This document provides an overview of root resorption, including definitions, classifications, mechanisms, and types. It discusses physiological versus pathological root resorption and defines internal and external resorption. Key cells involved in the resorption process are osteoclasts and odontoclasts. Resorption requires inflammatory stimuli and occurs via acidification and enzymatic degradation. Factors like trauma, pressure, and infection can lead to resorption if they damage the protective root layers. The document classifies and describes various types of internal and external resorption.

1. PRESENTED BY
RENJITH RAJ
III MDS

2.  Introduction
 Definitions
 Physiological mechanisms inhibiting root
resorption
 Key calls involved
 Mechanism of resorption
 Requirements for the presence of resorption
 Classification
 External resorption and its various types

3.  Internal resorption and types
 Journal review
 Conclusion

4.  Tooth resorption is considered as a reactive mechanism
of pulpal and periodontal tissues in response to
various injuries .
 Unlike bone, roots of permanent teeth are not resorbed
normally.
 If occurs, it is because of some pathological reasons-
considered an unfortunate and unpredictable
phenomenon.
 Decidous teeth show physiologic resorption before
they are shed off.

5. Resorption : (AAE,1944 ) : Resorption is a condition associated
with either physiologic or pathologic process resulting
in a loss of dentin, cementum or bone.
Root resorption : (C.W.Barclay) : It is a pathological process, of
internal or external origin, which occurs when the natural
protection of predentin and odontoblasts in root canal or
precementum and cementoblasts on the root surface are damaged
or removed.
Internal resorption : ( Grossman ): Internal resorption is an
idiopathic, slow or fast progressive resorptive process, occurring
in the dentin of the pulp chamber or root canals of teeth.
External resorption : ( Grossman ): External resorption is a lytic
process, occurring in the cementum or cementum and dentin of
the roots of teeth.

6.  Physiological process
 Necessary precursor to the eruption
of permanent teeth.
Permanent teeth root resorption
Pathological inflammatory processs
Results from injury to or irritation of pdl and or pulp

7.  Unlike deciduous teeth, permanent teeth rarely
undergo root resorption
 Even in the presence of peri-radicular inflammation,
resorption will occur primarily on the bone side of the
attachment apparatus and the root will be resistant to
it.
 Al-though many theories have been put forward, the
reason for the resistance of the root to resorption is not
fully understood.

9.  One theory maintains that remnants of the epithelial root
sheath surround the root like a net, therefore imparting a
resistance to resorption and subsequent ankylosis
 inhibitory effects of organic precementum and predentin
(hypothesis by Andreason). This theory is based on the
premise that the cementum and predentin covering on
dentin are essential elements in the resistance of the dental
root to resorption.
 Another function of the cemental layer is related to its
ability to inhibit the movement of toxins if present in
the root canal space into the surrounding periodontal
tissues

10.  another hypothesis for the relative resistance of tooth
to resorption maintains that intrinsic factors found in
predentin and cementum act as inhibitors of resorptive
cells.
 One such factor is Tumor Necrosis Factor
osteoprotegerin (OPG), a novel member of the tumor
necrosis factor(TNF) superfamily that has the ability to
inhibit osteoclast- mediated bone loss.
 Cementoblasts, periodontal ligament cells, and
human pulpal cells possess the ability to produce OPG

11.  KEY CELLS INVOLVED:-
Tooth resorption involves an elaborate interaction among
 Inflammatory cells
 Hard tissue cells
 Resorbing cells

12.  Monocytes
 Macrophages
 Osteoclasts
 Odontoclasts
(According to Pierce AM et al.)

13. 1. Bone-resorbing cells derived from
hemopoietic cells.
2. Can move between resorbing sites
3. Is a multinucleated giant cell
4. Characterized by specialized membrane
structures, clear zones and ruffled borders
5. Found in tiny depressions, HOWSHIP
LACUNAE in cementum, dentin and bone.
6. Stimulation is under the control of RANK-
RANKL-OPG system(downregulation of OPG
and upregulation of RANKL favour
differentiation of osteoclasts)

14. • Odontoclasts are smaller,
• Have a ruffled border,
• Contain fewer nuclei than Osteoclasts and
• Have smaller or no clear zone.
• Both cells have similar enzymatic and acid
phosphatase activity.
Odontoclasts or Dentinoclasts
( Boyde and Jones )

15.  Takes place as two events:-
Degradation of the inorganic crystal structures
 Hydroxyapatite
Degradation of the organic matrix
 Type I collagen

16.  By producing an acidic (ph-3 to 4.5)
 Highly active polarized proton pump
 Within the ruffled border of clastic cells
 Carbonic anhydrase II
 Present intracellularly
 Catalyses CO2 H2CO3
 Readily available source of H+ ion
 Acid phosphatase enzyme also favors resorption process

17.  Degradation of the organic structure
 By three groups of proteinase enzymes
 Act at / just below neutral pH of 7.4
 Collagenase
 Matrix metalloproteinase (MMP)
 Act at acidic pH
 Cysteine proteinase

18.  Regulatory factors
 Systemic regulatory factors
 Local regulatory factors

19.  Systemic regulatory factors
 Promote resorption
 Parathyroid hormone (PTH)
 1,25-dihydroxyvitamin D3
 Inhibit resorption
 Calcitonin

20.  Parathyroid hormone (PTH)
 Acts on osteoclasts
 Increase CA II activity
 Promotes fusion of marrow cells
 Forms osteoclastic multinucleated giant cells
 1,25-dihydroxyvitamin D3
 Increases resorptive activity of osteoclasts already present
 Calcitonin
 Inhibits cytoplasmic motility and produces cell retraction

21.  Local regulatory factors
 Secreted by inflammatory cells and osteoclasts.
 Cytokines
 Macrophage colony-stimulating factor (M-CSF)
 Interleukin 6 (IL-6)
 Interleukin 1 (IL-1)
 TNF – α
 Arachidonic acid metabolites (PGE2)
 Endotoxin (lipopolysaccharides)

22.  Cytokines
 Macrophage colony-stimulating factor (M-CSF)
 Proliferation of osteoclast progenitor
 Subsequent differentiation into mature osteoclasts
 Interleukin 6 (IL-6)
 Acts on osteoblastic stromal cells to induce osteoclast differentiation
factor
 Indirectly helps in the differentiation of osteoclast
 Interleukin 1 (IL-1)
 Acts indirectly through the osteoblast
 Act directly on the osteoclast
 Stimulates the production and release of prostaglandin E2
(PG2)
 TNF – α
 Stimulate osteoclastic activity

