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PATHOLOGIES OF CEMENTUM

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CONTENTS
• INTRODUCTION
• PERIODONTALLY INVOLVED CEMENTUM
• CEMENTUM IN AGGRESSIVE PERIODONTITIS
• DEVELOPMENTAL AND ACQUIRED ANOMALIES ASSOCIATED WITH CEMENTUM
– Cemental tears
– Cemental caries
– Cervical Enamel Projection
– Enamel Pearls
– Cementicles
– Hypercementosis
– Ankylosis
– Cemental aplasia and hypoplasia
– Cemental resorption

• CENTRAL LESIONS RELATED TO CEMENTUM


– Periapical cemental dysplasia,
– Benign Cementoblastoma
– Cementifying fibroma
– Gigantiform cementoma.
– Cemento- osseous dysplasia.

• CONCLUSION

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INTRODUCTION
• Cementum is a specialized mineralized connective tissue.
• Being exposed to pocket contents knowing variations.
• Cementum possesses unique characteristics.
• Cementum generally have properties (physical and chemical) similar to bone.

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PERIODONTALLY INVOLVED CEMENTUM

In the progress of periodontal disease cementum covering root surfaces becomes


exposed to the environment of the periodontal pockets and is then often called
‘periodontally involved cementum’.

Cemento phatia—(Gottlieb) according to this concept the "loss of cemental vitality" was
the primary etiologic factor in apical migration of the epithelial attachment, deep
pocket formation, and diffuse alveolar atrophy.

Uncalcified cementoid is necessary for "cemental vitality,"

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FEATURES OF PERIODONTALLY INVOLVED CEMENTUM

SURFACE CHARACTERISTICS –

• Waerhaug, 1956; Swartz and Phillips, 1957 of periodontally involved


cementum is rough and of an irregular nature This, is supposed, to
facilitate both the accumulation and retention of plaque and calculus.

• Herting, 1967 electron-microscopic studies demonstrating surfaces


‘pebbled’ in appearance and covered with layers of bacteria and bacterial
remnants

• Sottosanti and Garrett, 1975 Areas of cemental surface resorption.

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HARDNESS –

Nabers, Grant et al. Glickman Periodontally involved cementum is softer than


uninvolved cementum.

This decrease in hardness Of the diseased cementum


– demineralization by organic acids.
– resorption of collagen and protein polysaccharide matrix via enzyme
activities.

Glickman (1972) proteolysis of the embedded remants of Sharpey’s fibres by bacterial


products.

Rautiola and Craig and Warren et al found no significant differences between the
hardness of involved as compared with uninvolved cementum.

Yamada, Furseth A hypermineralized surface layer in periodontally involved


cementum .

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CHEMICAL COMPOSITION –

• Cloutier and Johansen No significant differences were found between the


amino acid composition of involved and uninvolved cementurn.

• IRON— FROM HEME

• Selvig and Zander Mineral content of exposed cementum is increased . this has been
explained by the penetration of mineral ions from either the gingival crevicular fluid
or the saliva into the cementum.

• Baumhammers and Stallard Salivary origin of the additional mineral ions throughout
the entire length of the involved cementum is unlikely thus, salivary components can
only become incorporated in those root surfaces exposed to the oral environment by
recession.

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STRUCTURAL FEATURES —

Resorption lacunae
• Adriaens et al , Hughes et al reported resorption lacunae in periodontally diseased
(but not in non-diseased) caries free teeth

Cracks
• Daiy et al also showed cracks within cementum from periodontally- involved root
surfaces.

Hypermineralization

• Selvig and Zander Microradiographic examination of the surface of involved


cementum has revealed a radio-opaque zone approximately 10-20 µm in width This
finding has been confirmed also in supragingival cementum exposed to saliva

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Furseth and Johansen Hypermineralization of cementum represents recrystallization
of the constituent mineral phase following exposure of the
cemental surface to either pocket or oral cavity fluids, or to
mineral concentrating bacterial plaque.

