Root resorption/ dental courses

• INDIAN DENTAL ACADEMY
• Leader in continuing Dental Education
www.indiandentalacademy.com

Studies suggest that:
• 1-16% of all maxillofacial trauma cases
account for Exarticulation / Avulsion
cases.
• Luxation injuries account for about 17% of
all dental injuries.

Unfortunately, the common forms
of dental trauma accounting for root
resorption include:
• Avulsions ( Most common).
• Severe forms of luxation injuries:
 Intrusive Luxation.
 Extrusive Luxation.
• Rarely other forms of dental trauma.

Factors common to these forms of
dental trauma
• Damage to the “ Attachment apparatus”.
• Insult to the “Dental pulp”.

SEQUENCE OF EVENTS LEADING
TO ROOT RESORPTION
CRUSHING / DAMAGE TO THE PDL
LOSS OF PRECEMENTUM LEADING TO
DENUDATION OF ROOT SURFACE
CHEMOTAXIS OF HARD
TISSUE RESORBING CELLS
MACROPHAGES AND
OSTEOCLASTS REMOVE DAMAGED
PDL AND CEMENTUM

The situation gets further
complicated by:
• Eventual exposure of dentinal tubules.
• Contents of the pulp i.e. Ischemic and
sterile or necrotic and infected.
• Presence/Absence of adjacent vital
cementoblasts.

Key cells and factors involved:
• Monocytes and macrophages
• Osteoclasts
• Odontoclasts

MONOCYTES AND MACROPHAGES:
• Initially monocytes are
recruited to the site of injury
by the release of pro-
inflammatory cytokines.
• These subsequently
differentiate into
macrophages.
• These macrophages are
similar to osteoclasts except
that they lack a ruffled
border. www.indiandentalacademy.com

OSTEOCLASTS:
• Derived from the
hemopoietic cells of
the monocyte-
macrophage lineage,
with a life span of
about 2 weeks.
• Multi-nucleated giant
cells ( 20 to 30
nuclei) , formed from
the fusion of
mononuclear
precursors.

ODONTOCLASTS:
• Similar to the osteoclasts.
• Contain fewer nuclei than the osteoclasts.
• Cells with a fewer nuclei, greater is the
dentinal resorption.

The resorption process is bimodal :
• Dissolution of the inorganic crystal
structure.
• Degradation of the organic structure of
collagen, principally type I.

Dissolution of the inorganic crystal
structure.
• pH levels below 5 , facilitate rapid
dissolution of hydroxyapatite.
• Polarised proton pump along the ruffled
border and the enzyme carbonic
anhydrase II play an important role.

Degradation of the organic structure
Three groups of proteinase enzymes are
involved:
• Collagenases
• Matrix metalloproteinases ( both act at
neutral pH ) and
• Cystene proteinases ( act at acidic pH).

ROOT RESORPTION
INJURY
STIMULATION

INJURY
• Mechanical
• Chemical
• Surgical
“Concerns the non-mineralized tissues
covering the external ( pre-cemental ) surface
of the root or the internal (pre-dentinal) surface
of the root”

STIMULATION
• Nature of cells present:
* At the time of injury.
* Site of injury.
• Site of tooth involved (Cemental or
Dentinal)
Concerns a wide array of factors like:

“ Resorption is a condition
associated with either a
physiologic or a pathologic
process resulting in loss of dentin,
cementum or bone”
Am. Assn of Endo.

Need for a classification
system:
“Apical Root Resorption”
1. Orthodontic treatment.
2. Inflammatory Root Resorption
following trauma.

Classification system based on
clinical presentation:
1. Pulpal infection root resorption.
2. Periodontal infection root resorption.
3. Orthodontic pressure root resorption.
4. Impacted tooth or tumor pressure root
resorption.
5. Ankylotic root resorption.
6. Idiopathic root resorption.

Classification system based on
histopathological presentation:
1. Internal root resorption.
# Metaplastic resorption.
# Inflammatory resorption.
2. External root resorption.
# Surface resorption.
# Inflammatory resorption.
# Replacement resorption.
3. Invasive root resorption.