23.  Prostaglandins
 PGE2
 Stimulates formation of osteoclasts
 Enhancing the fusion of osteoclastic precursors
 Increases the resorbing activity of existing cells

24.  Bacterial endotoxin / LPS
(lipopolysaccharide)
 Induction of osteolytic factors
 Lysosomal enzyme release
 Collagenase release from macrophages
 Osteoblastic secretion of osteolytic factors
 IL-1
 IL-6
 M-CSF
 PGE2

25.  The loss or alteration of the protective layer
 pre-cementum
 pre-dentin
 Sustained inflammation must occur to the
unprotected root surface

26.  Directly
 due to the trauma of a dental injury
 Especially intrusive injury
 Indirectly
 Inflammation in reaction to the traumatic injury
 varies according to the stimulus it is exposed to after
the injury
 has the potential to cause extensive damage to the
protective layer

27.  The inflammatory response caused by the
dental injury can be divided into two critical
phases
 Destructive phase
 Healing phase

28. Destructive phase
 where active resorption between the dried-out cells
with multinucleated giant cells takes place
 This destruction will continue as long as there is
stimulus present to allow the inflammation to develop
 stimulus only exist for a short period of time
 Healing will take place without intervention by the dentist
 If the inflammatory stimulus is long-standing
 the destructive root resorption will continue until either no root
structure remains or the stimulus is removed by the
intervention of the dentist.
 Identified by radiolucent appearance of the tooth and bone on
x-rays

30.  Healing phase
 The critical factor in determining the outcome after a
dental traumatic injury has occurred is the type of
cells that repopulate the root surface during the
healing phase
 Cementoblasts
 type of healing termed
 cemental healing or surface resorption will occur
 the outcome will be favorable
 Osteoblasts
 the conditions for healing will be unfavorable
 Ankylosis, replacement resorption or osseous replacement

31.  The type of tissue that will cover the root surface is
dependent on
 the surface area of the root damage
 destruction of over 20% of the root surface is required
for osseous replacement to occur
 the relative proximity of the cells to the root; i.e.
how far and how fast the cells can travel in order to
cover the damaged root surface

33.  surface area of root damage is dependent on
 the scale of the initial injury
 which cannot be reversed.
 the extent of the destructive inflammatory
response.
 opportunity here for the initial inflammation to be
minimized by actions taken both immediately after the injury
 where the way in which the tooth is handled is of crucial
importance
 by the pharmacological manipulation of the inflammatory
response

34. PRESENCE
OF
STIMULUS
ABSENCE OF
STIMULUS
CEMENTAL
HEALING
BONE
HEALING
SURFACE
RESORPTION
ANKYLOSIS
MORE
RESORPTION
< 20 %
DAMAGE
> 20 %
DAMAGE
INJURY
PHYSICAL DAMAGE
INFLAMMATION
ADDED PHYSICAL DAMAGE

35.  I) By ILAN ROTSTEIN & JAMES H. SIMON –
(Endodontic Topics 2006)
 A. Non-Infective Root Resorption
 B. Infective Root Resorption.
 A. Non-Infective Root Resorption (Non-Inflammatory)
 This process occurs as a result of a tissue response to non-
microbial stimuli in the affected tissues.
 It includes
 Transient root resorption.
 Pressure-Induced root resorption.
 Chemical-Induced root resorption.
 Replacement resorption
 Extracanal Invasive resoption.

36.  B. Infective Root Resorption (Inflammatory)
 This process occurs due to a vascular response to
microorganisms invading the affected tissues.
 It may occur in both the pulp space and the
periodontium and may be located either within the
root canal space (internal resorption) or on the external
root surface of the root (external resorption).
 a. Internal Resorption
 b. External Resorption. (Apical/ Lateral / Cervical)

37. CLASSIFICATION BY Trope & Chivian 1994
 Local causes of root resorption
 Pressure
 Orthodontic tooth movement
 Impacted tooth
 Tumours or cysts
 Inflammation
 External
 Apical
 Lateral
 Cervical
 Internal
 Dentoalveolar ankylosis and replacement resorption
 Systemic causes of root resorption
 Idiopathic resorption

38. CLASSIFICATION BY Ne et al, 1999
 Internal resorption
 Root canal (internal) replacement resorption
 Internal inflammatory resorption
 External resorption (according to its clinical and
histologic manifestations)
 External surface resorption
 External inflammatory root resorption
 cervical resorption with or without a vital pulp (invasive cervical root
resorption)
 external apical root resorption (EARR)
 Replacement resorption
 Ankylosis

39.  A. Pulpal infection root resorption
 B. Periodontal infection root resorption
 C. Orthodontic pressure root resorption
 D. Impacted tooth or tumor pressure root
resorption
 E. Ankylotic root resorption.

40. A. Internal Root Resorption
B. External Root Resorption
i. Transient Or Surface Resorption
ii.Progressive Resorption
a. Inflammatory Resorption – Apical Or Lateral
b. Cervical / Invasive Resorption
c. Replacement Or Ankylotic Resorption
d. Idiopathic Resorption

41. A. Pressure Induced Resorption
i. Orthodontic Resorption
ii. Tumor/Cyst Induced Resorption
iii.Impacted Teeth Resorption
B. Inflammation Induced Resorption
i. External Resorption
• Apical
• Lateral ( Surface/ Inflammatory)
• Cervical
• Ankylosis or Replacement Resorption
ii. Internal Resorption.

42. 1. Trauma induced tooth resorption
 Surface resorption
 Transient apical internal resorption
 Pressure resorption
 Orthodontic resorption
 Replacement resorption
2. Infection induced tooth resorption
 Internal inflammatory root resorption
 External inflammatory root resorption
 Communicating internal-external resorption

43. 1. External surface resorption/ Repair related
resorption
1. External infection related resorption /
Inflammatory root resorption
2. External trauma related replacement
resorption / Ankylosis
3. External spontaneous ankylotic resorption

44. 5.External multiple sites of ankylosis /
Infection related resorption
6.Cervical invasive resorption
7. Internal surface resorption
8. Internal infection related root resorption
9. Internal replacement resorption

45. The root resorption that is initiated in the periodontium and affecting
the external or lateral surfaces of a tooth.
Can be classified into four categories by its clinical and histologic
manifestations. (Rita F.ne, Guttman et al;quintessence international 1999)
External resorption
 Surface resorption
 lnflammatory root resorption
(a) Cervical resorption with or without a vital pulp
(b) External apical root resorption
 Replacement resorption
 Ankylosis

46. Definition
Small, superficial resorption cavities in the cementum
and the outermost layers of the dentin, without an
inflammatory reaction in the periodontal ligament
Andreason & Hjorting –Hansen (1966)
Etiology
Acute injury:- concussion, subluxation and
lateral luxation.
Chronic injury:-orthodontic treatment, traumatic
occlusion, pressure from cysts, ectopically
erupting teeth.

