment
 8. Kidney disease
 9. Bone dysplasia
 10.Genetic disorders
 11.Vitamin A deficiency
 12.Pregnancy
 13.Shingles
 14.Gancher’s disease
 15.Turner’s syndrome
 16.Kabuki syndrome (the presence of a
number of external root resorptions of the
lower central incisors and molars)
 17.Radiotherapy

10. CLASSIFICATION:
Tooth root resorption: etiopathogenesis and classification Marta Sak1
, Małgorzata Radecka1
, Tomasz M.
Karpiński2
, Anna Wędrychowicz-Welman1
, Anna K. Szkaradkiewic micro medicine 2016,vol 4

11. INTERNAL RESORPTION:
 Internal resorption is also called the internal granuloma, internal progressive
resorption, ,internal middle resorption, pulpoma or „pink tooth”.
 Internal resorption is a chronic, inflammatory disease of the dental pulp resulting in
resorption of dental hard tissues and mostly presents as an ovoid, radiolucent defect
in the root canal
 It starts in the dentine where there is a breach in the pre dentin (from the side of the
tooth cavity) and spreads in the direction of cementum.
 Most frequently this process is found in the teeth with has not finished its
development, in which a layer of dentin is thin, and tubules within it are broad.
Such a structure makes them more susceptible to any pathological processes
 Once the condition is detected and diagnosed, root canal treatment has to be done, as
removal of vital tissue is necessary for arresting the clastic activity.

12.  Unlike external resorption, this process is arrested once the pulpectomy is
done or remaining pulp becomes completely non-vital.
 In a study conducted by Thoma et al.,13
the authors reported internal root
resorption in only one tooth out of the 1000 teeth studied
 It has been shown that like the cells of the periodontal ligament which are
responsible for external root resorption, the pulp expresses
OPG(osteoprotegerin). While the RANK/RANKL facilitate stimulation of
clastic activity, the OPG is a potent inhibitor of the bone resorption

13. PATHOGENESIS:
 Like bone resorption, tooth resorption is brought about by the
multinucleated cells called odontoclasts, which though smaller in size, bear
a morphological similarity to osteoclasts and share a similar hard tissue
resorption pattern.
 Both produce similar enzymes namely, cathepsin, acid phosphatase and
matrix-metalloproteinase-9 and also show the presence of Howships
lacunae which are the resorption craters found on the surface of a
mineralized tissue.
 These are attracted to the site of injury or inflammation by various
proinflammatory cytokines.At the molecular level, signaling molecules
osteoprotegerin (OPG) /receptor activator of nuclear factor kappa B
(RANK)/ ligand (RANKL) of bone remodeling play a role in root
resorptive procedures also

14. HISTOPATHOLOGY

15. ANDEARSON CLASSIFICATION:
The internal and external types may be further divided into surface, inflammatory or
replacement types.
IR may also be classified according to the location of the lesion (apical or intraradicular);
mineral content of the defect (in ammatory or replacement) or
progress of resorption (transient or progressive).
internal external combined

16.  pink hue in the coronal part of the tooth and is named as the pink tooth of
Mummery after anatomist James Howard Mummery
 pink-hued area on the crown of the tooth which represents the
hyperplastic, vascular pulp tissue filled in the resorbed area, showing
through the overlying thin shell of the enamel.
 The progress of in ammatory resorption is arrested either by pulpal necrosis
which cuts off nutrient supply to resorbing cells; or by pulpectomy.
However, if pulpal necrosis leads to sinus tract formation, then the clastic
cells may obtain nutrition from the external environment.

17.  The pulp in the apical part of the root below the resorption place can remain alive and
pathologically unchanged, whereas in the resorption cavity and tooth chamber indicates
the presence of necrotic masses or pulp in the chronic inflammatory condition .The
process of resorption is stopped when the entire pulp dies.
 The main causes of internal resorption include:
Various factors that trigger this are trauma,orthodontic movement of the tooth,
anachoresis,cracked tooth,and even idiopathic changes
 chronic inflammation of the pulp due to caries, iatrogenic stimuli (eg. high
temperatures triggered during cavity preparation, or prosthetic reconstruc- tion
preparation),
 acute mechanical injury,
 biological treatment using the calcium hydroxide
formulations,in decidious dentition(resorption usually
occurs within the first twelve months after treatment).

