final_cementum.pptx

CEMENTUM IN
PERIODONTAL HEALTH
AND DISEASE.
1
PRESENTED BY:
DR PRINCY ANNA MATHEW.
1ST YEAR PG.
COORG INSTITUTE OF DENTAL SCIENCES.

CONTENTS
1) INTRODUCTION.
2) CEMENTOGENESIS.
3) FACTORS REGULATING CEMENTOGENESIS.
4) PHYSICAL CHARACTERISTICS.
5) BIOCHEMICAL COMPOSITION.
6) CELLS THAT ARE FUNCTIONALLY CONCERNED WITH CEMENTUM.
7) INCREMENTAL LINES OF CEMENTUM.
8) CLASSIFICATION OF THE CEMENTUM.
9) FUNCTIONS OF THE CEMENTUM.
10) CEMENTODENTINAL JUNCTION.
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11) CEMENTOENAMEL JUNCTION.
12) AGE CHANGES IN THE CEMENTUM.
13) PATHOLOGICAL CONDITIONS ASSOCIATED WITH THE CEMENTUM.
14) INFLUENCE OF SYSTEMIC DISEASES ON CEMENTUM.
15) CHANGES IN CEMENTUM.
16) CLINICAL CONSIDERATIONS.
17) CLINICAL IMPLICATIONS.
18) CEMENTUM AND IMPLANTS.
19) PRACTICAL CONSIDERATIONS AND FUTURE PROSPECTS.
20) CONCLUSION.
21) REFERENCES.
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INTRODUCTION
DEFINITION- Cementum is the calcified, avascular mesenchymal tissue
that forms the outer covering of the anatomic root. - Carranza.
The Cementum is a specialized mineralized tissue covering
the root surfaces and occasionally small portions of the crown.
-Jan Lindhe.
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 Cementum begins at the cervical portion of the tooth at the cemento enamel
junction and continues to the apex.
 Cementum furnishes a medium for the attachment of collagen fibres that bind
the tooth to the surrounding structures.
 Cementum is a component of the tooth as well as the bone tissue.
 It has many features common with the bone tissue.
 However cementum contains no blood vessels or lymph vessels, has no
innervations, does not undergo physiologic resorption or remodelling, but is
characterized by continuous deposition throughout the life.
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STRUCTURE OF CEMENTUM.
Both acellular & cellular cementum consist of a calcified interfibrillar matrix &
collagen fibrils.
The two sources of collagen fibers in cementum are:
Sharpey's (extrinsic) fibers, which are the embedded portion of the principal
fibers of the periodontal ligament and are formed by the fibroblasts, and
Fibers that belong to the cementum matrix per se (intrinsic) and are
produced by the cementoblasts.
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CEMENTOGENESIS
 Cementum formation in the developing tooth is preceeded by the deposition of dentin along the inner
aspect of Hertwig’s epithelial root sheath.
 Once dentin formation is underway, break occurs in the epithelial root sheath allowing the newly
formed dentin to come in direct contact with the connective tissue of the dental sac, the
undifferentiated mesenchymal cells derived from dental sac, differentiate into CEMENTOBLASTS.
 These cementoblasts are responsible for the formation of
the cementum.
 These cells have the ultrastructural characteristics typical of
cells actively synthesizing protein and polysaccharide.
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FACTORS REGULATING CEMENTOGENESIS
MOLECULAR FACTORS REGULATING CEMENTOGENESIS.
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Morphogenes & Growth factors Suggested Functions related to CEMENTOGENESIS
Growth factors
* Transforming growth factor superfamily
(Including BMPs).
Promotes cell differentiation & subsequently
cementogenesis during development & regeneration.
* Platelet derived growth factor & insulin like
growth factor (IGF-I,IGF-II).
Promotes cementum formation by altering cell cycle
activities.
* Fibroblast growth factor.
Promotes cell proliferation & migration & also
vasculogenesis – all key events for formation &
regeneration of periodontal tissues.
Adhesion molecules
* Bone Sialoprotein & Osteopontin.
Promotes adhesion of selected cells to the newly
formed root. Bone sialoprotein may be involved in
promoting mineralization, whereas Osteopontin may
regulate the extent of crystal growth.
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9
Morphogenes & Growth factors Suggested Functions related to
Epithelial / Enamel like factors
(EmdogainTM)
Epithelial – mesenchymal interactions may be
in promoting follicle cells along a cementoblast
pathway. Some epithelial molecules may promote
periodontal repair directly or indirectly.
Collagens
Type I & III collagens play key roles in regulating
periodontal tissues during development &
regeneration. In addition, type XII may assist in
maintaining PDL space v/s continuous formation
cementum.
Gamma carboxyglutamate Proteins.
• Matrix Gla protein & Bone Gla protein
(Osteocalcin)
These proteins contain γ- carboxy glutamic acid,
hence the name Gla proteins. Osteocalcin is a
for cells associated with mineralization & is also
considered to be a regulator for crystal growth.
Gla protein prevents abnormal ectopic
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PHYSICAL CHARACTERISTICS
Colour- light yellow (dentin is darker in colour with darker hue).
 Hardness - less than dentin.
 Thickness - varies from 16-60µm on the coronal half to 150-200µm in the apical
third and the furcation.
 It is thicker in the distal surfaces than in the mesial surface. Between 11-70 years of
age, average thickness increases threefold, greatest increase apical region.
 Permeability- In young animals, cementum is permeable and permits the diffusion
of dyes from pulp and external root surface.
- permeability of cementum decreases with the age.
(Orban’s Oral histology and embryology- 12th edition)
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 Petelin et al (1999) studied the permeability of human cementum in vitro by
electron paramagnetic resonance . Cementum samples cut from different parts
of the root were classified into four different groups:
(A) samples exposed to the oral environment,
(B) samples exposed to the periodontal-pocket environment;
(C) samples cut from periodontally involved teeth but not exposed to saliva
or periodontal pocket and
(D) samples from sound young teeth extracted for orthodontic reasons.
 Largest diffusion flux across the dental hard tissue was found in the samples
that had been exposed to the pocket environment. Authors thus concluded that
transport of the labelled molecules into and through the cementum dentine
samples depends on the structure of the dental hard tissues, which changes
during the course of periodontal disease.
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BIOCHEMICAL COMPOSITION.
INORGANIC PORTION ( 50%).
-Mainly calcium phosphate in the form of hydroxyapatite.
-It has the highest fluoride content.
ORGANIC PORTION (50%).
- Collagenous protein - Type I- 90% -Predominant followed by type III&XII.
- Type II-5% -less crosslinked.
- Type V,VI & XIV  trace amounts-extracts of mature cementum.
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 Sharpey’s fibres which constitute a considerable portion of the bulk of cementum,
are composed of mainly Collagen Type I.
 Type III collagen appears to coat the type I collagen of Sharpey’s fibres.
- Non-Collagenous Protein : Almost all non-collagenase proteins identified in
- cementum are also found in bone (Bosshardt 2005).
These include Bone sialoprotein, dentin matrix protein, dentin sialoprotein,
fibronectin, osteocalcin, osteonectin, osteopontin, tenascin, proteoglycans, proteolipids,
cementum growth factor, enamel proteins and cementum attachment proteins.
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CELLS THAT ARE FUNCTIONALLY CONCERNED WITH
CEMENTUM.
1) CEMENTOBLASTS
2) CEMENTOCYTES
CEMENTOBLASTS
 Cementoblasts line the root surface and when active, they contain numerous
mitochondria, well developed golgi complex and open-faced nucleus.
 However, in resting cementoblasts, these cytologic features become less
pronounced.
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Origin Of Cementoblasts.
 It is widely held that infilterating dental follicle cells receive a reciprocal inductive
signal from the forming dentin and differentiate into cementoblasts.
 However, there is increasing evidence that HERS cells may undergo epithelial
mesenchymal tranformation into Cementoblasts during development (Bosshardt
2005).
 Structural & immunocytochemical data support the possibility that cementoblasts
derive, at least in part, from transformed epithelial cells of HERS.
 A possibility has been raised that acellular extrinsic fibre cementum is formed by
HERS derived cells, whereas, cellular intrinsic fibre cementum is formed by cells that
derive from dental follicle (Zeichner etal. 2003).
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CEMENTOCYTES
 Cementocytes are located in lacunae in the cementum matrix and typically
have numerous processes lying in canaliculi.
 These processes may branch and frequently anastomose with those of the
adjacent cementocytes.
 Because cementum is avascular tissue, the processes of the cementocytes are
oriented towards the periodontal ligament for nutrition.
 As a result of continuous phasic deposition of the cementum, resting lines
known as SALTER LINES appear in the cementum.
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 While cementum is being deposited, cementoblasts retreat leaving behind the
formed cementum matrix.
 Occasionally however cementoblasts become entrapped in the forming matrix
and are called CEMENTOCYTES.
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INCREMENTAL LINES OF CEMENTUM.
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 Incremental line in acellular cementum tend to be close together,
thin and even.
 Incremental lines of Salter are seen in cellular and acellular
cementum (decalcified section).
 The different rates of cementum formation is also reflected in
the wider precementum layer and the more widely spaced
incremental lines in cellular cementum.