47.  Typical feature:-when the trauma or pressure is discontinued,
spontaneous healing takes place.
Pathogenesis
The injured tissue adjacent to the root and surface cementum are
removed by macrophages and osteoclasts.
Takes 2-4 weeks
Repair is by progenitor cells from the pdl, new cementum is formed
with insertion of pdl fibres.
Radiographic features
After 2-4 weeks , localised widening of the pdl space
Slight cavitations may be seen on root surface
Very limited size-cant be recogonized radiographically.

48.  T
Treatment
 100% repair takes place in almost all cases.
 Endodontic treatment not indicated.

49.  Combined injury to pulp and pdl and where bacteria
located in the pulp space and dentinal tubules trigger
osteoclastic activity on root surface.
 Can affect all parts of the root.
 Rapidly progressing-result in total resorption of the
root within a few months.
Etiology
Related to acute trauma
Intrusion and replantation of avulsed teeth

50.  Pathogenesis
 once the initial resorption has penetrated the cementum and
exposed the dentinal tubules, toxins from infected root canal
diffuse through the exposed dentinal tubules to pdl.
 Continuation of osteoclastic process and associated inflammation
in the pdl-resorption of adjacent alveolar bone.
 Process progresses, root dentin is resorbed and root canal becomes
exposed.
 If endodontic therapy is done-resorptive process will be arrested
and the resorption cavity filled with cementum or bone.

52. Clinical findings
 Increased mobility
 Dull percussion tone
 Sometimes tooth may be extruded
 Sensitivity test gives no response
 May exhibit a sinus tract

53. Radiographic findings
Progressive cavitations involving root and adjacent alveolar bone.
Result in total loss of tooth structure within a few months.

54.  Endodontic implications
Requires immediate endodontic treatment to control or remove the
osteoclast promoting factors.
Treatment
Goal is to remove bacteria in the root canal and dentinal
tubules.-allow healing in entire periradicular space.
Mature teeth
Endodontic treatment-prophylactic extirpation of the pulp
in replanted avulsed tooth
Biomechanical preparation with Naocl and Ca(OH).
Calcium hydroxide perform disinfection and canal can be
filled 2-3 weeks after treatment.

55. Immature teeth
Pulp becomes necrotic before root is fully devoloped- apical opening is
often too large to create a resistance to retain the root canal filling.
Apexification procedures using calcium hydroxide have been
performed with good success – disadvantage: –
takes many months to form an apical barrier to allow placement of a
root canal filling.
Long term use can weaken the dentin,by dissolving its organic
content-result in cervical root fracture on even slight impact.
Root canal filling can be done immediately without waiting for a
biological response if MTA is used as a physical barrier apically.

56.  Represents a sequel to a defect or injury to pdl cells, including the
cell layer next to the cementum.
Etiology
Acute trauma:- severe luxations
 Lateral luxations
 Intrusions
 Replantation of avulsed teeth
Homeostasis of pdl is lacking.
Healing events take place from adjacent healthy pdl or the bony
alveolus leading to formation of a normal pdl in former and a bony
bridge between socket wall and the root surface.

57. Moderate sized injuries(1-4mm2)
 An initial ankylosis forms.
 Tooth-allowed functional mobility by the use of a
nonrigid splint, small areas of resorption can be replaced
with new cementum and pdl attatchment. (Transcient ankylosis)
Extensive injuries(›4mm2 )
Progressive ankylosis-tooth becomes an integral part of bone
remodelling system
In children- active process- gradual infraocclusion and arrested
devolopment of the alveolar process.
Combination of resorption –loss of ankylosed teeth within 1-5 years.
Older individuals- replacement resorption is significantly slower and
often allows a tooth to function for much longer periods of time(5-
20 yrs).position of tooth remains the same.

59. Clinical findings
 Tooth appears very form in its socket.
 High metallic sound on percussion.
 Demonstrated 4-6 weeks post – trauma.
Radiographic findings
 Diagnosed radiographically within 2 months after injury
 Complete disappearance of the periodontal space
 Uneven root surface contour (Moth-eaten appearance)

61.  Treatment
 No treatment
 Very little can be done to reverse this initial
attachment damage, therefore the main focus of
treatment is to do everything possible to limit the
destructive inflammatory process that occurs
immediately after the injury. If the inflammation is
minimized, the surface area of damaged root surface
will also be kept to a minimum.

62.  Treatment strategies are therefore directed at
avoiding or minimizing the severity of the
initial inflammatory response
 Prevention of the initial injury
 Minimizing additional damage after the initial injury
 Pharmacological manipulation (shut down) of the
initial inflammatory response
 Possibly stimulating cemental, rather than bone,
healing
 Slowing down the osseous replacement when it is
inevitable

63. 1. Prevention of the initial injury
Preventive measures have been to found to limit
the occurence of tooth injuries
 Athletes-usage of mouth-guards and other protective
devices found to be proven protection against tooth
trauma.

64. 2. Minimizing Additional Damage after the Injury
 Luxations
 Gentle repositioning of the tooth in its original position as
soon as possible.
 Patient should be sent to emergency room or dentist .
 Splinting
 functional splint for 7-10 days
 splint should be constructed to allow adequate cleaning

65.  Examples of functional splints
 TTS splint (Titanium Trauma
Splint)
 This splint allows space for
adequate cleaning, thereby
minimizing infection due to plaque
and food debris
 It is flexible in a horizontal and
vertical direction
 Resin splint
 whilst allowing functional
movement, is too thick ,
impossible for patients to clean it.