18. MEDIATORS OF INTERNAL RESORPTION

19.  Internal replacement resorption as described by Ne et al.,
on the
other hand presents as a rough, irregularly oval enlargement of the
pulpal space which has a hazy appearance of mild radiopacity . This
is due to deposition of a metaplastic hard tissue which is similar to
bone or cementum instead of dentin.
 the loss of odontoblast layer and predentin initiate the resorption
process, the progress of the lesion depends on bacterial stimulation
of the clastic cells. Otherwise, the resorption will be self-limiting.

20. Discontinuity of lamina dura

21. INFLAMMATORY INTERNAL RESORPTION
 Internal inflammatory resorption is charac- terized by the rapid enlargement of the
tooth cavity as a result of the ongoing pathological process.
 only in 2% of cases may occur clinical symptoms. The results of tests on the pulp
viability often do not deviate from the normal. They may be negative in the case of the
canal perforation ongoing with the pulp necrosis.
Type A (intra coronal)
Kless and philppart classification

22. TYPE A
 type A resorption in clinical examination of the patient can be see the pink
color of the tooth crown (pink tooth), which is evidence of a very large local
destruction of dentin and luminous dispersion through a thin layer of enamel
granulation tissue
 The use of CBCT allows to evaluate the nature of resorption and its exact
location

23. TYPE B
 In the type B , resorption is seen bubble or oval, symmetrical widening of the
root canal with a clearly regular and well limited smooth walls.
 The resorption loss is uniformly saturated and flows into the tooth cavity.
Characteristic is also fixed position of the change regardless of the X-ray
projection
Intra root

24. TYPE C AND TYPE D
 In the case of the canal wall perforation additionally occurs thinning of the alveolar
bone structure in the vicinity of the perforation.
 Active electrode inserted into the canal lumen immediately indicates the apical
foramen, giving a false result.
 Use conserva- tive, surgical or conservative-surgical treatement.
 Each type of internal resorption due to irreversible inflammation of the pulp
requires endodontic treatment in order to stop the process of root resorption and
obtaining sealed reconstruction
TypeC -Perforation of canal wall Type D- Perforation of tooth crown

25. TREATMENT LINE:
 To halt the clastic activity of any resorptive lesion, it is necessary to
either remove the stimulant, reduce the osteoclastic activity or
stimulating repair.
 For internal root resorption, root canal treatment is the treatment of
choice to remove residual pulpal tissue responsible for nourishing
the odontoclasts to stop the clastic activity in an active lesion.
 Application of 90% trichloracetic acid also helps in arresting the
clastic activity.
 Teeth which are non-restorable and have a poor prognosis may be
referred for extraction.

26. ACCESS CAVITY
 Access cavity design should be done with conservation of the
remaining tooth structure in mind.
 The granulation tissue present in inflammatory type of resorption
may bleed profusely on removal.
 Sodium hypochlorite help to control bleeding and aid in
accessibility and visibility.
 Use of Dental Operating Microscope or loupes is helpful as it
provides a magnified view of the chamber and guides the clinician in
locating the canal orifice.
 A sharp spoon excavator may be used to scoop out the inflamed pink
tissue, sometimes leaving behind just a thin, transparent shell of
enamel

27.  Athin shell of enamel remaining after removal of hyperplastic “pink”
pulp tissue.

28. CHEMO MECHANICAL DEBRIDEMENT:
 Unusual shape of the resorption defect renders routine endodontic
instruments and techniques insuffcient for adequate debridement and
cleaning.
 In cases with replacement resorptive defects, long shank diamond burs
or diamond tipped endodosonics are helphul to negotiate the blocked
canals.
 Passive Ultrasonic Irrigation or sonic agitation of sodium hypochlorite is
useful to kill the bacteria harbored in the irregularities of the resorptive
defects .
 Additionally, intra-canal medicaments like chlorhexidine gel, antibiotic
paste or calcium hydroxide help in reducing the bacterial load.
 Also, calcium hydroxide left in the defect for a short period before
obturation to counteract the acidic environment of the clastic area.

