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DENTAL CEMENTUM
DR.SHRUTI JITENDRA JAISWAL
1st MDS POST GRADUATE
DEPARTMENT OF PERIODONTOLOGY
Contents:
 Introduction
 Development of cementum
 Molecular factors affecting cementogenesis
 Physical characteristics
 Chemical characteristics
 Histology of cementum
 Classification
 Cementodentinal junction
 Cementoenamel junction
 Functions
 Cementum resorption and repair
 Effects of ageing on cementum
 Cementum in oral environment
 Role of cementum in periodontal disease
 Changes in cementum in periodontal pathology
 Effectiveness of root planing
 Developmental anomalies
 Conclusion
 References
INTRODUCTION
HISTOLOGICAL SECTION GROUND SECTION
▪ Begins at the cervical portion of the tooth at the cemento
enamel junction upto the apical foramen.
▪ According to Denton,cementum was first demonstrated
microscopically by Fraenkel and Raschkow (1835) and
Retzius (1836) and has since become a part of general
knowledge in dentistry.
▪ The word cementum originated from the latin word ‘cement’
which means quarried stone.
▪ Anatomically-part of tooth
Functionally-part of periodontium
DEFINITION
▪ Cementum is the calcified, avascular mesenchymal tissue that
forms the outer covering of the anatomic root.
(Carranza 13th south asian edition)
▪ Cementum is a hard, avascular connective tissue that covers the
root of the teeth.
(Ten Cate’s oral histology 9th edition)
▪ Cementum is the mineralized dental tissue covering the
anatomic roots of human teeth.
(Orban’s oral histology and embryology 13th edition)
▪ The cementum is a specialized mineralized tissue
covering the root surfaces and, occasionally, small
portions of the crown of the teeth.
(Lindhe 6th edition)
▪ The thin, calcified tissue of ectomesenchymal
origin covering the roots of teeth in which
embedded collagen fibers attach the teeth to the
alveolus.
(Glossary of Dental Implantology)
Development of cementum
HERS-Corono apical
extension of IEE and
OEE induces the
secretion of enamel
proteins
Facing the
ectomesenchymal
cells of the dental
papilla diffrentiate
into odontoblasts
Odontoblasts start
forming the
predentin
Some cells from the fragmented root sheath form discrete masses
surrounded by a basal lamina k/as Epithelial cell rests of malassez which
persists in the mature PDL.
HERS becomes
interrupted &
ectomesenchymal cells of
inner portion of dental
follicle comes in contact
with the predentin
EM cells of the follicle
receive signals from
dentin & surrounding
HERS cells;diffrentiates
into cementoblasts
Cementoblasts lay down
cemental matrix which
undergoes maturation and
subsequently gets
mineralised resulting into
cementum formation
Enamel
Enamel epithelium
Cemento enamel junction
Dentin
Cementum
Cementoblast
Remnants of epithelial
Root sheath
Periodontal connective
tissue
Molecular factors regulating
cementogenesis
Physical characteristics
▪ Colour-
light yellow in colour
dull surface-lacks lusture
darker hue than enamel
▪ Hardness-
less than dentin
▪ Permeablility-
more permeable than dentin
decreases with age
▪ Thickness-
thinnest at CEJ 20-50 µm
thickest at apex 150-200µm
Chemical characteristics
▪ On dry weight basis,a fully formed permanent teeth consists
of-
Inorganic substance
45-50%
• Calcium phosphate in the form of hydroxy apatite crystals
Ca10(PO4)6(OH)2
• Highest fluoride content
 type I COLLAGEN fiber
 And protein polysaccharide-
proteoglycans,osteopontin,osteonectin,osteocalcin,
osteonectin, fibronectin,bone sialoprotein.
 Other collagen –Type III,V,VI,XII
Suggested Function Related to Cementogenesis
Growth Factors
Transforming
growth factor β
superfamily
(including bone
morphogenetic
proteins)
Reported to promote cell differentiation and
subsequently cementogenesis during
development and regeneration.
Platelet-derived
growth factor
and insulin-like
growth factor
Existing data suggest that platelet-derived growth
factor alone or in combination
with insulin-like growth factor promotes cementum
formation by altering cell
cycle activities.
Fibroblast growth
factors
Suggested roles for these factors are promoting cell
proliferation and migration
and also vasculogenesis—all key events for formation
and regeneration of
periodontal tissues.
Adhesion Molecules
Bone
sialoprotein
Osteopontin
These molecules may promote adhesion of selected
cells to the newly forming
root. Bone sialoprotein may be involved in promoting
mineralization, whereas
osteopontin may regulate the extent of crystal
growth.
Epithelial/Enamel
Proteins
Proteins
Epithelial-mesenchymal interactions may be involved
in promoting follicle cells
along a cementoblast pathway.
Some epithelial molecules may promote periodontal
repair directly or indirectly.
Collagens Collagens, especially types I and III, play key roles in
regulating periodontal
tissues during development and regeneration.
In addition, typeXII may assist in maintaining the
periodontal ligament space
versus continuous formation of cementum.
Gla Proteins
Matrix Gla
protein/bone Gla
protein
(osteocalcin)
These proteins contain γ-carboxyglutamic acid, hence
the name Gla proteins.
Osteocalcin is a marker for cells associated with
mineralization—that is,
osteoblasts, cementoblasts, and odontoblasts—and is
considered to be a regulator
of crystal growth. It has also been proposed to act as a
hormone regulating energy
metabolism through several synergistic functions
favoring pancreatic β-cell
proliferation, increasing insulin secretion (in the
pancreas) and sensitivity in
peripheral tissues, and promoting energy expenditure (in
brown adipose tissue)
and testosterone production by Leydig cells in testes.
Matrix Gla protein appears
to play a significant role in preventing abnormal ectopic
calcification.