66.  Avulsions
 replanting the tooth as soon as possible
 extra-oral dry time must be minimized
 appropriate storage medium
 Milk
 Sterile saline
 Saliva
 Hank’s Balanced Salt Solution
 ViaSpan

67. 3. Pharmacological manipulation (shut down) of the initial
inflammatory response
 Drugs that affects osteoclasts present at the site of resorption
 Tetracyclines
 Sustained antimicrobial effect
 Anti-resorptive properties
 direct inhibitory effect on osteoclasts and collagenase
 Significantly more cemental healing
 Drugs that affect the recruitment of osteoclasts to the injury
site –reduce osteoclastic bone resorption.
 Glucocorticoids
 Topical dexamethasone was found to be useful while systemic
usage was not
 Bisphoshonates
 Alendronate
 Amino acids
 Taurine

68.  Combination of the two types of drugs
 synergistic effect on the inhibition of root resorption
 Ledermix
 a drug combining tetracycline and corticosteroids
 ART (Antiresorptive Regenerative Therapy )
by Pohl et al 2005
 Comprises a combination of different treatment
strategies for a synergistic effect
 Local application of a glucocorticoid
 Systemic and local application of tetracyclines
 Use of Enamel Matrix Derivative (EMD) e.g. Emdogain

69. 4. Stimulate Cemental Healing
 ‘Conditioned Medium'
 supernatant of cultured gingival
fibroblasts, that contain a number
of biologically active factors
 ViaSpan
 Emdogain (Enamel Matrix
Protein; Biora, Malmo, Sweden)
 for teeth with extended extra oral
dry times
 makes the root more resistant to
resorption
 stimulates the formation of new
periodontal ligament from the
socket
Emdogain placed on tooth and
in the socket before replantation

70. 5. Slow down 'inevitable' osseous replacement
 When the periodontal ligament on the root surface is
definitely destroyed
 intrusive injuries
 avulsion injuries with extended extra-oral dry times
 Intrusive injuries
 the tooth is repositioned
 inevitable osseous replacement accepted

71.  Avulsion injuries with extended dry times
 All remaining periodontal ligament debris is
removed from the root by thorough curettage
 Fluoride
 root is soaked in fluoride for 5 min before replantation
 effectively slow down remodeling of the root to bone
 Bisphosphonates
 slows down the osseous replacement
 More expensive than fluoride
 Emdogain A

72.  When there is no known etiology
 First reported-mueller & rony(1930)
2 TYPES:-
-APICAL
-CERVICAL
(Lydiatt et al 1989, Yusof & Ghazali 1989)

73.  Mostly seen in young adults
 Maxillary teeth frequently involved
 Resorption starts apically, progresses coronally
 Gradual shortening and rounding of roots
Cervical type
Starts in cervical region and approaches pulp.
Does not seem to be mediated from pulp space.

74.  Pathogenesis
Suspected that triggering factors exist for osteoclastic and
odontoclastic activity producing root resorption
 Treatment
Not mediated from pulp space- so interceptive endodontic
procedures are not indicated.

75.  Appear to begin at mesial or distal CEJ
 Initially presents as a radiolucency with
scalloped margin
 In time found to undermine enamel
Single idiopathic root resorption
Can be confused with root caries
Clinical and radiographic findings are helpful in
establishing correct diagnosis.

76. Root caries
 Lesion of dentin with
gingival recession
 Clinically soft to the
touch of an explorer
 Radiographically
illdefined, saucer like
and radiolucent.
Sharp edge of cavity
border –diagnostic
finding
Cervical resorption
 Gingival condition
might appear either
normal or inflammed
 Covered by soft tissue
 Almost same –
incidental
radiographic finding

77. Treatment
 No preventive or therapeutic regimen for this type
of resorption.
 Not mediated from pulp space- endodontic
treatment wont do any good. There is no known
preventive or therapeutic regimen for this
condition, and monitoring accompanied by
periodontal maintenance is recommended
 Usually observation and extraction of teeth.
 Further studies needed to identify the specific
cellular mechanism responsible to determine
therapeutic measures.

78.  A 27-year-old male was referred to the Endodontic
Department of Shiraz University of Medical Sciences,
School of Dental Medicine by his family dentist for
evaluation of extensive root resorption affecting most
teeth.
 The patient was a truck driver with no history of
medical disorders. A family history revealed no early
tooth loss in parents or grandparents. His two brothers
and three sisters were also examined, and panoramic
radiographs revealed no similar condition.

79.  Clinical examination revealed normal soft tissues
and normal dentition particularly the morphology
and size of the crowns.
 The periodontal condition was normal with no
abnormal pocketing. Tooth mobility was within
the physiological range.
 A panoramic radiograph and tracing together
with the periapical radiographs revealed extensive
apical root resorption in all teeth except teeth 18,
23, 31–34, 37and 41–44. Eighteen teeth had apical
root resorption, mostly in the maxilla

83.  On the basis of the history, clinical examination and
radiographic evaluation, a diagnosis of multiple
idiopathic apical root resorption was made.
 The patient was given instructions to maintain proper
oral hygiene and was scheduled for frequent recall
visits in order to prevent periodontal bone loss and
further compromiseof crown : root ratio.

85.  Nomeclature
 Inflammatory root resorption of endodontic origin
 is usually known as apical inflammatory root
resorption
 External apical root resorption (EARR)

87.  Definition
External apical root resorption is a pathological
condition, characterized by the resorption of hard
tissues (cementum, dentin) and sustained by a local
inflammatory reaction , in most cases because of the
presence of infected necrotic dental pulp, which is able
to maintain the whole process
Hammarstrom & Lindskog 1985

88.  Cause
 All causes of apical periodontitis
 Infected necrotic pulp
 caries (predominant cause)
 Overinstrumentation during endodontic therapy
 Trauma

89.  Features
 intact cementum on the root surface (in most routine
cases)
 communications primarily through the apical
foramina or, occasionally, through accessory canals
 Invariably, slight resorption of the root at the
cemento-dentinal junction

90. Clinical features
 Early stages-asymptomatic
 As the process progresses, teeth become
symptomatic.
 Periradicular abscess devolop
Radiographically
 Radiolucency observed at external surface of
dentin and adjacent bone.