29. OBTURATION:
 In such defects, the primary objective of a 3-dimensional sealing of root
canal can only be achieved satisfactorily with a flowable obturating material
like thermoplastisized gutta percha.
 Even cold-injectable sealer materials like Gutta-flow or MTA Fillapex can be
used along with solid core material to fill complex canal anatomies .Clinicians
have even used fowable composite resin restorative materials to fill internal
resorption defects.
 However, in situations where the clastic activity is extensive leading to a
perforation of the root/ crown wall, mineral trioxide aggregate (MTA) is
preferred owing to its biocompatibility and established efficacy in repairing
furcal and lateral root perforations by forming hydroxyapattite crystals at the
dentine-material interface.
 Recent bioactive materials such as Biodentine induce a local re-
mineralization and thus, might be of use in such cases.

30.  If the defect has caused widening of the canal and compromised dentin
thickness, a light transmitting post may be used to reinforce the canal, followed
by obturation and restoration.Final restoration may be done with composite
restorative materials which strengthen the remaining weakened coronal
structure and make it more resistant to fracture, or MTA if the lesion is
perforating in nature.
 Biodentine was used because it has some features which are superior to
MTA; for example, its consistency is better suited to the clinical use than MTA’s
and Biodentine does not require two-step obturation as in the case of MTA
because of its faster setting time of about 12 minutes .
 Biodentine powder is mainly composed of tricalcium silicate, calcium
carbonate, and zirconium oxide as the radiopacifier, while Biodentine liquid
contains calcium chloride as the setting accelerator and water reducing agent.
It has the capacity to develop watertight interfaces both with dental structures
and with adhesive systems . Biodentine shows deposition of apatitic structures
which might increase the marginal sealing of the material

31. Type B

32.  Type A and D (non-perforating) resorption is easy to treat. In the case of minor
changes the dentin loss is filled with glass- ionomer cement. The outer layer of
filling is made from composite material.
 Type C-Place of the perforation is closed using a surgical access with MTA
material. Other methods of surgical treatment are: apicectomy (if the perforation is
located in the apical one third of the root), hemisection, intended replantation or
extraction . The effect of untreated internal resorption may be spontaneous fracture
of the tooth crown or root, most frequently leading to extraction.

34. NON PERFORATING INTERNAL RESORPTION (MTA)

35. PERFORATING INTERNAL RESORPTION(MTA)

36.  XP-ENDO FINISHER:Respects the original root canal anatomy and effectively
cleans the irregular areas because of its reputed increased flexibility and its
ability to expand to adapt to the root canal three-dimensionally
 Remnants of intracanal medicaments jeopardize the effectiveness of root canal
filling by preventing sealer penetration into dentinal tubules
 XP-endo Finisher file and Passive ultrasonic irrigation were superior to the use of
endoactivator and canal brush.
 use of XP with a combination of NaOCl and EDTA could improve the removal of
CH from simulated internal resorptions
JOE — Volume 43, Number 1, January 2017

37.  IN RESORPTION AREA

38.  CaH-induce chronic inflammatory response which could influence the
macrophages to fuse and form Odontoclasts either through direct
stimulation, or indirectly by stimulating stromal odontoblasts/fibroblasts.
 when CaH is placed in deciduous teeth, it is very likely that the same high
alkaline pH could trigger existing pre-odontoclasts (stromal
undifferentiated mesenchymal cells) to transform into odontoclasts.

39. REPLACEMENT RESORPTION:
 The causes of replacement resorption are probably mild
irritations, e.g. irreversible chronic inflammation of the
pulp or weak injury.
 This change is characterized by resorption of dentin with simultaneous
deposition of hard tissues resembling bone or cementum in the tooth cavity.
 On the x-ray is visible widening of the tooth cavity and deposition of the
loose tooth structures in the light. This can be cause of partial obliteration of
canals or (in the long progressive changes) total obliteration of the chamber
and root canal