Yamada, Furseth and Johansen Breakdown of the organic matrix of the cementum, as
evidenced by partial or complete loss of collagen cross-
banding, has also been observed in these densely
mineralized zones .

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PATHOLOGIC GRANULES –

• Pathologic granules of involved cementum were first described by Bass (1951)

• The clinical significance of these pathologic granules is related to the possibility that
they may be derived from or contain bacterial toxins which would contribute to the
pathogenicity of the cementum.

• However, as no direct evidence is yet available to explain the origin of these


granules, the need for their removal by root planing is still conjectural.

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PERMEABILITY –

• Wainwright, 1953 using radioactive iodine mouth rinses on the teeth revealed
some penetration of the iodine into the exposed cervical portions of the roots.

• No significance, however, can be drawn from this investigation with respect to any
changes in penetrability of periodontally involved subgingival cementum.

• Thus, there is no evidence as yet available Of any alteration in the permeability of


cementum when involved in periodontitis

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ENDOTOXIN —

• Hatfield and Baumhammers that periodontally involved cementum is toxic to cell


cultures. Suggesting the presence of cytotoxic substances associated with the
cementum.

• One such substance, endotoxin, a lipopolysaccharide

• The endotoxin which has been found in the cementum also may act to produce
direct labilization of the lysosomal enzymes found within the cells of the tissue
which then spill out into the tissue to effect their resorptive activities.

• Antigen activating the complement system.

• Thus, cementum may act to perpetuate the destructive effects of periodontal


disease by acting as a reservoir for potentially Destructive materials.

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• Eide et al mineralized surface coating is derived from components of inflammatory
exudate within periodontal pockets and that this might be a reservoir of cementum-
associated LPS.

• Recent studies by Nakb etal, Eide et al, lughes &L Smales have shown that the
endotoxins adhere to the surface of the root cementum rather than penetrate the
cementum as previously claimed, and also that the "binding" of the endotoxins to
the surface appears to be weak.

• These findings suggest that extensive removal of cementum would not be necessary
to render the root free of bacterial endotoxins

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CEMENTUM IN AGGRESSIVE PERIODONTITIS

• In 1923 Gottlieb described the disease now known as localised aggressive


periodontitis as a "diffuse atrophy of the alveolar bone". He later suggested that it
was caused by a defect in the dental cementum (Gottlieb 1928).

• The total lack of cementum in teeth affected by juvenile periodontitis may be


interpreted in two ways

– Organic Cementum matrix which failed to undergo mineralization had been


deposited in the hypo plastic areas

– cementum matrix had never been present on the root surface

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• The hypoplastic areas probably lacked periodontal attachment.

• The impaired attachment of the teeth to the alveolar bone may favor penetration
by motile bacteria such as spirochetes and flagellated rods.

• These microorganisms dominate plaque from teeth with aggressive periodontitis.

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DEVELOPMENTAL AND ACQUIRED ANOMALIES
ASSOCIATED WITH CEMENTUM
CEMENTAL TEARS –

• Cemental tear has been described as an rare periodontal condition characterized by


a total or partial separation of the cementum.

• According to the current classification of periodontal diseases.

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• Men mean age of 63.1 years, involving single-rooted vital or nonvital teeth,
especially the incisors and premolars.

• Etiology – traumatic occlusion , dental trauma , or a poor capacity of tissue repair


due to age.

• The cementum fragments, exposed or not to the oral environment, can initiate a
localized attachment loss

• Clinical sign is the presence of localized periodontal pockets with exudates and
localized pain.

• Treatment approaches have been suggested: scaling and root planning , open flap
debridement , bone graft, GTR, and extraction in cases of poor prognosis .

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ROOT SURFACE CARIES

Miller depicted these lesions as shallow, widely extended excavations


without distinct margins and with little similarity to cavities of the crown.