Transcription Factors
Runt-related
transcriptionfactor 2
(Runx-2)
Osterix
As for osteoblasts, these may be involved in
cementoblast differentiation.
Signaling Molecules
Osteoprotegerin These molecules mediate bone and root resorption
by osteoclasts.
Receptoractivated
nuclear
factor κB ligand
Receptoractivated
nuclear
factor κB
Sclerostin Antagonist of Wnt and promotes cementum
formation
Wingless-related
integration site
(Wnt)
Regulates stem cell populations and
differentiation of cementoblasts
Cementum-Specific Proteins
Cementum
protein 1
(cementumderived
protein
23)
May play a role as a local regulator of cell
differentiation and extracellular matrix
mineralization.
Histology of cementum
▪ Histologically,cementum shows
a. Cells,fibers,ground substance
b. Cemento enamel junction
c. Cemento dentinal junction
Cementoblasts Cementocytes
Cementoclasts
Cells of cementum
• Cementoblasts
Characteristics-numerous mitochondria,well
formed golgi apparatus,large number of granular
endoplasmic reticulum
Synthesizes collagen & protein polysaccharide
forms organic matrix of cementum
 After the matrix is laid down,it begins mineralisation
 The cells are found lining the root surface
• Cementocyte
 Spider shaped cells -cellular
cementum.
 During the formation of cellular
cementum, cementoblasts get
entrapped within their own
cemental matrix due to rapid
deposition resulting
in the formation of cementocyte.
 Similar to osteocytes,they lie in
lacunae.
 Canalicular processes branch and
anastosomes with adjacent cells.
 These processes are directed
towards PDL.
 Deeper layers of cementum(60µm
from nutrition)cementocytes shows
definite signs of degeneration such
as cytoplasmic clumping,
vesiculation & sometimes empty
lacunae.
Cementoclast
 Found in howship’s lacunae
 Unilocular/multilocular
 Function-resorption of
cementocytes
 Major role-resorption and repair
Incremental lines of salter
▪ These lines represent rhythmic periodic deposition of cementum
▪ Appears as dark lines running parallel
to root surface
 Highly mineralized areas with less
collagen & more ground substance
 Seen in both acellular and cellular
cementum
 Predominantly in acellular cementum
Types of cementum
i.Based on location
a.radicular cementum
b.coronal cementum
ii.Based on cellularity
a.Acellular cementum
b.Cellular cementum
iii.Based on presence of collagen fibers in matrix
a.Afibrillar cementum
b.Fibrillar cementum
ACELLULAR CEMENTUM CELLULAR CEMENTUM
• Primary cementum • Secondary cementum
• Present on cervical 3rd or half • present on apical 3rd of the root
of the root
• cells are absent • cells are present
• forms before the tooth reaches • forms after the tooth reaches the
the occlusal plane the occlusal plane
• more calcified • less calcified
• sharpey’s fibers are main compo • sparse number of sharpey’s fibers
-nent are present
• perpendicular to root surface • parallel to root surface
• rate of development is faster • rate of development is slower
•incremental lines are wide apart • incremental lines are closer
• thickness ranges from 30-230µm • thickness ranges from 150-200µm
iv. Based origin of the matrix fibers
a.extrinsic fiber
b.intrinsic fiber
c.mixed fiber
 Extrinsic fiber-
− Also known as ‘sharpey’s fiber’
− Embedded portion of the principal
fibers of PDL
− Formed by fibroblasts
 Intrinsic fiber
− Belongs to cementum
− Formed by cementoblast
Intrinsic
fibers of
cementum
Mixed fiber
− Composed of extinsic sharpey’s fiber & intrinsic fiber
− Co-product of cementoblast and fibroblast
Mixed fibers of cementum
Schroeder classification(1986)
i. Acellular afibrillar cementum(AAC)
ii. Acellular extrinsic fiber cementum(AEFC)
iii. Cellular mixed stratified cementum(CMSC)
iv. Cellular intrinsic fiber cementum(CIFC)
Acellular afibrillar cementum(AAC)
▪ contains neither cells nor extrinsic or intrinsic
collagen fibers.
▪ only mineralised ground substance.
 product of cementum,seen in crown portion
of tooth
▪ thickness - 1-15µm
▪ no known fuction around CEJ.
 Acellular extrinsic fiber cementum(AEFC)
 densely packed bundles of sharpey’s fiber,
no cells.
 co-product of fibroblast & cementoblast.
 found in cervical 3rd of root,may extend
apically.
 thickness- 30-230µm
 function-anchorage in especially single
rooted teeth.
.
.
 Cellular mixed stratified cementum(CMSC)
▪ composed of both intrinsic & extrinsic
sharpey’s fibers.
▪ may contain cells.
▪ co-product of fibroblast & cementoblast.
▪ function-adaptation & repair
 Cellular intrinsic fiber cementum(CIFC)
-contain cells but no extrinsic collagen fiber.
-formed by cementoblasts.
-fills the resorption lacunae.
Intermediate cementum-
is a poorly defined zone near the cementodentinal junction
of certain teeth that appear to contain cellular remnants of
Hertwig sheath embedded in calcified ground substance.
- seen in apical 3rd of root and apices, & in furcation area.
-thickness- 10-1000µm
-function-adaptation of fibers
Cementodentinal junction
▪ Interface between dentin and
cementum.
▪ In deciduous teeth-scalloped
permanent teeth-smooth.
▪ Areas of dentin adjacent to CDJ
granular in ground substance
due to coalescing and looping the
terminal portion of dentinal tubules
and is called ‘Tomes Granular Layer’.
 Terminal apical area of cementum where it joins
the inteernal root canal dentin.
 During RCT,the obturating material should be at
CDJ.
 No increase /decrease in width(2-3µm)
Cementoenamel junction
▪ It is the preface between cementum & enamel at cervical region
of teeth is variable.