CLASSIFICATION OF CEMENTUM.
Cementum is classified on the basis of :
1. Presence or absence of the cells.
2. Time of its formation.
3. Based on its location.
4. Presence or absence of fibres.
5. Origin of fibres.
6. Schroder’s classification.
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ACELLULAR CEMENTUM v/s CELLULAR CEMENTUM
ACELLULAR CEMENTUM CELLULAR CEMENTUM
First layer of cementum deposited. Formed after acellular layer.
No cells. Lacunae & canaliculi containing
Cementocytes & their processes.
Sharpey’s fibers make up the bulk; are
completely calcified.
•Sharpey’s fibers occupy a smaller portion; are
partially or completely calcified.
At least 1 layer over all of the root, with many
layers near cervical 1/3rd.
Layered over acellular mainly in apical 1/3rd ,
especially interradicular region.
Formed at a slower rate. Formed at a faster rate.
Precementum layer virtually absent. Precementum layer present.
Border with dentin not clearly demarcated. Clearly demarcated.
Incremental lines relatively close together. Relatively wide apart.
Width constant over time. Layers sometimes added over time.
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BASED ON THE LOCATION
 CORONAL CEMENTUM.
 RADICULAR CEMENTUM.
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BASED ON PRESENCE OR ABSENCE OF FIBRES
*AFIBRILLAR CEMENTUM FIBRILLAR CEMENTUM
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BASED ON ORIGIN OF FIBRES
 EXTRINSIC FIBRES.
 INTRINSIC FIBRES.
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TYPES OF CEMENTUM
Gottleib (1942):
According to Schroeder (1986, 1991)
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ACELLULAR CEMENTUM
(Primary Cementum)
CELLULAR CEMENTUM
(Secondary Cementum)
ACELLULAR AFIBRILLAR
CEMENTUM
ACELLULAR EXTINSIC FIBRE
CEMENTUM
CELLULAR MIXED STRATIFIED
CEMENTUM
CELLULAR INTRINSIC FIBRE
CEMENTUM
INTERMEDIATE
CEMENTUM