40. EXTERNAL ROOT RESORPTION
 The immediate cause of pathological external resorption of the cementum
is damage of cemento- blasts and cementoid by pathogenic stimulus, which
disturbs the balance between the activities of cementoblasts and osteoclasts.
 In the progressive process resorption involves the entire thickness of the
dentine and cementum, causing outside perfo- ration of the canal. It is also
characteristic process in the adjacent alveolar bone.
 Minor irritants can cause the transient resorption, reversible after
eliminating the causative stimulus

41. ETIOLOGY AND PATHOLOGY
1. apical inflammatory root resorption accompany- ing chronic apical
inflammations
2. lateral inflammatory root resorption accompany- ing post-traumatic necrosis
of the pulp
3.cervical resorption
4. ankylosis and replacement ankylosis resorption, osseous
replacement
5. resorption caused by the action of chronic mechanical trauma
6.resorption associated with systemic diseases.

42. EXTERNAL RESORPTION DUE TO THE LOCATION IS
DIVIDED INTO:
apical resorption
resorption of the central part of the root
cervical resorption

43. EXTERNAL INFLAMMATORY RESORPTION:
 External inflammatory resorption is the most common type of external resorption
.It is characterized by deep, bowl-shaped depressions in the cementum and root
dentine.
 This type of resorption is self-limiting in nature and usually occurs following
trauma. It manifests itself as small superficial lacunae in the cementum and may
extend in the outermost layer of dentin.
 The development of external resorption usually occurs when the infection overlaps
the injury. Etiological agent may also be endodontic, periodontal and orthodontic
treatment or pressure of impacted tooth for the root of adjacent tooth.
 Clinically very important is the fact that the osteoclasts colonize and resorbe root
tissues only in the presence of a stimulating agent. Its absence causes inhibition of this
process, and cavities are filled with osteoblasts reconstructed lost tissues.

44.  Apical root resorption is most common in the purulent inflammations and cysts,
less often in granulomas. An infectious inflammation is associated with the
production and release of the macrophage-chemotactic factor, osteoclast-
activating factor, and prostaglandins, which are known stimulators of hard tissue
resorption
 On the other hand lateral inflammatory root resorption is observed in the teeth
with dead, infected pulp or after endodontic treatment.

45.  Injury to or irritation of the periodontium from trauma, periodontal infection, caries or
orthodontic treatment initiates an inflammatory response within the periodontal
ligament and leads to resorption.
 The most common cause of external root resorption is trauma particularly in cases
where the injury results in pulpal necrosis and damage to the root surface, leaving
dentinal tubules exposed.
 This creates a communication between the internal and external surfaces of the root.
Bacteria, bacterial byproducts (lipopolysaccharide,muramyl dipeptide,lipoteichoic
acid)and tissue breakdown products from within the root canal system stimulate
inflammation in the adjacent periodontal tissues and lead to aggressive and
progressive inflammatory resorption of the root
 In the X-ray image in both types of resorption is visible loss of hard tissues, both in the
root and in the surrounding bone. The shape of the cavity is irregular with a faint
outline. It is located asymmetrically with respect to the tooth midline. Resorption area
can "impose" on the course of the canal, which always remains visible and undefor-
med
 These excavations are sometimes seen on the radiograph as small irregularities on
the root surface with normal lamina dura and periodontal space

46. TRANSIENT RESORPTION
 This is reported as a temporary phenomenon in which the apex of the
tooth displays the radiographic appearance of resorption following
trauma(ortho) and generally returns to normal following repair in a period
of 1 year.
 The teeth respond normally to pulp tests and radiographically a widening
of the PDL space and blunting of apices may be seen. No treatment is
recommended as this an ephemeral type of resorption

47.  Its strong anti-bacterial effect and low solubility effect create a long term effect in
root canal.It increases the PH of the dentin,8-10 and inhibits the activity of
osteoclastic acid hydrolases and activates alkaline phosphotases in the periodontal
tissues.
 Calcium hydroxide may have activated the undifferentiated progenitor cells in the
surrounding mesenchyme to undergo mitotic division and differentiation into
function type of connective tissue cells (osteoblasts, cementoblasts,or fibroblasts).
 high pH neutralizes the acidic products of the resorptive cells, creating an
unfavorable environment for them
 high hydroxyl ion concentration may be a factor that induces calcification.
Interestingly, it has been demonstrated that calcium of calcium hydroxide is not
incorporated into the new hard tissue it induces. This calcium is derived from the
systemic circulation.