INTERNAL RESORPTION
ETIOLOGY: Damage to the predentinal
(inner) surface of the root and bacteria.
KEY FACTOR: Needs good vascular supply
to continue.
TYPES:
1. Root canal replacement
(metaplastic) resorption.
2. Internal inflammatory resorption.www.indiandentalacademy.com

Root canal replacement (metaplastic)
internal resorption.
• Low grade localised pulpal irritation such as
chronic irreversible pulpitis or partial necrosis.
• Trauma.
• Thermal insult.
ETIOLOGY:
It involves resorption of dentin and a
subsequent deposition of hard tissue that
resembles bone or cementum, but not dentin.

Clinical evaluation:
• Tooth remains asymptomatic and responds
normally to thermal or electric pulp testing.
• The condition becomes painful if the process
perforates the root or crown of the tooth.
Radiographic appearance:
• Enlargement of the canal space, including
discontinuity of normal space.
• This space is engorged with a less radiodense
material, giving the appearance of partial canal
obliteration. www.indiandentalacademy.com

Histologic evaluation:
• Gradual enlargement of pulp space because of
continuous formation of bone or osteodentin at
the expense of dentin.
• The normal pulp tissue is replaced by a
cancellous type of hard tissue.
VARIATIONS:
• Internal tunneling resorption.
• Pulp canal obliteration.

Metaplastic root resorption

Internal inflammatory resorption
Chronic irritation of pulp tissues when bacteria
and their components enter the root canals via
dentinal tubules that are exposed by mechanical
damage.
It involves progressive loss of root substance
without subsequent deposition of hard tissue
in the resorption cavity.
ETIOLOGY:

TYPES OF INTERNAL ROOT RESORPTION:
• Transient is self
limiting and is
repaired
presumably with
new hard tissue.
• Progresses till most of
the dentin gets
involved and
overtakes the
remaining vital pulp
tissue thus leading to
deprivation of the
tissue of the much
needed blood supply.
1 Transient
2 Progressive.

Diagnosis:
• Usually these teeth remain asymptomatic
and usually respond to pulp testing.
• The extensively internally resorbed teeth
show a typical “PINK” hue (Pink Tooth).
• Radiographically typically present as an
oval, circumscribed defect in the internal
wall of the root canal.

Inflammatory internal root
resorption

Histopathology:
• Normal pulp tissue with multinucleated
giant cells.

EXTERNAL ROOT RESORPTION:
Typically the external morphology of the
root is affected , unlike IRR where the
internal root canal morphology is
affected.
Types:
1) Surface resorption.
2) Inflammatory resorption.
3) Replacement resorption.

SURFACE RESORPTION
ETIOLOGY: Damage to the precemental
(outer) surface of the root and bacteria.
KEY FACTOR: Though vascularity seems to
be abundant, the key is the bacterial infection
from the pulp.
TYPES:
1.Transient
2.Progressive.www.indiandentalacademy.com

Features of Transient Surface Resorption:
• The most favorable and uncomplicated
mode of healing of traumatized teeth.
• Usually undetectable clinically and
radiographically.

INFLAMMATORY ROOT
RESORPTION
Contributory factors:
1. Injury to the periodontal ligament.
2. Initiation of Surface Resorption.
3. Establishment of communication between
the pulp and external root surface.
4. Patent dentinal tubules.
It is a clinical manifestation of progressive surface
resorption. Best described as a BOWL shaped
resorptive defect that penetrates dentin.

Diagnosis:
• H/o trauma ( Recent or longstanding)
• Clinical finding of Irreversible pulpitis (rarely) or
Pulp necrosis.
• Tooth mobility associated with tenderness.
• Dentoalveolar resorption radiographically.
Inflammatory root resorption can initiate and
involve the root extensively , in a duration as short
as 4-6 weeks.

INFLAMMATORY ROOT
RESORPTION

REPLACEMENT RESORPTION
KEY FACTOR: Colonisation of the damaged root
surface by osteoblasts, absence of vital
cementoblasts.
TYPES:
1.Transient
2.Progressive.
The root surface undergoes remodelling, until
all of it is replaced by bone.

TYPES OF REPLACEMENT ROOT
RESORPTION:
• Transient is self
limiting and involves
less than 20% of the
root area.
• Progresses till most of
the root is replaced by
bone. Should involve
atleast 30% root
surface to be branded
as Progressive
Replacement
Resorption.