1. Acellular afibrillar cementum (AAC)
 It contains neither cells nor any fibres.
 AAC is a product of cementoblasts and is found on the coronal
cementum in humans.
 Thickness is 1-15µm.
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2. Acellular extrinsic fiber cementum (AEFC)
 It is a product of fibroblasts and cementoblasts and is found in cervical third of
roots in humans but may extend further apically.
 Its thickness is 20-230µm. Has densely packed Sharpey’s fibres and no cells.
 Approximately 30,000 fibres/mm2 insert into it.
 Faster growth rate on distal than on mesial reflects
adaptation to functionally dictated alterations.
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3.Cellular mixed stratified cementum (CMSC).
 It is a co-product of fibroblasts and cementoblasts.
 Has extrinsic and intrinsic fibres and cells.
 In humans, it appears primarily on apical third of the roots and
in apices and furcation areas.
 Thickness is 100-1000µm.
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4.Cellular intrinsic fiber cementum (CIFC).
 Contains cells but no extrinsic collagen fibres.
 CIFC is formed by cementoblasts and it fills the resorption lacunae.
 Cementoblasts become entrapped in the cellular matrix they secrete.
 Its adaptive function maintains tooth in proper position.
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5.Intermediate cementum
.
 It is a form of secondary cellular intrinsic fiber cementum restricted to the apex of
the tooth.
 It is not involved in tooth attachment and has no
clinical significance.
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FUNCTIONS OF CEMENTUM.
Though different functions have been attributed for different cementum, it should
be understood that cementum functions as a single unit.
1. Anchorage and Attachment.
2. Adaptive and reparative function.
3. Walling in filled canals.
4. Repairing roots (horizontal fracture).
5. Sealing of necrotic pulps by occluding apical foramen.
6. Protecting underlying dentin.
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CEMENTODENTINAL JUNCTION.
 Terminal apical area of the cementum where it joins the internal root canal dentin is
known as cemento dentinal junction.
 In the root canal treatment, the obturating material should end here.
 It’s width is 2-3µm and appears stable even as the age increases.
 The dentin surface upon which the cementum is deposited is relatively smooth in
permanent teeth.
 The cementodentinal junction in deciduous teeth,
however is sometimes scalloped.The attachment of
cementum to dentin is quite firm, although the nature
of this attachment is not fully understood.
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 CDJ has fibril poor layer which contains a significant amount of proteoglycans &
fibrils intermingle between cementum & dentin.
 Yamamoto et al. (2001) examined CDJ in human maxillary incisors, canines &
premolars by SEM combined with NaOH maceration.
 Observations suggested that cemental fibrils intermingle with dentinal fibrils only
in places at the CDJ in both acellular and cellular cementum.
 They also proposed that the adhesion of proteoglycans is a main factor for the
cemento-dentinal attachment and that the fibril intermingling between dentin
and cementum is an accessory or secondary factor.
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CEMENTOENAMEL JUNCTION
 It is a point at which cementum and enamel meet. Three types of relationships
involving the cementum may exist at the CEJ.
A. 5-10% the cementum and enamel fail to meet.
B. In 30% an edge-to-edge butt joint exists.
C. In 60-65% of the cases, cementum overlaps the enamel.
 In the first instance, gingival recession may result in accentuated sensitivity because
the dentin is exposed.
 Neuvald L & Consolaro A (2000) observed a 4th
type of CEJ i.e. cementum overlapped by enamel,
on buccal & lingual side of specimens in 1.8 % of
the specimens.
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 According to Schroeder HE & Scherle WF (1988):
 In third molars, cementum overlap occurs in about 50% of the CEJ, the rest either
edge-to-edge contact or exposed dentine. showing
 Dentine exposure occurs more frequently on buccal but also on distal surfaces, at least
in maxillary and mandibular (exclusively on buccal surfaces) molars.
 As long as the CEJ is covered by healthy gingival tissues, the cementum-enamel
relationship may change from exposed dentine to edge-to-edge contact to cementum
overlap, simply because of cementum being formed with time. This sequence is
stopped definitively by the CEJ becoming exposed to the oral environment.
 The type of cementum which usually overlaps the enamel has been shown to be the
Acellular, afibrillar variety (Schroeder 1986). As long as this layer and the layer of
acellular, fibrillar root cementum is very thin, cementum overlap and dentine
exposure can hardly be seen light microscopically.
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CLINICAL DETECTION OF CE J
 Clinically, most commonly used method to detect CEJ is Manual Detection by
explorer or probe. Here, the instrument is run over the tooth surface until a catch is
detected. In physical this catch can be interpretated as an alteration in acceleration of
tip which has been caused by the anatomy of the CEJ.
 Recently, Advanced CEJ Detection systems have evolved which include:
 Automated periodontal probe (Jeffcoat et al. 1986): The probe tip automatically
enters the periodontal pocket & retracts under controlled force. As the probe tip
transverses the CEJ, the electronic system detects an alteration in the acceleration of
the probe tip.
 Dental Endoscope (Perioscopy system, Dental view, Irvine , CA)
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 Pressure controlled automated standardized hand piece or Florida PASHA
probe:
 In this, a Florida sleeve probe handpiece (Gibbs etal. 1988) is modified to create the
Florida PASHA probe. A flange or flare is created at the terminal end of the titanium
sleeve through which the probe tip reciprocates.
 The probe tip is 0.4 mm in diameter while the total diameter of the flange & sleeve
was 1.25 mm. The flange is large enough to catch the CEJ without being too bulky to
prevent interproximal access.
 For clinical recording of the CEJ, the probe is inserted into the pocket & sleeve is
advanced down over the probe until the flange engages the CEJ. The foot pedal is then
depressed to record the distance from the flange to the probe tip.
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 Ultrasonic calculus detection device (Siroson-L):
 The detection principle is based on the assessment of oscillation signals. A
piezoceramic oscillation stimulator of a ultrasonic handpiece causes these impulses
with a frequency of 100 Hz. These impulses result in tiny movements of
approximately 5 mm at the working tip.
 When the oscillating working tip touches different tooth surfaces, these also react
with characteristic oscillatory movements, which are reflected and then recognized by
the system via the working tip and the piezoceramic.
 The different surface types cementum and calculus can be distinguished by reflected
voltage patterns, which were then analysed to discriminate calculus and root surfaces.
(Meissner .G etal.2006)
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ACCURACY OF CEJ DETECTION ON PERIAPICAL FILMS.
 Brezniak et al. (2004) conducted a study to find the effects of angular changes
between the tooth and the film on the validity and reproducibility of identifying three
different CEJ points, ie, the most apical CEJ point between the crown and the root, the
most mesial CEJ point, and the most distal CEJ point. An extracted maxillary central
incisor was placed in a special jig and radiographed at four different tooth to film
angulations.
 The angular changes between the tooth and the film did have a statistically significant
effect on the identification of some of these CEJ points. The difference was
significant on the identification of the buccal and palatal points but not on the mesial
and the distal ones.
39