The lesions are commonly found in the roots of molars with a thick, white or
yellowish plaque deposit covering the abnormally rough, softened
cementum

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• Sumney et al found that root surface caries affected 49.2% of adult populations, was
usually incipient, and affected primarily the facial and lingual surfaces

• The characteristic histological pattern of caries in the cementum was explained by


Gottlieb on the basis that cementum is structurally similar to secondary dentin.

• Invasion rods

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• Furseth and Johansen noted considerable variation in the structural morphology of
carious cementum

– Thick mat of microorganisms covered the cemental surface and bacteria could
be seen in "lacuna-like spaces.“

– Regional differences of mineral distribution were observed which gave a


"brush-like" appearance due to alternating radiolucent and radiodense areas

• Also the cementum had a mottled appearance in some areas due to the variability in
mineral content.

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• Areas of demineralization are often related to root caries.

• Caries of the root may lead to pulpitis, sensitivity to sweets and thermal changes, or
severe pain. Pathologic exposure of the pulp occurs in severe cases.

• Caries of the cementum requires special attention when the pocket is treated.

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• CERVICAL ENAMEL PROJECTION

• Pathogenesis – If amelogenesis is not turned off before the start of root


formation, enamel may continue to form over portions of root normally covered by
cementum from odontogenic epithelium destined to form Hertwig’s root sheath

• Localised more common in mandibular


molars.

• Masters and Hoskins

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• ENAMEL PEARLS

• Pathogenesis –

• They appear to form as a result of localized failure of Hertwig’s root sheath to


separate from the dentin surface. The adhering epithelium becomes
amelogenetic and deposits of circumscribed globules of enamel which in turn
become covered by a layer of fibrillar cementum

• This anomaly consists of globules of enamel on the root surface in the cervical
region. They resemble small pearls up to several millimeters in diameter.

• While they may mimic calculus clinically and radiographicallyy, they cannot be
scaled off and elimination can only be accomplished by grinding. Large pearls
may contain pulp extensions.

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• CEMENTICLES –

• These are globular masses of acellular cementum, measuring less than 0.5mm in
diameter which are found within periodontal ligament. They generally exhibit
concentric appositional layers of afibrillar and/or fibrillar cementum

EMBEDDEDD

ATTACHED

FREE

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• Calcification of the epithelial cell rest of Malassez in the periodontal ligament
tissue.

• Calcification of the soft tissue between the Sharpey’s fiber

• Fragmentation and detachment of small piece of cementum from the root surface
due to excessive force on the tooth.

• Calcification of thrombosed blood capillaries within the periodontal ligament

• Generally, cementicles are not of clinical significance unless they become exposed
to oral environment where they may act as sites for plaque retention.

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• HYPERCEMENTOSIS

• Defined by Gardner and Goldstein

• Gottlieb demonstrated that all teeth continue to erupt throughout life and show a
slight increase in thickness of cementum
• physiologic process to maintain the integrity of the periodontium

• Zemsky stated that there was no general agreement of opinion on whether


hypercementosis was pathologic or physiologic.

• He reported five cases of unerupted, impacted, and malposed teeth exhibiting


marked hypercementosis with “no evidence of any pathologic condition

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• Humerfelt and Reitan Most frequent sites, are the maxillary and mandibular
premolar teeth. It occurs predominantly in adulthood, and the frequency increases
with age. It demonstrates a familial clustering, suggesting hereditary influence.

• ALEXANDER WEINBERGER on a basis of radiographic appearance

• The common type that cannot be differentiated from the original cementum has
been found associated with : (1) hypertrophic arthritis, (2) traumatic occlusion (3)
Paget’s disease (4) acromegaly.

• The second type, which in the radiograph appears more radiolucent than
cementum, has been identified with a history of rheumatic fever.