92.  External apical resorption can be of three types
 Periforaminal resorption
 Defined as the area of resorption not comprising the outline of
the foramen, but the surrounding area
 Foraminal resorption
 Defined as the resorption within the outline or perimeter of the
foramen
 Combined
Vier & Figueiredo 2002

93. Bacteria / by-products in root canal
Start an inflammatory reaction in the periapex
Resulting odema cause detachment of
periodontal ligament from parts of the root
Disappearance of cementum with consequent exposure of
the root which can be resorbed by phagocytic cells
Torabinejad & Finkelman 1994

94. Clinical evaluation
 Usually occurs without any clinical symptoms and forms
part of the periapical pathology associated with apical
periodontitis(Nair 1997)
radiographs for the clinical diagnosis
 Less than 20% of teeth revealed apical inflammatory
root resorption on a radiograph
 whereas 81% of teeth revealed apical inflammatory root
resorption by histology(Laux et al 2000)
 Histologic appearance
 resorption of the root at the cemento-dentinal junction is
routinely observed

95.  Treatment
 Removing the stimulus for the underlying inflammatory
process
 Working length determination
 Weine’s method
 Electronic method
 Application of intracanal medications
 Ca (OH)2
 Activ point(chlorhexidine 5%)
 Obtaining a good apical seal
 Ca (OH)2 for apexification
 Thermoplasticized gutta percha techniques

97.  Definition
External root resorption associated with
marginal periodontitis without pulpal
involvement is most commonly referred to as
cervical invasive root resorption (because of the
marginal location of the defect)
Heithersay 1999

98.  Nomenclature
 Peripheral cervical resorption
 Burrowing resorption
 Pseudo pink spot
 Subepithelial external root resorption
 Extracanal invasive resorption

99.  May occur after injury to the precementum,
apical to the epithelial attatchment , followed
by bacterial stimulation originating from
periodontal sulcus.
 Injury can be due to
dental trauma, bleaching procedures,
periodonal procedures, orthodontic treatment

101.  Bacteria from sulcus penetrate patent dentinal tubules
coronal to the epithelial attatchment and exit apical to
epithelial attatchment without penetrating pulp space.
 Damaged root surface –invaded by clast cells ,
penetrate the dentin though a small denuded area-
spread of resorption in root.
 Resorption process reach supragingival area of crown-
vascularised granulation tissue visible through enamel-
pinkish discolouration.

103. Radiographically,
 Single resorpton lacunae in the dentin usually
at the crestal bone level, especially to the
coronal and apical direction.
 Resorption progresses, radiolucency may be
observed at the alveolar bone adjacent to the
resorption lacunae of the dentin.

105.  Features
 inflammatory origin
 most often referred to as cervical root resorption
 occurs immediately below the epithelial attachment of the
tooth, usually but not exclusively in the cervical area of the
tooth
 Also called
 Extracanal invasive resorption (Frank AL)
 Invasive cervical resorption (Heithersay GS)
 Subepithelial external root resorption (Trope M)
 The pulp plays no role in cervical root resorption
and is mostly normal in these cases(Frank &
Torabinejad 1998)

107.  Class 1- small invasive resorptive lesion near the
cervical area with shallow penetration in to dentin.
 Class 2- well defined invasive resorptive lesion
that has penetrated close to the coronal pup
chamber but shows little or no extension in to
radicular dentin
 Class 3 – deeper invasion of dentin by resorbing
tissue not only involving the coronal dentin , but
also extending in to coronal third of the root.
 Class 4 –a large invasive process that has extended
beyond the coronal third of the root

108.  Clinical appearance
 asymptomatic
 If extensive, symptoms of pulpitis will develop
 usually only detected through routine radiographs
 'pink spot'
 When the resorption is long-standing
 Granulation tissue can be seen undermining the enamel of
the crown of the tooth, resulting in a pinkish appearance
 Results in misdiagnosis
 Probing may result in profuse bleeding
 presence of inflamed tissue rather than normal attachment

109.  By investigating the resorption cavity walls
with an explorer, a hard, mineralized tissue
sensation will be felt, accompanied by a sharp,
scraping sound.
 This feature and the appearance of knife-edge
cavity borders are important in the differential
diagnosis from root caries. Caries lesions are
rather soft because the organic component of
the dentin has been disintegrated not by the
bacterial acid production but by proteolytic
enzymatic degradation.

110.  Histologic appearance
 appears similar to any external inflammatory root resorptive
process
 usually a small opening into the root, with large amounts of
granulomatous tissue inside the defect and multinucleated
giant cells resorbing the dentinal structure
 In extensive defects
 osseous tissue seen inside the granulomatous tissue
 indicating quiescent periods in the process where healing with
reformation of an attachment may have been attempted.
 Even in the most extensive defects, the
predentin/odontoblastic layer is unaffected, demonstrating the
resistant nature of this tissue

111. Tooth immediately after careful
extraction. (Right) Same tooth after exca-
vation of the granulation tissue. Notice
the layer of dentin and predentin that
separated the resorbing tissue from the
dental pulp

112.  Radiographic appearance
 resorptive process occurs mesially or distally on the root
surface
 Single resorption lacunae in the dentin usually at the crestal bone
level
 The radiolucency expands coronally and apically in the dentin,
and reaches, but usually does not perforate, the root canal
 irregular, diffuse radiolucency of nonuniform radio-density
(Makkes & van Velzen 1975).
 resorptive process is buccal or palatal-lingual
 the radiographic picture depends on the extent to which the
resorptive process has spread in the dentin
 It can be seen as a radiolucency at the attachment level or have
spread a considerable way coronally or apically with a mottled
appearance
 Because the pulp is not involved, root canal outline can
usually be distinguished through the resorptive defect

113. Pinkish discoloration of the left central incisor
caused by invasion of the cer-vical region of the
tooth by fibrovascular tissue derived from the
periodontal ligament. (Right) The parallel
radiograph shows a rather irregular
radiolucency , involving not only the coronal
dentin but also ex-tending to the coronal third of
the root. The characteristic radiopaque line
separating the lesion from the root canal can be
identified.

114.  Treatment
 The aim of treatment is two-fold:
 Stop continuation of resorption
 removing all the granulomatous tissue from the root
 In cases where removal of granulomatous tissue would cause
unacceptable damage to supporting structures, an attempt is
made to severe the blood supply to the granulomatous tissue, thus
killing the resorptive cells and inhibiting progression of the
resorptive process
 Replace the unprotected root surface with a foreign material
that clastic cells cannot be attached to or penetrate
 Any well-sealing dental restorative material
 inhibits attachment by clastic cells
 also does not allow attachment by those cells that provide for a normal
periodontal ligament
 root attachment will only occur apical to the filling material, leaving a
periodontal pocket that is unacceptable

115.  Treatment approaches
 Internal approach
 External approach
 combinations

117. External Approach
 determine the exact location of the
defect (buccal or lingual-palatal)
 Angled radiographs
 full thickness flap is raised
 granulomatous tissue is removed
from the root and the bone defect
 with a curette or bur
 also remove granulomatous tissue
from sound, healthy bone
 so that revascularization of the
resorbing tissues will not occur
 The opening into the root should be
as conservative as possible
 The root defect is filled with a
restorative material
 flap replaced in a way as to
minimize the periodontal defect
after healing
 Indications
 For the small coronal defect
The flap is raised, meaning the
blood supply to the granulomatous
tissue in the root has been cut. B.
The tissue is removed from the root
and bone and C. the
root is filled with a composite resin
filling.

