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Tooth resorption
Resorption is a condition associated with either a physiologic or a pathologic process
resulting in a loss of dentin, Cementum or bone.
Etiology
Traumatic luxation injuries
orthodontic tooth movement
chronic infections of the pulp or periodontal structures.
Process
Similar to that of bone resorption.
Involves an elaborate interaction among inflammatory cells, resorbing cells, and hard
tissue structures.
The clastic cell is the key cell type responsible for all hard tissue resorptive processes. It
is joined by cells like Macrophages and Monocytes in resorptive activities. Collectively, these cells
orchestrate a complex interplay of molecular biologic events, involving cytokines, enzymes, and
hormones, that influence the resorptive activity.
key cells and factors involved in the mechanisms of resorption
Monocytes macrophages, osteoclasts,
they are found in tissue sections adjacent to bone-resorbing surfaces of rheumatoid arthritis,
periodontal disease, peri-radicular granulomas and cysts, and in metastatic bone tumors.
Interaction of Monocytes- cytokines- macrophages ( whose major role is wound
debridement).
Although macrophages have a structure similar to that of osteoclasts and, like
osteoclasts, can also become multinucleated giant cells, macrophage lake a ruffled border that is
attached to hard tissue substrate during resorption and do not create lacunae on the dentinal surface.
Osteoclasts
Bone-resorbing cells derived from hemopoietic cells of the Monocytes-macrophage
lineage
life span of approximately 2 weeks
active cell and has ability to move between resorbing sites
highly vacuolated and have numerous mitochondria (20 to 30 nuclei)
characterized by specialized membrane structures, clear zones, and ruffled borders.
found in tiny depressions, pits or irregular grooves, termed Howship lacunae.
Resorptive mechanism
Establish a microenvironment between the ruffled border and the bone in which resorption
takes
process is bimodal-involving the degradation of the inorganic crystal structure of hydroxyapatite
and the organic structure of collagen, principally type I.
The activated osteoclasts produce an acidic pH (3.0 to 4.5)
at Ph 5.0 or lower, the solubility of hydroxyapatite increases dramatically, and re-sorption of
hard tissue can occur.
Acidic environment is primarily achieved through the action of a highly active polarized
proton pump contained within the ruffled border.
Osteoclasts
contain enzyme carbonic anhydrase II (CA II) -specific to osteoclasts,
CA II catalyzes the intracellular conversion of CO2, to H2 CO3---provides a readily available
Source of H+ ions to be pumped into the subosteoclastic region.
organic matrix degradation
accomplished by three groups of proteinase enzymes:
collagenases
matrix metalloproteinase's (MMP)
both act at neutral or just below neutral pH (7.4)
cysteine proteinase family
act at an acidic pH.close to the ruffled border
Systemic regulatory factors
Parathyroid hormone (PTH)
active at the resorbing surface
1.25-dihydroxyvitamin D3 -calcitonin
PTH- promote bone resorption by increasing both the number of cells present and the rate of
activity among individual clastic cells- multifactor.
1.
Stimulation of osteoblasts using a receptor-mediated, cAMP-dependent pathway to
increase the production of neutral proteases and to decrease the amount of protease inhibitor and
matrix deposition.
2.
Direct action on the osteoclasts to increase CA II activity by cAMP-mediated
phosphorylation of the enzyme.
3.
Promotion of the fusion of marrow cells, leading to the formation of the multinucleated
giant cell of osteoclastic phenotype.
Systemic regulatory factors
D3 -increase the resorbing activity of osteoclasts
Calcitonin- inhibits resorption by inhibiting cytoplasmic motility and producing cell retraction.
Local regulatory factors
macrophage colony-stimulating factors:
(M-CSF),(IL-1),(IL-6),(IL-11) and (TNF-α)
Macrophage colony-stimulation factor is probably the most important soluble factor.
Interleukin-6 acts on osteoblastic stromal cells to induce osteoclast differentiation
factor.
Interleukin-1 was one of the first bone-resorbing cytokines to be identified .
The major effect of TNF-α on hard tissues is to stimulate osteoclastic activity
Bacteria-induced resorption
Produce acids and proteases
production of osteolytic factor.
Odontoclasts
dissimilarities with osteoclasts
smaller in size
have a ruffled border
contain fewer nuclei
have smaller or no clear zone
Similarities with osteoclasts
enzymatic properties
intense tartrate-resistant acid phosphatase activity.
types
Mononuclear odontoclasts 4% -participate in tooth resorption.
Multinucleated odontoclasts 94% -form lacunae on the dentin. Having 10 or fewer nuclei.
Oligonuclear odontoclasts (cells with fewer than five nuclei) resorb more dentin per nucleus than do
cells with a higher number of nuclei
Types of tooth resorption
Internal resorption
external resorption
combined internal and external resorption.
Internal resorption
Rare in permanent teeth
asymptomatic discovered during a routine radiographic examination.
types :
root canal replacement resorption
internal inflammatory resorption
Root canal replacement resorption (metaplastic resorption)
Etiology: Low-grade irritation to pulp
localized to small area of the root canal
resorption of the dentin deposition tissue that resembles bone or Cementum but not dentin.
Clinical evaluation: Asymptomatic can become painful if perforate.
Radiographic evaluation: Enlargement of canal.
Histological evaluation: Pulpal tissue is replaced by a cancellous tissue.