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• ETIOLOGY –

– IDIOPATHIC
– LOCAL FACTORS (CAUSING LOCALISED HYPERCEMENTOSIS)

Chronic periapical infection,


Lack of function due to unopposed teeth,
And abnormal occlusal trauma.

• hypercementosis of a bulbous or nodular enlargement OR in the form of multiple


cemental spikes distributed throughout the entire length of root.

• Concresence is another localized form of hypercementosis in which fusion of two or


more adjacent teeth occurs by deposition of cementurn.”Due to close approximation
of roots

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• SYSTEMIC FACTORS—leading to generalized hyper cementosis

PAGETS DISEASE (OSTEITITS DEFORMANS)—

• was first described by fox in 1933 when he reported the case of a patient with
knoblike irregularities involving the roots of all the Maxillary teeth

• lucasi suggests that the presence of Generalized hypercementosis in a patient of


the appropriate age group (40y)should always lead to consideration of the
possibility of Paget’s disease.

• Rao and karasickzo stated "Paget hypercementosis can be Differentiated from other
etiologies by the complete absence of periodontal membrane and lamina dura.

• Histologically, the periphery of root exhibits deposition of an excessive amount of


cementum over the original layer of primary cementum. The excessive cementum
maybe hypocellular or exhibit areas of cellular cementum that resemble bone
(osteocementum)

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• TOXIC GOITRE—
Hypercementosis With toxic goiter was reported by Kupfer in 1951. He found that
80% of the 36 patients in his toxic Goiter group had radiologic evidence of
hypercementosis.

• ARTHRITIS—
Patients with hyper throphic arthritis have marked overgrowth of cementum it is
based on assumption that tooth morphologically considered as joint (gomphosis)
leading to excessive deposition of cemuntum and ocurrs after age of 40 years.

Other systemic conditions include CALCINOSIS,RHUEMATIC FEVER, VITAMIN A


DEFICIENCY.

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• Radiographically, the radiolucent shadow of the periodontal membrane and the
radiopaque lamina dura are always seen on the outer border of an area of
hypercementosis, enveloping it as it would normal cementum

• On the other hand, from a diagnostic standpoint, periapical cemental dysplasia,


condensing osteitis, and focal periapical osteopetrosis may be differentiated from
hypercementosis by the fact that all of these entities lie outside the shadow of the
periodontal ligament and lamina dura

• Hypercementosis may be completely asymptomatic and found on routine


radiographic examination. The diagnosis of hypercementosis is made based on the
characteristic radiographic features described. Hypercementosis does not require
treatment.

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ANKYLOSIS –

• Definition
(Brearley and mckibben, 1972)

• Etiology

• The etiology of ankylosis is essentially unknown, but several theories have been
proposed

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• Biederman (1962) suggested the disturbed local metabolism theory.

• Traumatic injury of the alveolar bone or of the periodontal ligament has been
suggested as causative factors by many authors (Kracke, 1975; Henderson,1979).

• Kurol and Magnusson (1984) a developmental disturbance indicating a genetic


tendency.

• Certain endocrine conditions and congenital diseases, like CLEIDOCRANIAL DYSOSTOSIS


AND ECTODERMAL DYSPLASIA have been linked to a high incidence of tooth ankylosis.

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• Distribution
– Incidence of ankylosis in the deciduous dentition varies from 1.3 % to 9.9% .
– Mandibular first deciduous molars tend to be ankylosed more frequently
than maxillary deciduous molars at a ratio 8-1.
– Ankylosis may affect permanent teeth, but primary teeth are involved
approximately 10 times more frequently than permanent teeth
– The permanent teeth that most frequently become Ankylosed are the
mandibular and maxillary first molars followed by maxillary canines and
incisors

• DIAGNOSTIC FEATURES
Dull sound to percussion, lack of physiological mobility , infra occlusion ,
obliteration of pdl space, maloclussion.