 If a apical radiographic film of the incisor is properly exposed, the development and
fixation processes are done according to the manufacturer’s guidelines and
instructions, and there is no overlapping between the different CEJ lines, there should
be two CEJ lines (shadows) on the film ie, the buccal and the palatal CEJ lines. The
distal CEJ points are the images of the lines on their respective sides.
 Sasamoto et al (2003) conducted a study to investigate the relationship between the
anatomical and the radiographical location of CEJ using Paralleling/Bisection
technique.
 Paralleling technique was proved to be more accurate than bisection technique, and
molars interproximal CEJ could be recognized easily because of the flat buccolingual
CEJ line.
40

AGE CHANGES IN CEMENTUM.
 Intrinsic & concomitant age changes occur in cementum.
 A linear relationship between the thickness of cementum & age is reported from the
studies in humans. More cementum is formed apically than cervically. Thick layers
of cementum may form in root grooves & furcation areas.
 Continual reapposition of new layers of cementum represents the ageing of tooth as
an organ & maintains the attachment complex intact.
 With increasing age, vascularisation of the cementum present at the root apices is
commonly observed.
 Cellular cementum exhibits degeneration & death of cementocytes. Empty lacunae
are eventually observed.
41

AGE ESTIMATION BY CEMENTUM
 Zander and Hurzeler (1958) stated that cementum is a better age estimating tissue
than others.
 Incremental lines in cementum can be used as most reliable age marker than any
other morphological or histological traits in skeleton.
 Evaluation of annual incremental lines of dental cementum is one of potentially
valuable methods for biological age estimation in forensic
anthropology and digitalized visual analysis system
enhances the count and provides better results.
42

Estimation of Age Using Cementum Annulations
 In 2015, Padavala et al conducted a study on estimation of age using cementum annulations.
 The study sample consisted of 20 teeth. Teeth extracted because of periodontal, orthodontic and
prosthetic reasons were used in the study. Teeth with carious lesions were excluded.
 Longitudinal ground sections of each tooth were prepared and examined.
 The chronological age of the individual was obtained as E = n + t. where
o Estimated age (E) , number of incremental lines (n) & Euption age of tooth= (t).
o Number of incremental lines (n) = X / Y where,
o X is the total width of cementum (from dentinocemental junction to cementum surface).
o Y is the width of cementum between the two incremental lines.
43

 Out of the 20 samples used in the study, 16 samples showed cementum annulations under
polarized microscopy. 4 samples did not show any cementum annulations due to the
overcrowding of cementocytes in the cementum. Inaccurate age estimation was obtained in
15 samples.There was no significant correlation between the ages among the overall 20.
 The rationale is that by proper sectioning and use of polarized microscopy and image
analysis, counting the cementum annulations could potentially be used as a means of age
estimation.
44

PATHOLOGICAL CONDITIONS ASSOCIATED WITH
CEMENTUM.
1) ANKYLOSIS.
 Cementum with alveolar bone with the obliteration of the periodontal ligament is
termed as ankylosis.
 Ankylosis may occur at any age.
 Most commonly seen in mandible and most commonly involved tooth is mandibular
first molar.
 Ankylosis may also develop after chronic peripheral inflammation,tooth replantation
and occlusal trauma around the embedded teeth.
45

 Clinically ankylosed teeth lack the physiological mobility of normal teeth and on
percussion, produce a sharp, solid metallic sound.
46

2) CEMENTICLES.
 Abnormal calcified bodies in the periodontal ligament.
 Remnants of the Hertwig’s epithelial root sheath.
 Usually ovoid or round.
 Appear in increasing number in aging persons.
 Local trauma may be the cause.
Cementicles may be :
 Free in the periodontal ligament.
 Attached to cementum and form excementosis.
 Embedded in cementum during its growth by age.
47

3) CONCRESCENCE.
 It is the fusion of the teeth by fusion of the cementum.
 It occurs only after the root formation is completed.
 Causes may be crowding of the teeth or trauma.
48

4) HYPERCEMENTOSIS.
 Hypercementosis is a non-neoplastic condition in which
 excessive cementum is deposited in continuation with
 the normal radicular cementum.
 Premolars are the most affected and bilateral involvement is not uncommon.
 Hypercementosis may be evident on the entire root or only parts of the root.
 Radiographically an altered root structure caused by the excessive build up of
cementum around all parts or part of the root is evident.
49

5) CEMENTOBLASTOMA.
 Cementoblastoma or true cementoma is a benign odontogenic tumour that arises
from cementoblasts.
 It forms a large mass of cementum or cementum like tissue on the root.
 Seen more commonly in males below 25 years of age.
 Mandible is more involved and can deform bone cortices.
 Radiographically, the calcified mass is attached to the root, with loss of root
contour due to root resorption and fusion with the tumour.
50