118. Internal Approach
 trichloracetic acid (Heithersay)
 The acid will chemically burn the granulomatous
tissue, thus necrosing it and providing space for the
filling material internally
 calcium hydroxide
 but may take multiple applications to achieve the
same results
 Theoretically, a bur could be used but the
chances of pulp exposure and/or extensive
attachment damage are very high with this
approach

120. External Approach
 Traditional approach
 remove the entire root cementum surface
adjacent to the granulomatous tissue in the
dentin
 Alternate approach
 remove the resorptive tissue from a small
opening at the most apical extent of the
affected root
 leaving coronal root surface onto which a new
attachment might develop
 opening repaired with an acceptable
restorative material
 the defect and denuded root surface is covered
with a spacer (freeze-dried bone), and the
entire area covered with a Gore-Tex
membrane (Gore Tex, W. L. Gore, Flagstatt,
AZ).

121.  Forced eruption
 If the remaining root apical to the resorption defect is long
enough to maintain the tooth
 The resorption defect is moved to a position coronal to the
adjacent attachment.
 Defect cleaned and restored
 Forced eruption/re-intrusion
 If the crown root ratio is not ideal
 after the repair is complete the tooth can be orthodontically
moved into its original position

 Intentional replantation
 if the practitioner is confident that the resorbed root will not
fracture on extraction
 with or without re-intrusion

122. External Approach/Internal Approach
 elective endodontic therapy is often the best choice in extensive
lesions
 A flap is raised and the granulomatous tissue is aggressively
removed from the bony defect only
 A barrier membrane is used
 To stop new tissue from growing into the root
 To stop revascularization of the necrotic tissue left inside the root
 After approximately one month, an opening is made externally
above the attachment and the necrotic granulomatous tissue is
removed and replaced with a filling material
 mineral trioxide aggregate (MTA)
 Indication
 Opening of the root defect is small
 If opening into the root is large
 the treatment plan should be re-assessed with extraction an option if a
large periodontal defect is to be expected after surgery

123. Internal Approach
 Not predictable enough in these extensive cases
 Should not be considered

124.  offer poor prognosis
 extraction and replacement
with an implant or fixed bridge
is the preferred approach

125.  A 22-year-old woman entered the clinic with a major
complaint of a discoloring upper right lateral incisor.
The patient had undergone intracoronal bleaching
treatment 3 years previously in her upper right central
incisor
 The intracoronal bleaching procedure was performed
with a mix of sodium perborate and 3% hydrogen
peroxide , resulting in overbleaching to allow better
color matching with time.
 The current clinical examination of the upper lateral
incisor tooth revealed a significant change in the color
of the cervical area of the tooth

126.  A periapical radiograph showed a significant
cervical radiolucent lesion, which led to the
diagnosis of a class 3 ICR lesion
 Tooth vitality tests produced positive and
normal results and a probe was used to
confirm the presence of a marginal bone defect
(examined under local anesthesia).
 The existence of a large labial-cervical defect
led to the clinical diagnosis of ICR.

127. Radiographic view presenting a
process of cervical resorption in the
maxillary right lateral incisor.
Frontal view of maxillary right
lateral incisor 3 years after
treatment of
the adjacent central. Note the
cervical discoloration

128.  A limited labial flap was raised, revealing a large
resorption lesion with soft tissue growing into the
tooth. The lesion borders included the cementoenamel
junction and down to the cervical part of the root.
 The lesion was cleaned with a slow speed handpiece,
exposing sound tooth material on all aspects, while
maintaining the pulp’s integrity and vitality.
 The lesion was sealed with a temporary filling material
(IRM; Dentsply, Tulsa, OK), and the flap was repo-
sitioned, with hidden sutures secured to the palatal
tissue

129. Flap elevation of the cervical
lesion. Note the granulation tissue.
After removal of the granulation
tissue.

130.  Following the patient’s request, all efforts were made
to keep the tooth. Therefore, it was decided to try and
pull the root rapidly from within the alveolar socket by
using orthodontic extrusion combined with
fiberotomy.
 The patient received all the necessary information
including the risks and the immediate need for a root
canal treatment before onset of movement .
 The orthodontic movement pulled the tooth from
within the alveolar socket successfully, rapidly
bringing the lesion out of the bone above the crest.
Fiberotomy was performed twice during the
movement, and the temporary restoration material was
replaced with a glass ionomer filling material when the
lesion’s apical borders could be controlled

131. Orthodontic root extrusion,
onset of movement. After second fiberotomy procedure.
Note exposed gingival lesion
borders

132. Radiographic view close to end
of movement

133.  The tooth was then secured to the adjacent teeth
for a retention period of 3 weeks, and after this
stabilization period, a provisional acrylic
restoration was provided.
 Tooth mobility was examined and found to be
acceptable, and after a comprehensive evaluation
,it was decided to continue and prepare a crown
for that tooth.
 A composite post and core restoration was
prepared indirectly on healthy and sound tooth
margins that were cleaned carefully with 90%
trichloroacetic acid.

134.  After cementing the composite post and core, a second
provisional acrylic restoration was prepared to enable
full tissue maturation after the orthodontic process
Impressions were taken for the fabrication of a
zirconium coping.
 The coping’s accuracy was checked and sent for
porcelain layering. The final result fully met the
patient’s expectations .
 The restored tooth is examined as part of the patient’s
periodic maintenance and shows properly healed
tissues and uneventful function

135. Occlusal view of root prepared
for a post and core, leaving
sound dentin treated with TCA
Follow-up at 42 months: clinical
and x-ray examination.