49. TREATMENT:
 Treatment of small resorptions consists of to determine the cause of the disease and
its elimination. Minor irritants such as trauma or a history of orthodontic treatment
can cause transient type of surface resorption
 Treatment in these cases is during several sessions and relies on temporary filling of
canals with calcium hydroxide
 or antibiotic-steroid preparations. Once the disinfection is obtained canal should be
filled .In the case of the wide apical foramen as a result of the ongoing resorption
process it is recommended to supply this place with MTA material on the min. 3 mm
.Extensive resorptions of permanent teeth are indications to resection, amputation or
root hemisection, and in some cases, to extraction of the tooth.

50. CERVICAL RESORPTION:
 Cervical resorption is quite often occurring phenomenon, appearing always in the
place of epithelial attachment damage and formation of the periodontal pocket.
The etiology of this process is not fully understood. The most common factors
that cause this type of resorption are: intracavity teeth whitening, damage of the
cemen- tum surface due to tooth trauma, improperly performed periodontal
procedures (scaling) or orthodontic treatment
 . In the course of this disease process there is resorption of cementum, enamel
and dentin, and in the final stage of resorption may also include pulp. In
connection with such a way of resorption spreading inside the root, cervical
resorption it is also known as invasive
 This form of resorption spreads generally in the direction of the root, but it rarely
leads to perforation of the canal wall. In a signi- ficant destruction of dentine
around the tooth neck during the examination of the patient is observed the pink
spot in the crown of the tooth.

52.  diffusion of bleaching agents through dentinal tubules initiates the inflammatory
response
 Caoh can be placed intracoronally after removal of the bleaching agent ,and this
turns the ph into alkaline thus by preventing root resorption
 placement of a base over the guttapercha to prevent penetration of caustic
bleaching agents
 leaving the guttapercha filling at a more coronall level so that the bleaching agents
are completely restricted to the pulp chamber.
 oxygen peroxide may denature dentin, which is then, as an alien tissue, removed by
multinucleated giant cells

53. Postbleaching radiograph at 26 months. This 1-yr follow-up
radiograph demonstrates that rapid and extensive external cervical
root resorption had occurred during the preceding 12 months. Although
not as apparent, there was some evidence of resorption
occurring along the mesial surface of the remaining root. Calcium
hydroxide therapy was instituted at this time (April 1985).

54. TREATMENT:
 If the tooth is alive and during surgery could result in the exposure of the pulp, it
should be first performed endodontic treatment.
 Traditional methods of procedure depend on surgical exposure of the lesion site,
removing of resorption granulation by curettage and filling of the root loss with
composite, glass-ionomer cement, compomer or MTA .
 An alternative method of treatment is to eliminate the resorbing tissue by
chemical means. Used for this purpose is a 90% aqueous solution of
trichloroacetic acid. Depending on the amount of resorption tissue acid is applied
for 2-4 minutes. After this time, dead tissue should be remove and filling of the
resorption cavity should be begin

56. UNDERSTANDING THE EXTERNAL CERVICAL RESORPTION PATTERN
IN ENDODONTICALLY TREATED TEETH –MAVRIDOU
(INTERNATIONAL ENDODONTIC JOURNAL)-DEC 2017
 It was shown that the vital pulp tissue and the Pericanalar Resorption Resistant Sheet
(PRRS) can affect ECR, as they have been observed to obstruct its progression.
 However, during endodontic treatment the pulp tissue and the resorption resistant
area (PRRS) that surrounds the root canal space (Mavridou et al. 2016a) are removed
and this is believed to have a significant impact on the evolution of ECR.
 Furthermore, the altered chemical composition of root dentine, after endodontic
treatment (Sim et al. 2001, Zehnder 2006), can also have a significant influence the
ECR progression.
 it has been proposed that hypoxia plays a major role in the initiation process of ECR,
as it reduces or disrupts the supply of oxygen to the PDL