 Although cementoblastoma and hypercementosis are typical conditions with distinct
clinical evolution, atypical cases may present diagnostic difficulties.
 Because cementoblastoma is neoplasm with unlimited growth potential, the usual
treatment is complete surgical removal, while the conservative treatment is
recommended for hypercementosis.
51

INFLUENCE OF SYSTEMIC DISEASES ON CEMENTUM.
1) PAGET’S DISEASE.
 Paget’s disease is characterized by enhanced resorption of the bone.
 Etiology - viral infection, inflammatory causes, autoimmune causes.
 Middle age, both males and females are affected.
 Facial bone involvement- LEONTIASIS OSSEA.
 Maxilla - progressive enlargement, alveolar ridge widened, palate flattened,mobile
tooth.
 Mandible-findings are similar, not as severe as maxilla.
52

 Generalized HYPERCEMENTOSIS of the tooth is seen.
 Radiographically, cotton wool appearance of the Paget’s bone is seen.
 Characteristic feature - Jigsaw or Mosaic pattern.
 Treatment - no specific treatment.
2) HYPOPHOSPHATASIA.
 Hypophosphotasia is a rare metabolic bone disease that is charecterized by a deficiency of
tissue specific alkaline phosphatase.
 The histopathologic examination of either a primary
or permanent tooth that has been exfoliated from an
affected patient shows an absence or a marked
reduction of cementum that covers the root surface.
53

3) GIGANTISM.
 It is the childhood version of growth hormone excess and is charecterized by the
general symmetrical overgrowth of body parts.
 Clinical features include prognathic mandible, frontal bossing, dental malocclusion,
interdental spacing etc.
 Intraoral radiograph may show HYPERCEMENTOSIS of the root.
4) ACROMEGALY.
 Abnormal growth of the hands, feet and face, caused by the overproduction of growth
hormone by the pituitary glands after the growth plates are closed.
 Dental radiograph demonstrates large pulp chambers and EXCESSIVE DEPOSITION
OF CEMENTUM on the roots.
54

NEOPLASMS OF CEMENTUM
1. CEMENTOMA : (Periapical Cemental Dysplasia,Periapical Osteofibroma,
Osteofibrosis, Cementifying fibroma, Localized fibro-osteoma,
Cementoblastoma, Periapical fibrous Dysplasia).
Histologically it has 3 phases:I. Osteolytic phase.
II. Cementoblastic phase.
III. Mature phase.
2. BENIGN CEMENTOBLASTOMA (True Cementoma) :
It is a true neoplasm of functional cementoblasts which forms a large mass of
cementum or cementum like tissue on the tooth root.
55

33. GIGANTIFORM CEMENTUM : (Familial Multiple Cementoma).
Histologically the tumor consists of dense, highly calcified, almost totally acellular
cementum which is poorly vascularized and frequently becomes infected with ensuing
suppuration & sequestration.
4. FOCAL CEMENTO OSSEOUS DYSPLASIA:
Is a benign cemento osseous lesion that occupies a portion of the spectrum between
periapical and florid cemento osseous dysplasia. Histologically, trabeculae of woven bone
and cementum like material are interspersed throughout the fibrous frame work.
56

ALTERATIONS OF CEMENTUM
1. ROOT CARIES:
 It is soft progressive lesion found anywhere on the root surface which has lost C.T
attachment and exposed to oral environment.
 Exposure to oral fluid and bacterial plaque results in proteolysis of the embedded
remnants of Sharpey’s fiber. The cementum may be softened & undergo
fragmentation & cavitation.
 Involvement of the cementum is followed by bacterial penetration of the dentinal
tubules, resulting in destruction of the dentin & finally pulpal involvement.
 In severe cases, large section of necrotic cementum becomes detached from the tooth
and separated from it by masses of bacteria.
 Since cementum is formed in concentric layers the micro-organism spread laterally
between various layers.
57

2. CEMENTAL TEAR :
 Cemental tears or separations can occur either as a split within the cementum that
follows one of its incremental lines or more commonly as a complete separation along
the cemento-dentinal border.
 Tears have been observed within unexposed cementum as well as in cementum
exposed within the pocket. The cemental fragment can remain partially attached or be
completely detached from the root surface.
 Causes : Occlusal trauma due to parafunctional habits and localized trauma.
 Significantly thicker cementum has been observed on tear surfaces than on like-
surfaces without tears and may predispose the cementum to mechanical separation.
58

 Predisposing Factors : 1) Impairment of the repair capacity.
2) Decreased extensibility of collagen.
3) Increased strength of principal fibres.
4) Reduced occlusal support.
 Within the subgingival environment, cementum lining the walls of periodontal pockets
becomes more mineralized which may render it more brittle.
 Consequences of Cemental tear:
59

3. Abrasion :
 It is pathologic wearing away of tooth substance through abnormal mechanical
process. Abrasion usually occurs on the exposed root surfaces of teeth.
 They cause remarkable wear of cementum & dentin if the tooth brush carrying
abrasive dentifrices is used injudiciously.
 V-shaped or wedge-shaped ditch is seen on the root side of the CEJ with some gingival
recession.
60

4. Cementopathia :Loss of cemental vitality.It causes :
* Apical migration of epithelial attachment.
* Deep Pocket formation..
* Diffuse alveolar atrophy.
 The significance of cementum change in periodontal disease may lie within 2 realms.
The first possibility that exists is that the cementum of certain individuals through
some acquired physical or chemical defect renders that individual more susceptible to
periodontal disease.
The second & more likely situation is that the complex inflammatory, enzymatic &
molecular biologic influences which accompany periodontal disease may produce physical
or chemical changes which are detectable in Cementum.
61