REPLACEMENT
RESORPTION

INVASIVE/ CERVICAL
RESORPTION
“ a type of resorption that involves the cervical
area of a tooth below the epithelial attachment
and often proceeds from a small surface
opening to involve a large part of dentin between
the cementum and the pulp.”

INVASIVE/ CERVICAL
RESORPTION

Contributory factors:
1. Injury to the cementum apical to the
epithelial attachment.
2. Bacterial stimulation originating from the
periodontal sulcus.
Injuries:
Dental trauma.
Chemical insult Eg: Bleaching
Orthodontic treatment.
Periodontal procedures.
Dentoalveolar surgery.
Secondary bone grafting.

Pink Hue

PRESSURE RESORPTION
1. Orthodontic forces.
2. High occlusal forces.
3. Pressure from impacted, supernumerary teeth
etc.
4. Pressure from tumors and cysts.
This is also a form of external inflammatory root
resorption.
ETIOLOGY:

PRESSURE RESORPTION

KEY FACTORS:
• Pulp not involved, atleast initially.
• Resorption arrests on withdrawl of
stimulus.

IDIOPATHIC RESORPTION

Transient apical breakdown
• The tooth is often asymptomatic and responds
normally to vitality tests.
• Radiographically a transient change in the size of
the apical pdl space,ranging from two times the
normal width to a semicircular radiolucency,
combined with a blunting of the apex from
surface resorption may be observed.
It is a temporary phenomenon in which the apex
of the tooth displays the radiographic appearance
of root resorption that is linked to the repair
processes of a traumatically injured pulp and/ or
periodontium of a luxated mature tooth.

Transient apical breakdown

Combination of external and
internal resorption

Revisiting the clinical classification:
1. Pulpal infection root resorption.
# Internal resorption
# External resorption.
2. Periodontal infection root resorption.
# Invasive/ Cervical resorption.
# Rarely External resorption ( Indirectly).
3. Orthodontic pressure root resorption.
4. Impacted tooth or tumor pressure root resorption.
5. Ankylotic root resorption.

Management Strategies
“Prevention is better than Cure”

MANAGEMENT GUIDELINES:
Delay root resorption.
Prevent root resorption.
Delay root resorption:
• Application of stannous fluoride prior to
replantation of an avulsed tooth.

Prevent root resorption
• Identify and eliminate the strategic
underlying cause.
Eg: Pulpal infection, Periodontal Infection.
• Promote ideal healing
Eg: Repair by formation of new cementum.

Current strategies in managing root
resorption:
1. Calcium Hydroxide.
2. Calcium Hydroxide with IKI or
electrophoretically activated copper.
3. Enamel Matrix Derivatives.
4. Topical Alendronate.
5. Activ Point ( 5% chlorhexidine).
6. Calcitonin.

Mechanism of action of Calcium Hydroxide:
• Strong antibacterial effect.
• High pH, inhibits the activity of osteoclastic
acid hydrolases in the in the pdl tissues
and activates alkaline phosphatases.
• Prevents dissolution of the mineral
component by necrotising the cells of
resorption lacunae .

Enamel Matrix Derivative
• Based on the idea by
Slavkin & Boyde that
enamel matrix proteins from
Hertwig’s epithelial root
sheath initiate formation of
cementum (Primary
acellular cementum).
• EMDOGAIN, is a
commercially available
porcine enamel matrix
derivative.

Topical Alendronate
• Alendronate is a third generation
biphosphonate commonly employed to
treat diseases like osteoporosis, Paget’s
disease or other osteolytic malignancies.

Possible mechanisms of action of
alendronate
1. Decrease in osteoclastic activity with minimal
effects on recruitment.
2. The interference of receptors on the
osteoclasts for specific bone matrix proteins.
3. Promoting the production of an osteoclast
inhibitor, thus reducing the life span of
osteoclasts.
4. Obstructing resorption by interfering with the
ruffled border.

ACTIV POINT
• It is an intracanal medicament containing
5% Chlorhexidine.
• Has strong anti-bacterial effect upto
depths of 500µ.

CALCITONIN
• Calcitonin, is a hormone produced by the
thyroid gland and is a potential inhibitor of
osteoclastic bone resorption.
• They used porcine calcitonin paste.
• Has scope for use in cases of
IDIOPATHIC RESORPTION.

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Root resorption/ dental courses

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