57.  This is possibly due to infection (e.g. bacteria due to plaque and/or poor oral
health), continuous mechanical forces (e.g. orthodontic treatment), variable (load,
frequency, duration) mechanical forces (e.g. parafunctional habits, occlusion)
and/or a combination of these factors. Indeed in this study and in all examined
cases, factors (e.g. trauma, poor oral health, malocclusion etc.) that could influence
the local vascular supply of the PDL, due to chronic inflammation or mechanical
force, were recorded. This would potentially lead to a local hypoxic micro-
environment
 Microorganisms can act by maintaining irritation and as a hypoxic inducer.
 Hypoxia is believed to play a vital role in the evolution mechanism of ECR in
both endodontically and teeth with vital pulps.
 Hypoxia is a driving force of angiogenesis and could play a role in the continuous
development of highly vascularized granulation tissue accompanying ECR
(Ronbouts et al. 2016).

58. PATTERNS:
 All ECR cases of endodontically treated teeth shared common
characteristics:
(1)the portal(s) of entry (initiation point of resorption),
(2) the three-dimensional resorption pattern and
(3) the repair and substitution of the resorbed tissues by
bonelike tissue

59. PORTAL OF ENTRY
 The portal(s) of entry was found to be apical to the gingival epithelial attachment in an
area that originally was probably covered by cementum
 Macroscopical observation and histological analysis of this area revealed the presence
of granulation tissue. Expansion of the oral epithelium into the portal of entry was also
observed
 In addition, multinucleated clastic cells located mainly into resorption lacunae,calculus,
plaque and microcracks filled with bacteria were noticed
 In particular, no ingrowth of the adjacent bone tissue and fusion with the tooth structure
were observed This is possibly due to the lack of vital pulp tissue, which could regulate
the oxygen tension (as observed in teeth with vital pulps) and control localized hypoxia
in the resorption cavity.
 Hypoxia is believed to play a vital role in the evolution mechanism of ECR in both
endodontically and teeth with vital pulps.

62.  on the basis of etiology, a local destruction/disruption of the normal PDL
architecture and homeostasis took place
 This led to localized inflammation and the formation of granulation tissue
 This granulation tissue could reach the dentine through an exposure in the
cementum-enamel junction (CEJ).
 This “gap” could be either due to a localized cementum removal, brought
about by traumatic damage or cemental tear or due to a natural incomplete
closure of enamel over cementum at this area

64. RESORPTIVE PATTERN
 ECR invaded the tooth by resorbing cementum, dentine and enamel, and expanded
up to the filling material of the root canal.
 This ECR expansion occured in a three dimensional way, creating a large
resorption cavity and the resorption channels extended from the portal(s) of entry,
through the root dentine until the filling material.
 A dense inflammatory lymphoplasmacytic infiltrate also extended until the filling
material. Histological analysis of the resorption cavity and resorption channels
revealed large multinucleated cells. These cells could be either found within the
resorption lacunae, in close proximity to the root filling material, or detached from
the resorption lacunae.
 Furthermore, the border between resorption and tooth tissue was visible as a
basophilic line, which ultimately became the repair border between newly formed
reparative bonelike tissue and resorbed dental tissue.

66. REPAIR AND SUBSTITUTION OF THE RESORBED TISSUES
 This repair process took place by substitution of the resorbed tooth structure by
mineralized tissues. Histological analysis of the areas of repair showed osteoid
formation and reparative tissue, resembling lamellar trabecular bone tissue
 Remodeling of the reparative tissue was visible in close proximity to the resorption
lacunae of dentine structure.

69.  it has been shown that hypoxia accelerates bone resorption by increasing
osteoclast activity and viability in a time- and oxygen-dependent manner .
 It also inhibits bone formation by hindering osteoblast growth,
differentiation and collagen production
 However, despite the many similarities observed between endodontically
treated teeth and teeth with vital pulps, one main difference is the considerably
Higher intensity of the resorption observed in endodontically treated teeth
 The absence of a vital pulp and of a Pericanalar Resorption Resistant Sheet
(PRRS) PRRS is a resistant area that surrounds the pulp tissue in teeth with
vital pulps and helps the pulp retain its vitality by hindering the invasive
actions of the clastic cells