136. Prevention
 Nonvital bleaching
 Protection of the dentinal tubules
 Remove the gutta-percha apical to the cervical line to remove
discolored dentin, but do not extend the preparation into the
root. Use the crestal bone as a guide.
 Place a layer of cement (IRM, Cavit, glass ionomer) to prevent
ingress of the bleaching agent apically and into the cervical
dentinal tubules
 Use of calcium hydroxide beneath the access restoration
 Do not use heat
 30% hydrogen peroxide activated with heat damages the
cementum layer through the dentinal tubules

137.  Avoid etching the dentin
 Some techniques suggest etching of the dentin before
bleaching; however, a recent study showed similar bleaching
results with and without etching
 Do not use Superoxol as it is caustic
 Some advocate sodium perborate (USP) and water for the
walking bleach and report excellent results with no history of
external resorption
 Others showed in vitro the effectiveness of sodium perborate
and water as a bleaching agent, though it took longer to work
 Use of Carbamide peroxide for intracoronal
bleaching

138.  Orthodontic therapy
 All orthodontic forces, in particular tipping forces,
should be as light as possible
 in order that they do not crush the attachment apparatus while
the tooth is being uprighted
 Surgical procedures
 Avoid surgical procedures, including excessive use of
surgical elevators
 Surgical procedures that could damage the cervical
margin, for example the canine wire lasso, before the
orthodontic movement of an impacted canine should
not be used; rather, surgical exposure and banding
with acid etch and resin should be used to facilitate
coronal movement
 Periodontal procedures
 Avoid procedures that leave the root surface denuded

140.  Pressure
 orthodontic tooth movement
 impacted teeth
 tumors
 Orthodontic tooth movement
 In most cases, 'controlled' trauma
 pressure is spread evenly over a root area
 minimizing the inflammatory response
 favors resorption of the bone rather than the root
 In rare cases
 pressure is localized to the apical region
 cause cemental damage and apical root resorption.
 considerable shortening of the root
 Orthodontic root resorption
 'sterile' inflammation

141.  1st comprehensive study on root resorption
after orthodontic treatment by Ketcham
 2 types of root resorption in connection with
orthodontic treatment
 Small superficial resorptions that undergoes repair
 Resorption in the apical area which leads to
permanent root shortening
 Superficial resorption
 Frequently preceded by the hyalinization of the
periodontal ligament

142. Clinical features
 Asymptomatic.
 Shortening of roots.
 Pulp is usually vital.
Radiographs
 Resorption seen in apical third.
 no radiolucency observed in bone or root

144.  Root resorption due to orthodontic pressure has
always been considered to be external root resorption.
However, this is not necessarily true. Damage takes
place at the apex of the tooth near the cemental-
dentinal junction due to the orthodontic pressure.
Therefore, protective damage can be either cementum
or predentin. Because the predentin can also be
affected, it is not unusual to see radiographic evidence
of internal apical resorption during the active stage of
the process. In 1997, Bender et al. suggested the term
periapical replacement resorption (PARR) for
describing this type of resorption

145.  Pressure resorption due
to orthodontic
treatment. A. Teeth at
the start of orthodontic
treatment. B. Severe
root resorption on the
left central incisor after
orthodontic treatment.
Note that, even though
considerable resorption
has taken place,
favorable healing at the
apex with cementum
can be seen. (Courtesy
Dr IB Bender)

149.  Healing of Orthodontically Induced Root Resorption by Ultrasound
in Man
 ULTRASOUND
 Root resorption is one of the adverse outcomes of orthodontic tooth
movement
 It compromises the crown-root ratio
 leads to increased malpractice litigation against orthodontists
 Previous researches have shown that Low-intensity pulsed
ultrasound (LIPUS) can enhance healing of traumatized different
types of connective including dental tissues without any adverse
effect
 SEM study showed statistically significant decrease in number and
the area of resorption lacuanae in the LIPUS treated premolars.
 Histological examination revealed healing of the resorped root
surface by deposition of new cellular reparative cementum. Also,
LIPUS application enhances the formation of more cementum
deposition on top of the regular old cementum.
 May provide a valuable and clinically acceptable method for
minimizing orthodontically induced root resorption in human.
(T. EL-BIALY and I. ELSHAMY, 2003)

150.  For impacted teeth or tumors, the resorption
will occur wherever the pressure from the
impaction/tumor occurs
 Usually slow growing lesions- Cysts,
ameloblastoma, fibro osseous lesions and giant
cell tumours.
 Tooth asymptomatic, pulp is vital
 Treatment is relatively easy, in that removal of
the source of the pressure will result in the
cessation of resorption in the majority of cases

152.  According to shafer- Internal resorption is an
unusual form of tooth resorption that begins
centrally within the tooth , apparently initiated
in most cases by a peculiar inflammation of the
pulp.
Features
 rare in permanent teeth
 Pulp usually remains vital
 characterized by an oval-shaped enlargement of the root canal
space
 Typically asymptomatic and discovered on routine radiographs
 Pathognomic feature is pink spot appearance of tooth.

153.  Etiology
 Presence of chronic inflammatory tissue in the pulp
 pulp tissue becomes inflamed due to an infected coronal
pulp space
 Traumatic injuries
 Iatrogenic injuries
preparation of tooth for crown
deep restorative procedures
application of heat over pulp
pulpotomy using ca(oh)
 Idiopathic

154. Internal resorptive lesions
 The margins are smooth and
clearly defined
 Their distribution over the
root is symmetrical but may
be eccentric
 The radiolucency is of
uniform density
 The pulp chamber or canal
cannot be followed through
the lesion
 The walls of the root canal
system may appear to balloon
out
External resorptive lesions
 The borders may be ill defined
 Their distribution is not
symmetrical and may occur
on any root surface
 There may be variations in
radio –density in the body of
the lesion
 If the lesion is superimposed
on the root canal system, it
should be possible to follow
the canal walls unaltered
through the area of the defect
GARTNER ET AL 1976

155.  The odontoblastic layer and predentin are lost or
altered
 Trauma frequently has been suggested as a cause
 Luxation injuries 2%
 2 types
 transient type
 progressive type requiring continuous stimulation by
infection

156.  Radiographic appearance
 fairly uniform radiolucent
enlargement of the pulp canal
 original outline of the root canal
is distorted
 Usually bone changes not
evident
 rare occasions adjacent bone show
radiographic changes
 when the internal resorptive defect
penetrates the root and impacts the
periodontal ligament

157.  Treatment
 Nonsurgical endodontic treatment
 Placement of intracanal medicaments
 Calcium hydroxide
 Obturation using a softened gutta-percha techniques
 Surgical treatment in rare cases
 extremely large internal resorptive defects in the apical part of
the canal
 surgically remove the defective root
 place an endodontic implant in order to maintain stability of the
tooth

159. Etiology
 Low grade irritation of pulpal tissue
 Chronic irreversible pulpitis
 Partial necrosis
 Absent or damaged odontoblastic layer and
predentin
 Trauma
 Application of extreme heat to the tooth

160.  Pathophysiology
 Resorption of dentin
 Subsequent deposition of hard tissue that resembles bone or
cementum but not dentin
 Clinical evaluation
 Typically asymptomatic
 May respond within normal limits to thermal or electric pulp
test
 Radiographic evaluation
 Generally appears as enlargement of canal space
 Discontinuity of the normal canal space
 Engorged with a less radiodense material at later stage.