SURFACE CHANGES IN CEMENTUM
 The SEM analysis of surface of Cementum in relationship to normal tissue is characterized by
projection above the mineralized plane.
 Areas of cementum which are exposed to periodontal disease show varying changes depending on their
location:
 At the base of pocket, most recently exposed cementum may show a partial filling in one of the
spaces between the projections.
 Cementum which has undergone a larger exposure shows a complete covering of the normal
projections with flat sheet like plaque & calculus formations.
 Cementum near CEJ demonstrates extensive flat sheet like calculus formations.
 Cementum is also covered with cuticular material whose thickness is 1-4 μ & is of lamellar nature. The
cuticle may represent a zone of homogenous collagen degradation in areas of root exposure to the oral
environment. The roughness of the root surface probably is due to the uneven deposition of this cuticle.
62

CHEMICAL CHANGES IN CEMENTUM.
 The nature of difference between periodontally normal & diseased teeth basically can
be characterized as either an absorption onto or a depletion from the cementum of
major mineral components such as Mg, Ca & of certain trace elements such as Si, Cu,
Fe etc.
 Areas of hypermineralization - minerals increased are calcium, magnesium ,
phosphorus and fluoride.
 Cementum in association with pocket wall picks up Fe which is a breakdown product
of heme molecules. Also, demineralized cementum once in contact with oral
environment binds Ca from the saliva.
 The ability of cementum to absorb substances from its environment may be harmful if
absorbed materials are toxic.
63

CYTOTOXIC CHANGES IN CEMENTUM.
EFFECTS ON CELL PROLIFERATION:
 In 1974, Aleo et al demonstrated for the first time that endotoxin &/or endotoxin like products are
found in the cementum of the periodontally involved teeth.
 These products limit the proliferation of fibroblasts in vitro & are lethal in high concentrations.
When compared to commercial endotoxin preparations, the cementum bound products are approx.
50 times more toxic , suggesting that the biologic activity of the cementum bound products is
different in that they contain other heat resistant toxic substances.
EFFECTS ON CELLATTACHMENT :
 Aleo et al also studied the in- vitro attachment of human gingival fibroblasts to both normal &
periodontally exposed root surfaces. It was found that cultured gingival fibroblasts do not attach
normally to the root surface of periodontally involved teeth. Whether an initial attachment of cells
occurred followed by rapid detachment or lysis could not be established.
64

STRUCTURAL CHANGES IN CEMENTUM
 PRESENCE OF PATHOLOGIC GRANULES
 Pathologic granules have been observed with optical & dense electron microscopy & may represent
areas of collagen degradation or areas where collagen fibrils have not been mineralized initially. These
granules extend 3- 12 μ into the surface of cementum from overlying plaque.
 Granules appear in 4 basic morphologic patterns:
 Grape like structure, long chain aggregate, small isolated vacuoles or a very long fissure like area.
 Hypothesis for the formation of these granules includes 3 basic events:
 Upon exposure to oral environment, unmineralized areas of cemental collagen are denatured,
resulting in loss of structural characteristics such as cross banding.
 Areas where cemental collagen has been denatured, subsequently mineralize by picking up ions from
the oral environment.
 Upon decalcification in the laboratory, areas where cemental collagen has been denatured & / or
deposited are unmarked & become visible.
65

AREAS OF CELLULAR RESORPTION OF CEMENTUM AND DENTIN:
 Are common in roots unexposed by periodontal disease. These areas are of no
particular significance because they are symptom free, and as long as the root is
covered by the periodontal ligament, they are apt to undergo repair.
 However, if the root is exposed by progressive pocket formation before repair , then
these appear as isolated cavitations that penetrate into the dentin..
 These areas can be differentiated from caries of the cementum by their clear-cut
outline and hard surface. They may be sources of considerable pain, requiring the
placement of a restoration.
66

 Shafik et al (1992) evaluated the root surfaces adjacent to periodontal pockets in
Juvenile & Adult periodontitis.
 The observations of the Adult periodontitis (AP) specimens showed frequent coverage
of the affected root surfaces by calculus and different types of plaque bacteria.
 In the Juvenile periodontitis (JP) specimens, bacterial plaque and calculus were found
on the cervical third of root surfaces. The middle part of the affected root surfaces
appeared cracked with defects in cementum. Further apically, the cracks increased in
number and magnitude and appeared as furrows with some areas devoid of cementum.
In JP the severe cracking and focal loss of cementum may indicate a potential
impairment of periodontal fiber attachment which may have a bearing on the
significant bone destruction observed in JP.
67

CEMENTAL RESORPTION
 Cementum of erupted as well as unerupted teeth is subject to Resorptive changes that
may be of microscopic proportion or sufficiently extensive to present a
radiographically detectable alteration in the root contour.
 Microscopically cemental resorption appears as “Bay-like” concavity in the root
surface.
 Multinucleated giant cells and macrophages are found adjacent to cementum
undergoing active resorption.
 May be caused by local or systemic causes or may occur without apparent etiology
(i.e., idiopathic).
69

 Several sites of resorption may coalesce to form a large area of destruction.
 The resorptive process may extend into underlying dentin and even into the pulp,
but is usually painless.
70

CEMENTAL REPAIR
 Cemental resorption is not necessarily continuous and may alternate with periods of repair and
the deposition of the new cementum.
 The newly formed cementum is demarcated from the root by deeply staining irregular line,
termed as “Reversal line” which de-lineate the border of the previous resorption.
 Cementum repair requires the presence of viable connective tissue.
 If the epithelium proliferates into the area of the resorption, repair will not take place.
 Cementum repair can occur in devitalized as well as vital teeth.
 Regeneration of the cementum requires cementoblasts, but the origin of cementoblasts and the
molecular factors regulating their recruitment and differentiations are not fully understood.
71

 Epithelial cell rests of Mallasez have some function in cementum repair and
regeneration under specific conditions.
 They help in cementum repair by activating their potential to secrete matrix
proteins that have been expressed in tooth development, such as amelogenins,
enamelins and sheath proteins.
72