70.  The change of the chemical composition of root dentine. It has been
reported that during endodontic treatment, the use of irrigants such as
NaOCl, EDTA, citric acid, H2O2 etc. could alter the chemical
composition of root dentine). In particular, variations in the matrix and
protein content could interfere in bone cell activity and function

71.  However in endodontically treated teeth, the absence of a vital pulp alters the oxygen
content in such a way that resorption is favored in comparison to repair. Therefore in
endodontically treated teeth an extensive and more aggressive ECR is observed.
 POINTS TO BE NOTED:
 At the portal of entry no ingrowth of the adjacent bone tissue and fusion with the tooth
structure were observed.

72.  In the resorption stage, ECR invaded the tooth structure by destroying cementum,
dentine and enamel. The absence of a Pericanalar Resorption Resistant Sheet (PRRS)
possibly accelerated the invasive actions of the clastic cells.
 At the reparative stage, repair took place through the formation of mineralized tissue,
which substituted the resorbed tooth structure. These reparative areas were more
limited in comparison to the large scale reparative patterns met in all teeth with vital
pulps. This observation could be linked to the limited action of the coupling
mechanism between clastic and blastic cells.

73. EXTERNAL REPLACEMENT RESORPTION AND ANKYLOSIS
 Dentoalveolar ankylosis is characterized by a combination of the root structure of the
tooth directly with bone tissue, while replacement resor- ption is the process of the
loss of root tissues and replacing them through the bone .
 As the cause of ankylosis and replacement resorption most frequently are mentioned
injuries, including tooth dislocation, axial and lateral intrusion, as well inflammatory
infection of the dead pulp, pressure, disorder in the local blood circulation, genetic
fac- tors, vitamin A deficiency and hormonal imbalance.
 Dentoalveolar ankylosis and repla- cement resorption are most common in young
people (8-16 years old). Their origin is connected with damage of cementum and
perio- dontal fibers. This process may be reversible, when applies less than 20% of
the root surface .The earliest post-traumatic ankylosis can be recognized after
approx. 2 months after the onset of the injury

74.  Repair with cementum like tissue occurs within 2-3 weeks if the damaged
surface does not cover a large surface area.if the damaged root surface is
large the bone cells will be able to attach to the root before cementum
producing cells. Ankylosis is the result of this process.

75. Replacement resorption of the tooth 24.
Replacement resorption of the tooth 46.
Replacement resorption of mesial root of the tooth 36.

76. FINDINGS:
 Symptoms of both resorption types are: no physiological mobility of the tooth,
metallic flicking sound and radiologically absence of periodontal slit
 In advanced form of resorption characteristic is X-ray image of "root eaten by
moths.“
 In extremely severe cases can occur almost complete replacement of cementum and
root dentin by bone tissue until completely blurring of the tooth outline in X-ray. In the
initial stage of changes intraoral X-ray can not demonstrate any deviations from the
norm, because ankylosis develops on the lingual and labial sites. In such cases, it is
useful execution of CBCT. In young patients ankylosis prevents physiological mesial
movement of teeth and inhibits the local growth of alveolar bone, which is sinking into
the surrounding alveolar ridge – infraposition.

77. TREATMENT:
 The most effective treatment of replacement resorption in young people in the
period of growth is decrowning .This procedure consists in cutting off the tooth crown
1.5-2 mm below the edge of the bone and leaving the root, which as a result of
replacement resorption will be replaced by bone.
 This method is intended to prevent the loss of alveolar bone, stimulate its growth
and provide optimal conditions for future prosthetic reconstruction. After about 18
years of age, when will be completed the growth process, even at partial replacement
of the tooth root by bone, is possible to perform the implantation.
 In older patients it is acceptable to leave the tooth affected by resorption to the
appearance of the symptoms of inflammation. In the case of the bite disturbances with
severe crowding of the teeth and the unfavorable profile it is acceptable as possible
atraumatic removal of such tooth and making autologous premolar transplantation.