▪ It is also an important landmark as a clinical consideration while
scaling and root planing.
Funtions of cementum
▪ Provides medium for the attachment of collagen fibers of PDL.
▪ Cementum is harder than alveolar bone & is avascular and
doesn’t show resorption on masticatory or orthodontic forces.
▪ Thus during heavy orthodontic forces tooth integrity is
maintained & alveolar bone being elastic in nature changes its
shape,fulfilling orthodontic requirements.
▪ Acts as a covering for root surface, a seal for open dentinal
tubules.
▪ Prevents dentinal tubules from
sensitivity.
Reparative nature
▪ Aid in maintaining the teeth in functional occlusion (in
chronic bruxism, deposition of cementum on apical aspect of
the teeth) [passive eruption].
Cementum resorption and repair
▪ Permanent teeth do not undergo phyioslogic resorption as
primary teeth.
▪ Local factors-
▪ Systemic factors- Ca deficiency,
hypothyroidism,paget’s disease,
Hereditary fibrous
osteodystrophy
▪ Microscopically ,bay-like concavities seen over tooth surface.
Multi nucleated giant cells, mononuclear macrophages are
generally found adjacent to the site of active resorption.
▪ Painless
▪ Reversal line-?
▪ Repair – i.anatomic repair
ii.functional repair
▪ Occurs in vital and non vital tooth both
Effects on ageing in cementum
▪ Becomes irregular due to calcification of some bundle fibers
where they were attached to cementum
▪ Cemental width may increase 5-10 times
(deposition continues after eruption)
▪ Increase in width is greater apically &
lingually
▪ In ageing, a continuous increase of
cementum in apical zone may
result in obstruction of apical
foramen
What happens to cementum when
exposed to oral cavity?
Cementum becomes exposed to the oral environment in cases
of gingival recession and as a consequence of loss of
attachment in pocket formation
The cementum is sufficiently permeable to be penetrated in
these cases by organic substances, inorganic ions, and
bacteria
Bacterial invasion of the cementum occurs commonly in
periodontal disease
 Cemental caries
Clinical considerations
 In periodontal pockets, pathologically exposed cementum,
altered cementum interfere with healing
 Root planing (hypomineralised cementum)
 Cellular cementum- avascular, no nerve supply -scaling
produces no pain, but if cementum is removed, dentin is
exposed causes sensitivity
 Precementum – natural barrier to excessive apical
migration of junctional epithelium
 Biomodification of root surface
Role of cementum in
periodontal disease
The surface on which plaque &
calculus is attached, the role
therapy is to remove these
accretions as a part of the
treatment plan
It forms the inner wall of the
periodontal pocket.
This tissue is relatively static as
compared to surrounding dynamic
tissues, so any change will have
long term effects.
Its intimately involved in all phases
of the PD process so it must be
returned to a healthy state before
any progress in disease control,
soft tissue regeneration & repair.
ROLE OF CEMENTUM IN
PERIODONTAL DISEASE
DCNAVol 24. No. 4, 1980
by Joseph J. Aleo
Changes in cementum associated
with periodontal disease
▪ Structural changes
▪ Pathologic granules in exposed cementum by Bass and Benson
– proven by SEM studies that vacuole like formations exist
▪ Partial demineralisation by Selvig et al
▪ Reprecipiation of dissolved minerals
▪ Decrease or loss of cross banding of collagen
▪ Subsurface condensation of organic material of exogenous
origin
▪ Chemical changes
▪ increase in calcium & phosphate levels by 7-10% -increased
radiopacity in electron probe analysis by Selvig & Hal
▪ Increase in flouride coincides with Ca & P (1.3-1.9%)
▪ Decrease in sodium levels (0.3%)
▪ Absorption of Ca P & F –highly calcified –resistant to decay
▪ Absorbed materials –foreign to surrounding tissues
▪ Demineralisation/mineralisation of cementum –ability to
absorb or deplete mineral or organic compounds
Cytotoxic changes
▪ Effects on Cell proliferation
-Hatfield & Baumhammers- inhibitory substance penetrates
surface of exposed cementum that prevents growth of epithelial
cells in tissue culture
-Presence of endotoxins- Aleo et al 1974 –limit fibroblast
proliferation – detrimental to the arrest of disease
-Cementum bound endotoxins -50 times more toxic –heat
resistant toxic substances (Limulus amoebocyte lysate)
-Destructive physical changes –cavitation, partial
demineralisation
Cytotoxic changes
• Effects on Cell attachment
• Cultured human gingival fibroblasts do not attach
to the diseased tooth –Aleo et al 1975
Effects on Cell attachment
• Inhibitory principle of matrix
• Morris 1975
• diseased roots inhibited the development of implanted
marrow whereas demineralised healthy roots did not
• demineralised diseased roots showed most inhibtion (masked
by superimposed apatite crystals)
• toxins must have seeped into root matrix during pocket
formation & demineralisation removed the toxins allowing
development of marrow
▪ According to inhibitory principle of matrix –
▪ drastic phenol extraction usually required to
remove toxins from bacterial cell wall is not
necessary to make diseased cementum receptive
to cell attachment – milder treatments may
accomplish the same thing
▪ in early and moderate periodontitis -acellular
cementum (coronal half of the root) is affected
▪ damage extends to cellular cementum in most
advanced and furcally positioned lesions
▪ these surfaces are almost always covered by
cellular cementum during successful regeneration;
whether this is adequate is unclear.