REPARATIVE v/s ORIGINAL CEMENTUM
(Philipson et al 1990)
REPARATIVE CEMENTUM :* formed on instrumented root surface.
* morphologically different.
* has a fibre orientation parallel to the root surface.
* appears not to be firmly attached to the underlying dentine.
* cementoblasts showed characteristics of actively synthesizing cells.
ORIGINAL CEMENTUM :* formed during root development.
* has palisade like orientation of fibres.
* mineralized zone appears darker and clear from the unmineralized zone.
* cementoblasts contained few ribosomes and nuclei with irregular chromatin
thus leading to low cementum producing activity.
73

REGENERATION OF CEMENTUM
DEFINITION : Regeneration is the growth & differentiation of new cells & intercellular
substances to form new tissues & parts.
 The process of periodontal tissue regeneration starts at the moment of tissue damage by
means of growth factors and cytokines released by the damaged connective tissue and
inflammatory cells.
 It is well accepted that in order to improve periodontal healing, root planing or root
conditioning is a necessary antecedent to mesenchymal cell migration and attachment
onto the exposed root surface. Acid treatment, in particular with citric acid, has been
found to widen the orifices of dentinal tubules, thereby accelerating cementogenesis
and increasing cementum apposition and connective tissue attachment.
 However, a systematic review performed by Mariotti (2003) suggested that the use of
citric acid, tetracycline or EDTA to modify the root surface provides no clinical
significant benefit for regeneration in patients with chronic periodontitis.
74

1. CEMENTUM REGENERATION BY GTR.
 Nyman et al. (1982), using Millipore membranes, introduced the concept of a
membrane barrier, which excludes the apical migration of gingival epithelial cells
and provides an isolated space for the inwards migration of periodontal ligament
cells, osteoblasts and cementoblasts.
 Recent systematic reviews indicate that, in the treatment of intrabony and furcation
defects, GTR is more effective than open flap debridement (Zeichner, 2006).
 It has been questioned whether GTR produces true cementum regeneration or only
cemental repair. The newly formed cementum has been characterized as a Cellular
Cementum that is usually poorly attached to the dentin surface (Kostopoulos et al
2004).
75

 It is suggested that Periodontal healing with GTR therapy occurs in two stages. :-
1st stage comprises * an initial healing phase with the formation of a blood clot,
* transient root resorption/demineralization,
* deposition of acellular cementum on the root surface and
* formation of connective tissue.
2nd stage comprises * a remodeling process  resulting in a regenerated
cementum ~ pristine cementum, as maturation proceeds over time (Graziani et al 2005).
76

2. BONE GRAFTS & CEMENTUM REGENERATION.
 Studies in monkeys have suggested that PerioGlas (synthetic bone particulate) can
achieve superior bone repair and cementum regeneration, and retard epithelial down-
growth compared with other similar materials (Fetner et al 1994).
 A recent systematic review on the efficacy of bone replacement grafts compared with
other interventions in the treatment of periodontal osseous defects was performed by
Reynolds et al (2003). Meta-analysis indicated that for the treatment of intrabony
defects, bone grafts are effective in reducing crestal bone loss, increasing bone level &
clinical attachment level and reducing probing depth compared with open flap
debridement procedures.
77

o Histological studies showed that demineralized freeze-dried bone allografts support
the formation of a new attachment apparatus in intrabony defects; however, the
available data indicate that alloplastic grafts support periodontal repair rather than
regeneration, and that the best treatment is a combination of bone grafts with barrier
membranes.
o Nevertheless, these strategies are directed mainly to enhance alveolar bone and
periodontal ligament repair and have the problems that they do not address
cementogenesis and therefore do not completely regenerate the architecture of the
original periodontium.
78

3. ROLE OF GROWTH FACTORS .
 New strategies, utilizing growth factors to induce cell migration, proliferation and
differentiation, are being developed to repopulate the damaged periodontal tissues with
periodontal ligament cells.
 Putative growth factors common to both cementum and bone include members of the
TGF-beta superfamily, such as the BMPs, as well as IGF-I and IGF-II, platelet-derived
growth factors (PDGFs), epidermal growth factor (EGF), and the fibroblast growth
factors (FGFs). In addition, cementum-derived growth factor (CGF), an isoform of IGF-
I, appears to be cementum-specific.
79

 These growth factors can be further subdivided into those that stimulate osteogenesis
(e.g. bone morphogenetic proteins), those that promote cellular differentiation (e.g.
platelet-derived growth factor) and angiogenesis (e.g. vascular endothelial growth
factor), and those that regulate the epithelial mesenchymal interactions involved in
initial tooth formation (e.g. Emdogain™).
 Emdogain™ (Strauman AG, Basel, Switzerland), a mixture of enamel matrix proteins,
primarily amelogenins, isolated from developing porcine teeth, has been approved by
the U.S. Food and Drug Administration (FDA) for regeneration of angular intrabony
periodontal defects.
80

 Although the mode of function is not known, the proposed mechanism behind using
enamel matrix proteins is that these proteins are believed to be involved in forming the
periodontal attachment apparatus during initial tooth development. The addition of
these proteins to periodontal defect sites may be effective at promoting periodontal
regeneration by recapitulating the environment during initial tooth attachment.
 Recent studies [Suzuki et al 2005] have shown that Emdogain™ contains both TGF-
beta and BMP growth factors, that may contribute to its clinical effectiveness. A
systematic review of published clinical trials [Esposito M etal. 2005] suggests that
Emdogain™ affords results similar to those seen with the use of GTR.
81