78.  This procedure results from the necessity of the extraction treatment of the
malocclusion. In cases of punched teeth stored for a long time in a dry
environment resorption can be delayed (but not stopped!), if the root
surface is coated with a layer of fluoride before the replantation
 Fluoride probably acts directly on the bone tissue, cementum and dentin,
by converting hydroxyap-atite into fluorapatite, or by a specific inhibitory
action on the clastic cells, or even an association of both hypotheses.
Another property of fluoride is its ability to inhibit microbial growth and
metabolism,decreasing cell pH

79.  Loss of pre-cementum, cementoblasts,and epithelial rests of Mallassez results in
the denuded root surface being chemotactic to hard tissue resorbing cells.
Macrophages and osteoclasts subsequently remove damaged periodontal ligament
and cementum.
 When pulp necrosis occurs following luxation and avulsion injuries, the necrotic
tissue is susceptible to bacterial contamination.The combination of bacteria in the
root canal and cemental damage on the external root surface results in external
in£ammatory root resorption.
 If the resorptive process exposes dentine, toxins from bacteria present in the
tubules and/ or the infected root canal can be transmitted to the periodontal
ligament. Stimulators of hard tissue resorption (including macrophage chemotactic
factor, osteoclast activating factor, prostaglandins) are released

80.  .In£ammation in the periodontal ligament and osteoclastic activity lead to
resorption of the lamina dura and adjacent bone. The process usually progresses
until the root canal is exposed.
 Once in£ammatory resorption has been arrested, the resulting defect is repaired by
cementumor bone, according to the type of vital tissue found next to the
resorption site (periodontal ligament or bone marrow-derived tissue).
 If less than 20% of the root surface is involved, a transient ankylosis may occur,
which can later be resorbed due to functional stimuli, providedthe tooth in the
healing period is stabilised with a splint which allows a minimum amount of
mobility, or is nonsplinted
 In larger injuries (>4mm2), a permanent ankylosis is created.The tooth thus
becomes an integral part of the bone remodelling system, the resorbing cells being,
primarily, osteoclasts
 The medium in which the tooth has been stored affects the levels of root
resorption and pulp healing.
 Prolonged drying of the root is detrimental due to loss of vitality of the periodontal
ligament and dehydration of the pulp

81.  the risk of early resorption is increased in teeth that have additional
damage or contamination of the root, or are kept in dry conditions for
longer than 15min
 The hydrated periodontal ligament cells will maintain their viability,
allowing them to reattach on replantation without causing any more than
minimal destructive in£ammation
 Suitable media, in order of preference, are: Hank’s pH balanced salt), cold
fresh milk, saliva, physiologic saline
 Andreasen recommends delaying endodontic treatment for 1week after
replantation to prevent the development of ankylosis and in£ammatory
resorption,and allow time for reattachment of periodontal fibres.
 If pulp therapy of a replanted tooth with a closed apex is initiated within
7^10 days of injury, the pulp should be necrotic with little or no infection

82. RESORPTIONS CAUSED BY CHRONIC ACTION OF
MECHANICAL TRAUMA
 Chronic mechanical injuries are the result of pressure by the unerupted teeth or
improperly erupted, expanding cysts, tumors and as a result of points of premature
occlusal contacts.
 These factors can cause resorption of the roots of adjacent teeth.
 External resorption of the teeth roots is also often a consequence of orthodontic
treatment. The location and extent of the post-resorption defects depend on the
direction, time of action and size of the force applied in orthodontic apparatus. On
the X-ray is found a widening of periodontium space and shorten of the roots that
appear like cut off. Treatment of this resorption type is to eliminate the causative
agent

83. RESORPTION ASSOCIATED WITH SYSTEMIC DISEASES
 Internal and external resorptions may be accompanied by some systemic
diseases.
 For these include: hyperparathyroidism and hypoparathyro- idism,
hyperthyroidism, Paget's disease, Gaucher's disease, Turner syndrome,
cancers within the facial part of the skull. Frequently these resorptions
concern several teeth and are chronic

84. REFERRENCES:
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 Management of a Perforating Internal Resorptive Defect with Mineral Trioxide
Aggregate: A Case Report Emre Altundasar, DDS, PhD,* and Becen Demir, DDS,
PhD,, JOE — Volume 35, Number 10, October 2009
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86. THANK YOU