(MacNeil and Somerman, 1999)
Role of cementum molecules in
periodontal regeneration
▪ growth factors and adhesion molecules present in
cementum are also active toward cells of the
gingiva, periodontal ligament, and alveolar bone
(Narayanan and Bartold,1996; Bartold et al.,
2000)
▪ it is possible that these cementum components
have the potential to participate in the
regeneration of these tissues
▪ not significant because the growth factors present
in cementum remain bound to the cementum
matrix
▪ even if the inflammatory process releases them,
their relative concentrations are likely to be less
than those available from the blood and
inflammatory cells
▪ therefore, contributions by cementum molecules
to the regeneration of other periodontal tissues
are likely to be marginal
Effectiveness of Root planing
in removing toxins
▪ In vitro- human gingival fibroblasts attach normally to
periodontally diseased roots that have diseased
cementum mechanically removed
▪ In vivo- Jones & O’Leary 1978
▪ -subgingival root planed
-supragingival root planed
-periodontally involved with calculus
-gross scaled in vitro
-healthy uninvolved
▪ All were planed and checked with Hartzell No. 3 explorer
& then assayed for endotoxin –planed had 1ng more
endotoxin
Chemical modification of
cementum
Addition of zinc to cultures relieved endotoxin induced
depression of cellular proliferation.
▪ Chelation of zinc enhanced cellular toxicity of endotoxin -
Aleo et al
▪ Studies analysing effect of zinc on cell attachment are still
underway
▪ Register & Burdick- tested effects of partial
demineralisation by acid on reattachment (adult dogs)
▪ Results –production of cementum pins –reattachment with
cementogenesis
–repair of chronic interproximal defects
–complete alveolar bone repair over labial defects by 1 year
Role of cementum in periodontal
regeneration
▪ Not significant because the growth factors present in
cementum remains bound to the cemental matrix.
▪ Even if the inflammatory process releases them, their
relative concentrations are likely to be less than those
available from the blood & inflammatory cells.
▪ Therefore,contributions by cementum molecules to the
regeneration of other periodontal tissues are likely to be
marginal.
DEVELOPMENTAL ANOMALIES
LOCATED ON CEMENTUM
▪ Enamel Projections
If amelogenesis does not stop before
the start of root formation, enamel
may continue to form over portions
normally covered by cementum.
▪ Enamel Pearls
This consists of globules of enamel
on the root surface in cervical region
(act as plaque retentive areas)
Hypercementosis
▪ refers to a prominent thickening of the cementum .
▪ It may be localized to one tooth or
affect the entire dentition
(Pagets disease)
▪ occurs as a generalized
thickening of the cementum,
with nodular enlargement of
the apical third of the root.
The etiology of Hypercementosis
▪ spike like type of hypercementosis -results from
excessive tension from orthodontic appliances
or occlusal forces
▪ generalized type -occurs in teeth without antagonists,
hypercementosis is interpreted as an effort to keep pace
with excessive tooth eruption
▪ In teeth subject to low-grade periapical irritation arising
from pulp disease, it is considered compensation for the
destroyed fibrous attachment to the tooth
Factors leading to hypercementosis
• TFO
• Orthodontic movement
• Pressure from non-aligned erupting
tooth
• Cysts,tumors
• Teeth without functional antagonist
• Periapical disease
Local factors
• Calcium deficiency
• Hypothyroidism
• Hereditary fibrous osteodystrophy
• Paget’s didsease
Systemic
factors
▪ Other systemic disturbances that may lead to ormay be
associated with hypercementosis include
acromegaly,arthritis, calcinosis, rheumatic fever, and
thyroid goiter.
Cementoblastoma
 Only neoplasm of cementum
 Cementum like tissue is deposited
in roots of tooth as irregular or rounded
mass.
•Age <25
 Often involves the mandibular molars
or premolars
 Tooth usually has a vital pulp
 Attached to root and may cause its resorption, may involve the
pulp canal, grows slowly, tends to expand the overlying cortical
plates
 Enlargement produced is usually asymptomatic
Cementoma
•Benign cementoblastoma / Cemental Dysplasia
•Represents an unusual reaction of bone
•Caused due to occlusal trauma
•Present usually at apex of mandibular
incisors
•Almost exclusively found in black
persons
•Age 20-40 years
•Expansion of jaw
Concrescence
▪ Form of fusion which occurs after root
formation has been completed.
▪ Thought to arise as result of traumatic
injury or crowding of teeth with
resorption of interdental bone so that
two roots are in approximate contact
and become fused by deposition of
cementum between them.
▪ May occur before or after teeth have
erupted.
Hypophosphatasia
▪ This is a hereditary disease that is characterized by the total
absence of cementum.
▪ It results in early loss of the teeth.
▪ It occurs because of the deficiency of enzyme alkaline
phosphatase in serum and tissues.
Cementicles
 calcified bodies sometimes seen in the periodontal
ligament.
 may be round or ovoid.
 singly or in multiple numbers near the cemental surface.
Origin
 not established.degenerated epithelial cells form the nidus
for their calcification.
 also believed could be due to trauma, the calcification of the
ends of the sharpey’s fibers occurs that can result in the
formation.
▪ Types of cementicles:
▪ Free cementicles : lamellated
cemental
bodies that lie freely in the PDL.
▪ Attached cementicles : cemental
bodies which are attached to the
root surface.
Ankylosis
▪ •Fusion of the cementum and alveolar
bone with obliteration of the periodontal
ligament is termed ankylosis.
•occurs in teeth with cemental resorption,
may represent a form of abnormal repair.
•may develop after chronic periapical
inflammation, tooth replantation, occlusal
trauma.
•results in resorption of the root and its
gradual replacement by bone tissue.
Conclusion
▪ Cementum is an important tissue of the periodontium,
the attachment apparatus of the tooth and has an
important role in tooth movements.
▪ Cementum deposition is a continuous process but this
tissue is comparatively static as compared to the
surrounding dynamic tissues therefore it has to be taken
in account while performing various dental procedures.