 The expression of both BMP-2 and BMP-7 during periodontal tissue morphogenesis suggests that
optimal therapeutic regeneration may require the combined use of the two BMPs. BMP-7-treated molar
furcation defects in baboons resulting in substantial cementogenesis, while BMP-2 showed limited
cementum formation but greater amounts of mineralized bone and osteoid; however, the combined
application did not enhance alveolar bone regeneration or new attachment formation over and above that
obtained by separate applications of the two BMPs (Ripomanti et al 2001).
 Recently, it was shown that the application of a synthetic BMP-6 polypeptide to a periodontal
fenestration defect in rats resulted in increased formation of new bone and cementum (Huang et al 2005).
 Perhaps the use of other members of the BMP family, such as growth and differentiation factor-5, 6, and
7, might provide better and more complete regenerative outcomes. These factors have been detected
during the process of periodontal development at the surfaces of alveolar bone, cementum and
periodontal ligament fiber bundles (Sena et al 2003).
 Limitations for the regular use of BMPs are the need for high doses, non-specific activity on different
cell lineages in time and space, and the rapid loss of topically applied growth factors (Beertsen et al
1997).
82

 The goal of gene-enhanced periodontal regeneration (GETE) is to reclaim the lost regenerative
capacity within the PDL space.
 This approach is intended to mimic the normal biological process that occurs , as these tissues
are formed early in development.
 While GETE can be used in conjunction with stem cells, this technique has the greatest
potential if it can be adapted for use with easily harvestable fully mature cells (e.g. gingival
fibroblasts, periodontal ligament fibroblasts).
 GETE for periodontal regeneration is still in its infancy. A couple of preliminary studies have
confirmed that this is a promising approach. Syngeneic dermal fibroblasts transduced ex vivo
with an adenoviral vector expressing BMP-7 (Ad-BMP-7) in a gelatin carrier were implanted
into submerged, surgically-created periodontal-alveolar bone defects in the rat [Jin et al 2003].
Significant bridging of the alveolar defect was seen in conjunction with new cementum
formation and fibrous connective tissue attachment.
83

CLINICAL IMPLICATIONS
 When the Root surface is exposed to plaque & pocket environment, its surface is
contaminated by toxic substances, notably endotoxins. Evidence suggests that these
toxic substances are only superficially attached to the root substances & do not
permeate it deeply (Checcki.L etal. 1998; Cheetam W.A etal.1988). Removal of
extensive amounts of dentin & cementum is not necessary to render the roots free of
toxin & should be avoided (Lowenguth R.A etal.1995).
 Root surface of pocket can be treated to improve its chances of accepting the new
attachment of gingival tissues (Root Biomodification) which is hampered by bacteria
& their products. Several substances have been proposed for this purpose which
include Citric acid, Fibronectin, Teteracycline etc.
84

PRACTICAL CONSIDERATIONS AND FUTURE PROSPECTS.
 While it is anticipated that in the future, gene-enhanced tissue engineering approaches
will afford great potential for periodontal regeneration, this approach would currently
face significant regulatory hurdles prior to government approval.
 With the continued development of improved methods for gene delivery to cells as well
as advances in our knowledge of the molecular basis of tooth formation and periodontal
homeostasis, it is reasonable to anticipate that a simple chairside protocol could be
developed in the future.
 This might involve either the direct delivery of the DNA of interest to the periodontal
tissue, or the isolation of a small amount of gingival tissue from the patient,
transduction/transfection of the DNA at chairside, and reimplantion of the gene-
enhanced cells into the tooth or periodontal ligament space.
85

 In the future, the incorporation of biomimetic motifs into matrices (eg : addition of
cementum-derived attachment protein), a cementum-derived protein that appears
to promote adhesion of mineral-forming mesenchymal cells to root cementum
holds significant potential for increasing the success rate of periodontal
regenerative protocols.
86

CEMENTUM AND IMPLANTS
 Titanium implants are ankylosed to bone without any intervening connective tissue.
 Buser et al, 1990, did a study on implants, where he placed the implants in contact
with retained root tips ,whose PDL served as source for cells which could participate
in the healing process.
 Microscopically, it revealed that distinct layer of cementum on the implant surface was
formed and a periodontal ligament with collagen fibres perpendicularly oriented to
implant surface, implanted into the cementum on the implant surface, as well as the
opposing bone.
87

CONCLUSION
Cementum forms the inner wall of the periodontal pocket. Because this tissue is
relatively static when compared to the dynamic equilibrium & biologic turnover
that exists for surrounding tissues, any change in its structure or chemical make
up will have long term effects.
With the newer concepts of regenerative cementogenesis and the role of
cementum in implants, the need for us to better understand the basic tissue
should be understood and implemented.
Thus cementum should not be ignored because it is intimately involved in all
phases of the disease process and must be returned to healthy state before any
progression is made in disease control, soft tissue regeneration & repair.
88

REFERENCES
• Joseph P. Fiorellini, David M. Kim, And Satoshi O. Ishikawa, The Tooth – Supporting
Structures, Newman, Takei, Carranza, Carraza’s Clinical Periodontology Tenth Edition,
Elsevier, 2009, 75-79
• Orban’s Oral Histology & Embryology-12th Edition, Elsevier, 2008, 137-154
• Ten Cate’s Oral Histology; Development, Structure And Function. 8th Edition, Elsevier,
2013, 205-212.
• Clinical Periodontology and Implant dentistry- Jan Lindhe, 5th edition.
• Shafer’s Textbook Of Oral Pathology Fifth Edition, Elsevier, 2006, 1213-1215
89

• Development and general structure of the periodontium Periodontology 2000, volume 24,
2000, 9-27.
• Atypical hypercementosis versus Cementoblastoma - British Institute of Radiology, Jan 28,
2014.
• Cementum in Periodontal disease. 1975 ; 6-12.
• Corbett EF etal. JCP 1993 ;20: 420- 432. Ramfjord S.P., Kerr D.A., Ash M.M.:World Work
Shop in Periodontics, 1966. 43-44.
90

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