Variations: Internal tunneling resorption.
Treatment: RCT / Critical that the pulp and granulation tissue with odontoclasts be removed to
arrest.
Internal inflammatory resorption
Etiology: progressive loss without deposition of hard tissue. Chronic inflammation of the
pulp. Most commonly, internal resorption is found in the cervical region.
Clinical evaluation: may be symptomatic
the process of resorption is active only if part of the pulp remains vital; therefore, pulp testing
can be positive. However, usually the coronal pulp is necrotic while the apical pulp is vital, resulting in a
non-responsive test.
Can be transient or progressive. The transient type of resorption occurs frequently in
traumatized teeth or in teeth that have undergone orthodontic or periodontal treatment. While
progressive is via tubules.
Radiographic evaluation: Circumscribed, oval enlargement (radioleucency) continuous with the
root canal wall,
Histological evaluation: A necrotic zone containing bacteria is usually found coronal to
resorbing tissue.
Treatment: Non-surgical root canal therapy.
External resorption of teeth
type
1. External surface resorption
2. External inflammatory root resorption
3. Ankylosis
4. Replacement resorption.
External resorption can be differentiated from internal resorption by its radio-graphic
presentation.
External surface resorption
Transient phenomenon
spontaneous destruction and repair in all teeth
likely normal physiologic response
self limiting process
requires no treatment
Etiology indirect physical injury-physiological.
trauma.
Histologic evaluation- small lacunae in Cementum
radiographic evaluation- when visible, it appears as small excavations on the root surface with normal
lamina dura and periodontal space.
Treatment- nil
External inflammatory root resorption (EIRR)
Most common
bowl-shaped
resorptive defect that penetrates dentin and associated with a djacent bony radioleucency.
Typically in the apical area.
Involve any tooth with necrotic pulp.
Replanted teeth that have not had RCT often show these resorptive lesion laterally as well as Apically
etiologyInjury
pressure
pressure-bone lesions
periodontium infection
orthodontic treatment-initiates an inflammatory response cause.
Bacteria, bacterial by-products, and tissue breakdown products from within the root
canal system stimulate inflammation in the adjacent periodontal tissue and lead to aggressive
progressive inflammatory resorption of the root.
cervical resorption
Can occur following injury to the epithelial cervical attachment apparatus and
to the area of the root surface just below the attachment apparatus.
Etiology
All forms of tooth trauma
surgical procedure
Orthodontic treatment
bruxism
periodontal root planning and scaling
Chemical injury- 30% hydrogen peroxide used for internal bleaching- gingival or periodontal tissues can
become irritated as the hydrogen peroxide leaches through cervical dentinal tubules
Apical External inflammatory resorption (EIRR)
etiology
pulp remains vital.
1.Trauma 2.Periradicular periodontitis. 3.Orthodontic treatment in which the
It is hypothesized that the excessive forces initiate inflammation either as a result of stimulation of a
phagocyte process by tissue breakdown products or through some form of Neurogenic inflammation.
The resorption can begin 2 to 12weeds after injury. It progresses rapidly, especially after tooth
re-plantation in patients between the ages of 6 and 10 years.
For resorption to continue, resorbing cells require continues stimulation.
The progressive type of external inflammatory re-sorption occurs when the source of
inflammation is not removed, causing an ongoing resorptive process.
Apical Enternal inflammatory root resorption (EIRR)
radiographic evaluation With EIRR, the periodontal ligament space becomes widened and there
is a loss of adjacent lamina dura and tooth structure.
Treatment of external inflammatory root resorption is dependent on the etiology:
1.
Calcium hydroxide
2.
Post-treatment complications; High rate of recurrence as inflammatory resorption
becomes arrested, ankylosis can occur.
Ankylosis
Ankylosis is union of bone and tooth, with no intervening connective tissue.
Etiology- luxation injuries
Ankylosis can be progressive or transient. The likelihood of progressive ankylosis increases dramatically,
when greater then 20% of the root surface is damaged.
Ankylosis is not a disease process. It occurs as a mistake” because cells involved in the remodeling of
bone are not able to distinguish among root, Cementum, dentin, and bone.
Resorption of root surface-substitution by bone resulting in ankylosis
Resorb tooth structure replaced by bone – ankylosis
RCT has no effect.
Clinically High pitch or metallic tone.
Lose of mobility occurs when more than 10% of the root surface is ankylosed.
RADIOGRAPHICALLY-A complete disappearance of the periodontal space and an uneven root surface
contour is common.
COMPLICATIONS- malocclusion or super-eruption as opposing teeth.
External replacement resorption:
ETIOLOGY
It differs from ankylosis because of the presence of intervening inflamed connective tissue.
CLINICALLY such resorption typically follows an asymptomatic course.
Radio graphically Disappearance of the periodontal ligament space.
treatment this type of resorption usually progresses until where is little or no root left, and tooth
extraction is necessary.
Transient apical breakdown (TAB)
a temporary phenomenon
invariably follows surface resorption or pulp oblitration.The injured peri-radicular tissue
generally returns to normal following repair, which usually takes place 1 year after trauma
Etiology moderate injuries to the pulp, infections, orthodontic treatment , and occlusal insult to the
periodontium.
Radio logically Transient apical break-down can only be found in teeth with fully formed roots and
closed or half-closed apices.
Treatment nil