References
▪ Carranza Clinical periodontology south asian edition 13th
▪ CEMENTUM- Recent concepts related to periodontal
disease therapy – Joseph J. Aleo (DCNA)
▪ LINDHE’s Clinical periodontology & implantology,6th edition
▪ Shafer’s textbook of oral pathology, 6th edition
▪ Orban’s Oral histology & Embryology edition,14th edition
▪ Tencate’s oral histology 9th edition
THANK YOU!

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cementum.pptx

  • 1.
  • 2. DENTAL CEMENTUM DR.SHRUTI JITENDRA JAISWAL 1st MDS POST GRADUATE DEPARTMENT OF PERIODONTOLOGY
  • 3. Contents:  Introduction  Development of cementum  Molecular factors affecting cementogenesis  Physical characteristics  Chemical characteristics  Histology of cementum  Classification  Cementodentinal junction  Cementoenamel junction
  • 4.  Functions  Cementum resorption and repair  Effects of ageing on cementum  Cementum in oral environment  Role of cementum in periodontal disease  Changes in cementum in periodontal pathology  Effectiveness of root planing  Developmental anomalies  Conclusion  References
  • 5.
  • 7. ▪ Begins at the cervical portion of the tooth at the cemento enamel junction upto the apical foramen. ▪ According to Denton,cementum was first demonstrated microscopically by Fraenkel and Raschkow (1835) and Retzius (1836) and has since become a part of general knowledge in dentistry. ▪ The word cementum originated from the latin word ‘cement’ which means quarried stone. ▪ Anatomically-part of tooth Functionally-part of periodontium
  • 8. DEFINITION ▪ Cementum is the calcified, avascular mesenchymal tissue that forms the outer covering of the anatomic root. (Carranza 13th south asian edition) ▪ Cementum is a hard, avascular connective tissue that covers the root of the teeth. (Ten Cate’s oral histology 9th edition) ▪ Cementum is the mineralized dental tissue covering the anatomic roots of human teeth. (Orban’s oral histology and embryology 13th edition)
  • 9. ▪ The cementum is a specialized mineralized tissue covering the root surfaces and, occasionally, small portions of the crown of the teeth. (Lindhe 6th edition) ▪ The thin, calcified tissue of ectomesenchymal origin covering the roots of teeth in which embedded collagen fibers attach the teeth to the alveolus. (Glossary of Dental Implantology)
  • 10. Development of cementum HERS-Corono apical extension of IEE and OEE induces the secretion of enamel proteins Facing the ectomesenchymal cells of the dental papilla diffrentiate into odontoblasts Odontoblasts start forming the predentin Some cells from the fragmented root sheath form discrete masses surrounded by a basal lamina k/as Epithelial cell rests of malassez which persists in the mature PDL.
  • 11. HERS becomes interrupted & ectomesenchymal cells of inner portion of dental follicle comes in contact with the predentin EM cells of the follicle receive signals from dentin & surrounding HERS cells;diffrentiates into cementoblasts Cementoblasts lay down cemental matrix which undergoes maturation and subsequently gets mineralised resulting into cementum formation
  • 12. Enamel Enamel epithelium Cemento enamel junction Dentin Cementum Cementoblast Remnants of epithelial Root sheath Periodontal connective tissue
  • 14. Physical characteristics ▪ Colour- light yellow in colour dull surface-lacks lusture darker hue than enamel ▪ Hardness- less than dentin ▪ Permeablility- more permeable than dentin decreases with age ▪ Thickness- thinnest at CEJ 20-50 µm thickest at apex 150-200µm
  • 15. Chemical characteristics ▪ On dry weight basis,a fully formed permanent teeth consists of- Inorganic substance 45-50% • Calcium phosphate in the form of hydroxy apatite crystals Ca10(PO4)6(OH)2 • Highest fluoride content
  • 16.  type I COLLAGEN fiber  And protein polysaccharide- proteoglycans,osteopontin,osteonectin,osteocalcin, osteonectin, fibronectin,bone sialoprotein.  Other collagen –Type III,V,VI,XII
  • 17. Suggested Function Related to Cementogenesis Growth Factors Transforming growth factor β superfamily (including bone morphogenetic proteins) Reported to promote cell differentiation and subsequently cementogenesis during development and regeneration. Platelet-derived growth factor and insulin-like growth factor Existing data suggest that platelet-derived growth factor alone or in combination with insulin-like growth factor promotes cementum formation by altering cell cycle activities. Fibroblast growth factors Suggested roles for these factors are promoting cell proliferation and migration and also vasculogenesis—all key events for formation and regeneration of periodontal tissues. Adhesion Molecules Bone sialoprotein Osteopontin These molecules may promote adhesion of selected cells to the newly forming root. Bone sialoprotein may be involved in promoting mineralization, whereas osteopontin may regulate the extent of crystal growth. Epithelial/Enamel Proteins Proteins Epithelial-mesenchymal interactions may be involved in promoting follicle cells
  • 18. along a cementoblast pathway. Some epithelial molecules may promote periodontal repair directly or indirectly. Collagens Collagens, especially types I and III, play key roles in regulating periodontal tissues during development and regeneration. In addition, typeXII may assist in maintaining the periodontal ligament space versus continuous formation of cementum. Gla Proteins Matrix Gla protein/bone Gla protein (osteocalcin) These proteins contain γ-carboxyglutamic acid, hence the name Gla proteins. Osteocalcin is a marker for cells associated with mineralization—that is, osteoblasts, cementoblasts, and odontoblasts—and is considered to be a regulator of crystal growth. It has also been proposed to act as a hormone regulating energy metabolism through several synergistic functions favoring pancreatic β-cell proliferation, increasing insulin secretion (in the pancreas) and sensitivity in peripheral tissues, and promoting energy expenditure (in brown adipose tissue) and testosterone production by Leydig cells in testes. Matrix Gla protein appears to play a significant role in preventing abnormal ectopic calcification.