161.  Histologic evaluation
 normal pulp tissue replaced by a cancellous type of
hard tissue
 Continuous formation of bone or osteodentin
 Gradual enlargement of the pulp space
 Variations
 Internal tunneling resorption
 Arrest of resorptive process
 Complete pulp canal obliteration
 Treatment
 Nonsurgical root canal therapy

162. Internal inflammatory resorption
Progresive loss of dentin is present without the deposition of
any form of hard tissue in the resorption cavity
 Etiology
 Chronic inflammation of pulp
 Most commonly found in the cervical region
 Pathophysiology
 Progressive loss of root substance without depositin of hard tissue
in the resorption cavity
 Clinical evaluation
 Generally asymptomatic
 Pain if perforation occurs
 Usually coronal pulp is necrotic
 Can be of 2 types
 Transient
 Progressive

163.  Transient type
 Frequently in traumatized teeth that has undergone
orthodontic/periodontic treatment
 Only loss of odontoblasts and predentin
 Is very shallow
 Is self limiting
 Repaired with new hard tissue
 Progressive variety
 Ongoing stimulation by bacteria

164.  Radiographic evaluation
 Appears as a circumscribed ,oval enlargement continuous with
the root canal wall
 Histologic evaluation
 Normal pulpal tissue is present
 Transforms into granulomatous tissue with giant cells that resorb
the predentin of the root canal
 Necrotic zone containig bacteria usually found coronal to
resorbing tissue
 Treatment
 Perforation absent
 Nonsurgical root canal therapy
 Perforation present
 Root canal therapy
 Access for repair
 Periodontal procedure
 Root extrusion

165.  Internal root resorption has been described as
intraradicular or apical accordingto the location in
which the condition is observed . (shanon patel,
dominico ricucci JOE july 2010)
Intraradicular internal resorption
 is an inflammatory condition that results in
progressive destruction of intraradicular dentin and
dentinal tubules along the middle and apical thirds of
the canal walls.
 The resorptive spaces might be filled by granulation
tissue only or in combination with bone-like or
cementum-like mineralized tissues.
 The condition is more frequently observed in male
than female subjects

166.  Compared with intraradicular internal resorption,
apical internal resorption is a fairly common
occurrence in teeth with periapical lesions.

167. Chemomechanical Debridement of the Root Canal
 Ultrasonic activation of irrigants after mechanical
preparation of root canals has been shown to reduce the
number of bacteria.
 Given the inaccessibility of internal root resorption lesions
to chemomechanical debridement, ultrasonic activation of
irrigants should be viewed as an essential step in the
disinfection of the internal resorption defect
 However, even with the use of ultrasonic instruments,
bacteria might still remain in confined areas
 Thus, an intracanal, antibacterial medicament should be
used to improve disinfection of the inaccessible root
resorption defects

168.  Calcium hydroxide is antibacterial and has been shown to
effectively eradicate bacteria that persist after chemomechanical
instrumentation.
 Calcium hydroxide has also been shown to have a synergistic
effect when used in conjunction with sodium hypochlorite to
remove organic debris from the root canal
 Nevertheless, some case reports demonstrated the inability of
calcium hydroxide to eliminate bacteria in ramifications because
of its low solubility and inactivation by dentin, tissue fluids, and
organic matter.
 Despite these limitations, the use of multiple calcium hydroxide
dressings has been advocated to enhance chemomechanical
debridement of the internal root resorption defects.

169. Obturation of the Root Canal
 The primary objective of root canal treatment is to
disinfect the root canal system. This is followed by
obturation of the disinfected canal with an appropriate
root-filling material to prevent it from reinfection.
 By their very nature, internal root resorption defects can
be difficult to obturate adequately. To completely seal
the resorptive defect, the obturation material should be
flowable.
 Gutta-percha is the most commonly used filling
material in endodontics

170.  thermoplastic gutta-percha techniques are significantly
better in filling resorptive cavities.
 In situations when the root wall has been perforated,
mineral trioxide aggregate (MTA) should be considered the
material of choice to seal the perforation.
 MTA is biocompatible and has been shown to be effective in
repairing furcation perforations andlateral root perforations
 The material is well-tolerated by peri-radicular tissues and
has been shown to support almost complete regeneration of
the periodontium.
 In addition, MTA has superior sealing properties when
compared with other materials.

171.  A hybridtechnique might also be used to obturate
canals; the canal apical to the resorption defect is
obturated with gutta-percha, and then the resorp-tion
defect and associated perforation are sealed with MTA
 When internal resorption has rendered the tooth
untreatable or unrestorable, extraction is the only
treatment option.

174.  Can occur
simultaneously on
the same tooth
 May appear on
separate or joined
defects
 May eventually
communicate

176.  Features
 Temporary phenomenon in which the apex of the tooth displays
the radiographic appearance of resorption
 Invariably followed by surface resorption and / or obliteration of
pulp canal
 Injured periradicular tissue generally returns to normal following
repair 1 year after trauma
 Breakdown process is related to
 Type of injury
 Stage of root development
 Only found in teeth
 with fully formed roots
 With closed or half - closed apices

177.  Etiology
 Moderate injuries to the
pulp
 Subluxation
 Extrusion
 Lateral luxation
 Moderate combined injury
to the peridontal ligament
and the pulp in mature
teeth
Other causes
 Infections
 Orthodontic treatment
 Occlusal insult to the
periodontium

178.  Radiographic evaluation
 Transient localised change in the size of the apical
periodontal ligament space
 Blunting of the apex from surface resorption
 Pulp canal obliteration may be seen
 Treatment
 No treatment

180.  Etiology
 Even with systemic diseases that cause bone
resorption, roots of teeth show remarkable resistance;
unless associated with
 Hormonal disturbances
 Renal dystrophy
 Increased oxalate concentration in blood
 Precipitation in hard tissues
 Cause resorption
 Genetic factors
 Resorption of no apparent cause seen in members of the same
family

181.  Systemic diseases and endocrine disturbances
 Hypoparathyroidism
 Calcinosis
 Gaucher’s syndrome
 Hyperparathyroidism
 Turner’s syndrome
 Paget’s disease (osteitis deformans)
 Herpes zoster
 Following radiation therapy

182.  Features
 Resorption in systemic disturbances
 usually occurs at the apex of several teeth
 is bilateral
Morse 1974
 Treatment
 Treatment of underlying systemic disease may cause
resorption to cease