  • 19. Transcription Factors Runt-related transcriptionfactor 2 (Runx-2) Osterix As for osteoblasts, these may be involved in cementoblast differentiation. Signaling Molecules Osteoprotegerin These molecules mediate bone and root resorption by osteoclasts. Receptoractivated nuclear factor κB ligand Receptoractivated nuclear factor κB Sclerostin Antagonist of Wnt and promotes cementum formation Wingless-related integration site (Wnt) Regulates stem cell populations and differentiation of cementoblasts Cementum-Specific Proteins Cementum protein 1 (cementumderived protein 23) May play a role as a local regulator of cell differentiation and extracellular matrix mineralization.
  • 20. Histology of cementum ▪ Histologically,cementum shows a. Cells,fibers,ground substance b. Cemento enamel junction c. Cemento dentinal junction
  • 22. • Cementoblasts Characteristics-numerous mitochondria,well formed golgi apparatus,large number of granular endoplasmic reticulum Synthesizes collagen & protein polysaccharide forms organic matrix of cementum
  • 23.  After the matrix is laid down,it begins mineralisation  The cells are found lining the root surface
  • 24. • Cementocyte  Spider shaped cells -cellular cementum.  During the formation of cellular cementum, cementoblasts get entrapped within their own cemental matrix due to rapid deposition resulting in the formation of cementocyte.
  • 25.  Similar to osteocytes,they lie in lacunae.  Canalicular processes branch and anastosomes with adjacent cells.  These processes are directed towards PDL.  Deeper layers of cementum(60µm from nutrition)cementocytes shows definite signs of degeneration such as cytoplasmic clumping, vesiculation & sometimes empty lacunae.
  • 26. Cementoclast  Found in howship’s lacunae  Unilocular/multilocular  Function-resorption of cementocytes  Major role-resorption and repair
  • 27. Incremental lines of salter ▪ These lines represent rhythmic periodic deposition of cementum ▪ Appears as dark lines running parallel to root surface  Highly mineralized areas with less collagen & more ground substance  Seen in both acellular and cellular cementum  Predominantly in acellular cementum
  • 28. Types of cementum i.Based on location a.radicular cementum b.coronal cementum ii.Based on cellularity a.Acellular cementum b.Cellular cementum iii.Based on presence of collagen fibers in matrix a.Afibrillar cementum b.Fibrillar cementum
  • 29. ACELLULAR CEMENTUM CELLULAR CEMENTUM • Primary cementum • Secondary cementum • Present on cervical 3rd or half • present on apical 3rd of the root of the root • cells are absent • cells are present • forms before the tooth reaches • forms after the tooth reaches the the occlusal plane the occlusal plane • more calcified • less calcified • sharpey’s fibers are main compo • sparse number of sharpey’s fibers -nent are present • perpendicular to root surface • parallel to root surface • rate of development is faster • rate of development is slower •incremental lines are wide apart • incremental lines are closer • thickness ranges from 30-230µm • thickness ranges from 150-200µm
  • 30. iv. Based origin of the matrix fibers a.extrinsic fiber b.intrinsic fiber c.mixed fiber  Extrinsic fiber- − Also known as ‘sharpey’s fiber’ − Embedded portion of the principal fibers of PDL − Formed by fibroblasts
  • 31.  Intrinsic fiber − Belongs to cementum − Formed by cementoblast Intrinsic fibers of cementum
  • 32. Mixed fiber − Composed of extinsic sharpey’s fiber & intrinsic fiber − Co-product of cementoblast and fibroblast Mixed fibers of cementum
  • 33. Schroeder classification(1986) i. Acellular afibrillar cementum(AAC) ii. Acellular extrinsic fiber cementum(AEFC) iii. Cellular mixed stratified cementum(CMSC) iv. Cellular intrinsic fiber cementum(CIFC)
  • 34. Acellular afibrillar cementum(AAC) ▪ contains neither cells nor extrinsic or intrinsic collagen fibers. ▪ only mineralised ground substance.  product of cementum,seen in crown portion of tooth ▪ thickness - 1-15µm ▪ no known fuction around CEJ.
  • 35.  Acellular extrinsic fiber cementum(AEFC)  densely packed bundles of sharpey’s fiber, no cells.  co-product of fibroblast & cementoblast.  found in cervical 3rd of root,may extend apically.  thickness- 30-230µm  function-anchorage in especially single rooted teeth. . .
  • 36.  Cellular mixed stratified cementum(CMSC) ▪ composed of both intrinsic & extrinsic sharpey’s fibers. ▪ may contain cells. ▪ co-product of fibroblast & cementoblast. ▪ function-adaptation & repair
  • 37.  Cellular intrinsic fiber cementum(CIFC) -contain cells but no extrinsic collagen fiber. -formed by cementoblasts. -fills the resorption lacunae.
  • 38. Intermediate cementum- is a poorly defined zone near the cementodentinal junction of certain teeth that appear to contain cellular remnants of Hertwig sheath embedded in calcified ground substance. - seen in apical 3rd of root and apices, & in furcation area. -thickness- 10-1000µm -function-adaptation of fibers
  • 39. Cementodentinal junction ▪ Interface between dentin and cementum. ▪ In deciduous teeth-scalloped permanent teeth-smooth. ▪ Areas of dentin adjacent to CDJ granular in ground substance due to coalescing and looping the terminal portion of dentinal tubules and is called ‘Tomes Granular Layer’.
  • 40.  Terminal apical area of cementum where it joins the inteernal root canal dentin.  During RCT,the obturating material should be at CDJ.  No increase /decrease in width(2-3µm)
  • 41. Cementoenamel junction ▪ It is the preface between cementum & enamel at cervical region of teeth is variable. ▪ It is also an important landmark as a clinical consideration while scaling and root planing.
  • 42. Funtions of cementum ▪ Provides medium for the attachment of collagen fibers of PDL. ▪ Cementum is harder than alveolar bone & is avascular and doesn’t show resorption on masticatory or orthodontic forces.
  • 43. ▪ Thus during heavy orthodontic forces tooth integrity is maintained & alveolar bone being elastic in nature changes its shape,fulfilling orthodontic requirements.
  • 44. ▪ Acts as a covering for root surface, a seal for open dentinal tubules. ▪ Prevents dentinal tubules from sensitivity. Reparative nature ▪ Aid in maintaining the teeth in functional occlusion (in chronic bruxism, deposition of cementum on apical aspect of the teeth) [passive eruption].
  • 45. Cementum resorption and repair ▪ Permanent teeth do not undergo phyioslogic resorption as primary teeth. ▪ Local factors- ▪ Systemic factors- Ca deficiency, hypothyroidism,paget’s disease, Hereditary fibrous osteodystrophy ▪ Microscopically ,bay-like concavities seen over tooth surface. Multi nucleated giant cells, mononuclear macrophages are generally found adjacent to the site of active resorption. ▪ Painless
  • 46. ▪ Reversal line-? ▪ Repair – i.anatomic repair ii.functional repair ▪ Occurs in vital and non vital tooth both
  • 47. Effects on ageing in cementum ▪ Becomes irregular due to calcification of some bundle fibers where they were attached to cementum ▪ Cemental width may increase 5-10 times (deposition continues after eruption) ▪ Increase in width is greater apically & lingually ▪ In ageing, a continuous increase of cementum in apical zone may result in obstruction of apical foramen
  • 48. What happens to cementum when exposed to oral cavity? Cementum becomes exposed to the oral environment in cases of gingival recession and as a consequence of loss of attachment in pocket formation The cementum is sufficiently permeable to be penetrated in these cases by organic substances, inorganic ions, and bacteria Bacterial invasion of the cementum occurs commonly in periodontal disease  Cemental caries
  • 49. Clinical considerations  In periodontal pockets, pathologically exposed cementum, altered cementum interfere with healing  Root planing (hypomineralised cementum)  Cellular cementum- avascular, no nerve supply -scaling produces no pain, but if cementum is removed, dentin is exposed causes sensitivity  Precementum – natural barrier to excessive apical migration of junctional epithelium  Biomodification of root surface
  • 50. Role of cementum in periodontal disease The surface on which plaque & calculus is attached, the role therapy is to remove these accretions as a part of the treatment plan It forms the inner wall of the periodontal pocket. This tissue is relatively static as compared to surrounding dynamic tissues, so any change will have long term effects. Its intimately involved in all phases of the PD process so it must be returned to a healthy state before any progress in disease control, soft tissue regeneration & repair. ROLE OF CEMENTUM IN PERIODONTAL DISEASE DCNAVol 24. No. 4, 1980 by Joseph J. Aleo
  • 51. Changes in cementum associated with periodontal disease ▪ Structural changes ▪ Pathologic granules in exposed cementum by Bass and Benson – proven by SEM studies that vacuole like formations exist ▪ Partial demineralisation by Selvig et al ▪ Reprecipiation of dissolved minerals ▪ Decrease or loss of cross banding of collagen ▪ Subsurface condensation of organic material of exogenous origin
  • 52. ▪ Chemical changes ▪ increase in calcium & phosphate levels by 7-10% -increased radiopacity in electron probe analysis by Selvig & Hal ▪ Increase in flouride coincides with Ca & P (1.3-1.9%) ▪ Decrease in sodium levels (0.3%) ▪ Absorption of Ca P & F –highly calcified –resistant to decay ▪ Absorbed materials –foreign to surrounding tissues ▪ Demineralisation/mineralisation of cementum –ability to absorb or deplete mineral or organic compounds
  • 53. Cytotoxic changes ▪ Effects on Cell proliferation -Hatfield & Baumhammers- inhibitory substance penetrates surface of exposed cementum that prevents growth of epithelial cells in tissue culture -Presence of endotoxins- Aleo et al 1974 –limit fibroblast proliferation – detrimental to the arrest of disease -Cementum bound endotoxins -50 times more toxic –heat resistant toxic substances (Limulus amoebocyte lysate) -Destructive physical changes –cavitation, partial demineralisation
  • 54. Cytotoxic changes • Effects on Cell attachment • Cultured human gingival fibroblasts do not attach to the diseased tooth –Aleo et al 1975
  • 55. Effects on Cell attachment • Inhibitory principle of matrix • Morris 1975 • diseased roots inhibited the development of implanted marrow whereas demineralised healthy roots did not • demineralised diseased roots showed most inhibtion (masked by superimposed apatite crystals) • toxins must have seeped into root matrix during pocket formation & demineralisation removed the toxins allowing development of marrow
  • 56. ▪ According to inhibitory principle of matrix – ▪ drastic phenol extraction usually required to remove toxins from bacterial cell wall is not necessary to make diseased cementum receptive to cell attachment – milder treatments may accomplish the same thing
  • 57. ▪ in early and moderate periodontitis -acellular cementum (coronal half of the root) is affected ▪ damage extends to cellular cementum in most advanced and furcally positioned lesions ▪ these surfaces are almost always covered by cellular cementum during successful regeneration; whether this is adequate is unclear. (MacNeil and Somerman, 1999)
  • 58. Role of cementum molecules in periodontal regeneration ▪ growth factors and adhesion molecules present in cementum are also active toward cells of the gingiva, periodontal ligament, and alveolar bone (Narayanan and Bartold,1996; Bartold et al., 2000) ▪ it is possible that these cementum components have the potential to participate in the regeneration of these tissues
  • 59. ▪ not significant because the growth factors present in cementum remain bound to the cementum matrix ▪ even if the inflammatory process releases them, their relative concentrations are likely to be less than those available from the blood and inflammatory cells ▪ therefore, contributions by cementum molecules to the regeneration of other periodontal tissues are likely to be marginal
  • 60. Effectiveness of Root planing in removing toxins ▪ In vitro- human gingival fibroblasts attach normally to periodontally diseased roots that have diseased cementum mechanically removed ▪ In vivo- Jones & O’Leary 1978 ▪ -subgingival root planed -supragingival root planed -periodontally involved with calculus -gross scaled in vitro -healthy uninvolved ▪ All were planed and checked with Hartzell No. 3 explorer & then assayed for endotoxin –planed had 1ng more endotoxin
  • 61. Chemical modification of cementum Addition of zinc to cultures relieved endotoxin induced depression of cellular proliferation. ▪ Chelation of zinc enhanced cellular toxicity of endotoxin - Aleo et al ▪ Studies analysing effect of zinc on cell attachment are still underway ▪ Register & Burdick- tested effects of partial demineralisation by acid on reattachment (adult dogs) ▪ Results –production of cementum pins –reattachment with cementogenesis –repair of chronic interproximal defects –complete alveolar bone repair over labial defects by 1 year
  • 62. Role of cementum in periodontal regeneration ▪ Not significant because the growth factors present in cementum remains bound to the cemental matrix. ▪ Even if the inflammatory process releases them, their relative concentrations are likely to be less than those available from the blood & inflammatory cells. ▪ Therefore,contributions by cementum molecules to the regeneration of other periodontal tissues are likely to be marginal.
  • 63. DEVELOPMENTAL ANOMALIES LOCATED ON CEMENTUM ▪ Enamel Projections If amelogenesis does not stop before the start of root formation, enamel may continue to form over portions normally covered by cementum.
  • 64. ▪ Enamel Pearls This consists of globules of enamel on the root surface in cervical region (act as plaque retentive areas)
  • 65. Hypercementosis ▪ refers to a prominent thickening of the cementum . ▪ It may be localized to one tooth or affect the entire dentition (Pagets disease) ▪ occurs as a generalized thickening of the cementum, with nodular enlargement of the apical third of the root.
  • 66. The etiology of Hypercementosis ▪ spike like type of hypercementosis -results from excessive tension from orthodontic appliances or occlusal forces ▪ generalized type -occurs in teeth without antagonists, hypercementosis is interpreted as an effort to keep pace with excessive tooth eruption ▪ In teeth subject to low-grade periapical irritation arising from pulp disease, it is considered compensation for the destroyed fibrous attachment to the tooth
  • 67. Factors leading to hypercementosis • TFO • Orthodontic movement • Pressure from non-aligned erupting tooth • Cysts,tumors • Teeth without functional antagonist • Periapical disease Local factors • Calcium deficiency • Hypothyroidism • Hereditary fibrous osteodystrophy • Paget’s didsease Systemic factors
  • 68. ▪ Other systemic disturbances that may lead to ormay be associated with hypercementosis include acromegaly,arthritis, calcinosis, rheumatic fever, and thyroid goiter.
  • 69. Cementoblastoma  Only neoplasm of cementum  Cementum like tissue is deposited in roots of tooth as irregular or rounded mass. •Age <25  Often involves the mandibular molars or premolars  Tooth usually has a vital pulp  Attached to root and may cause its resorption, may involve the pulp canal, grows slowly, tends to expand the overlying cortical plates  Enlargement produced is usually asymptomatic
  • 70. Cementoma •Benign cementoblastoma / Cemental Dysplasia •Represents an unusual reaction of bone •Caused due to occlusal trauma •Present usually at apex of mandibular incisors •Almost exclusively found in black persons •Age 20-40 years •Expansion of jaw
  • 71. Concrescence ▪ Form of fusion which occurs after root formation has been completed. ▪ Thought to arise as result of traumatic injury or crowding of teeth with resorption of interdental bone so that two roots are in approximate contact and become fused by deposition of cementum between them. ▪ May occur before or after teeth have erupted.
  • 72. Hypophosphatasia ▪ This is a hereditary disease that is characterized by the total absence of cementum. ▪ It results in early loss of the teeth. ▪ It occurs because of the deficiency of enzyme alkaline phosphatase in serum and tissues.
  • 73. Cementicles  calcified bodies sometimes seen in the periodontal ligament.  may be round or ovoid.  singly or in multiple numbers near the cemental surface. Origin  not established.degenerated epithelial cells form the nidus for their calcification.  also believed could be due to trauma, the calcification of the ends of the sharpey’s fibers occurs that can result in the formation.
  • 74. ▪ Types of cementicles: ▪ Free cementicles : lamellated cemental bodies that lie freely in the PDL. ▪ Attached cementicles : cemental bodies which are attached to the root surface.
  • 75. Ankylosis ▪ •Fusion of the cementum and alveolar bone with obliteration of the periodontal ligament is termed ankylosis. •occurs in teeth with cemental resorption, may represent a form of abnormal repair. •may develop after chronic periapical inflammation, tooth replantation, occlusal trauma. •results in resorption of the root and its gradual replacement by bone tissue.
  • 76. Conclusion ▪ Cementum is an important tissue of the periodontium, the attachment apparatus of the tooth and has an important role in tooth movements. ▪ Cementum deposition is a continuous process but this tissue is comparatively static as compared to the surrounding dynamic tissues therefore it has to be taken in account while performing various dental procedures.
  • 77. References ▪ Carranza Clinical periodontology south asian edition 13th ▪ CEMENTUM- Recent concepts related to periodontal disease therapy – Joseph J. Aleo (DCNA) ▪ LINDHE’s Clinical periodontology & implantology,6th edition ▪ Shafer’s textbook of oral pathology, 6th edition ▪ Orban’s Oral histology & Embryology edition,14th edition ▪ Tencate’s oral histology 9th edition