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• CEMENTAL APLASIA AND HYPOPLASIA

• Charecterised by complete absence or decrease in cementum production

• ASSOCIATED WITH

Hypophospatemia —

• Hypophosphatasia (HPP) is a rare, inherited bone disease characterized by reduced


activity of the tissue non-specific (liver/bone/kidney) Isoenzyme of alkaline
phosphatase (TNSALP), due to deactivating mutations within the TNSALP gene
(Whyte, 2001).

• A consistent feature of HPP is premature loss of deciduous teeth (Chapple, 1993),


which is attributed to disturbed cementum formation ( Beumer et al., 1973)

• Cementum formation was almost Completely abolished in HPP, not only for acellular
cementum but also for cellular cementum.

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• Coffin–Lowry syndrome —

• Coffin–Lowry syndrome (CLS) is a rare genetic disorder.

• The syndrome presents with psychomotor retardation, short stature, skeletal


deformations, digit abnormalities, and distinctive facial features.

• Oral and dental findings in CLS are Common and they include thick prominent lips,
high palate, hypodontia, microdontia, delayed eruption, and early tooth loss.

• hypoplastic root cementum suggested as cause for primary loss of teeth in CLS

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• Cleidocranial dysostosis—

• Cleidocranial dysostosis (CCD) is a skeletal disorder associated with dental


anomalies such as failure or delayed eruption of permanent teeth and multiple
impacted supernumerary or permanent teeth.

• Smith and Sydney made detailed histological observations of the teeth of patients
exhibiting CCD and reported an almost complete lack of cellular cementum on both
the erupted primary and unerupted permanent teeth.

• Failure of disintegration of root sheath at the appropriate time leads to the


formation of the gap type of C-E junction. In the absence of cementum formation
at the crucial period of time, the lack of attachment of periodontal fibers may
probably lead to delayed eruption.

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CEMENTAL RESORPTION

• Under normal conditions, hard tissues are protected from resorption by their
surface layer of blast cell.

• Resorption of the mineralized tissues occur if clastic cells obtain access to the
mineralized tissue by a break in this barrier or when the precementum is
mechanically damaged or scraped off.

• The mineralized or denuded root areas attract resorbing cells to colonize the
damaged areas of root.

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• The cementum of erupted as well as unerupted teeth is a subject to resorptive
changes that may be of microscopic proportion or insufficiently extensive to present
a radiographically detectable alterations in root contour.

• Microscopic cementum resorption is very common. In one study conducted by


Henry and Weinmann, it occurred in 236 of the 261 teeth About 70% of all
resorption areas were confined to the cementum involving the dentin.

• apical third of the root 90.4%.


• middle third 19.2%
• 4% in the gingival third.

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• Cementum resorption appears microscopically as bay like concavities in the root
surface.

• Multinucleated giant cells and large mononuclear macrophages are generally


found adjacent to the cementum undergoing active resorption.

• The resorptive process may extend into the underling dentin but it is usually
painless.

• The newly formed cementum is demarcated from the root by a deeply staining line,
termed as the reversal line, which delineates the border of the previous resorption.
Embedded fibers of the periodontal ligament reestablish a functional relationship
with the new cementum.

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• THE VARIOUS CAUSES OF CEMENTAL RESORPTION ARE-

Local factors of cementum resorption:


1. Trauma from occlusion,
2. Orthodontic movement.
3. Pressure from malaligned teeth, cysts and tumors,
4. Teeth without functional antagonist
5. Embedded teeth.
6. Replanted and transplanted teeth
7. Periapical disease
8. Periodontal disease.

Systemic conditions predisposing to or inducing resorption are:


1. Calcium deficiency.
2. Hypothyroidism.
3. Hereditary fibrous osteodystrophy
4. Paget’s disease.
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CENTRAL LESIONS RELATED TO CEMENTUM
– Based on clinical, radiographic and histological features, bony lesions of
cementum were classified by Pinborg et al in 1971 as:

– PERIAPICAL CEMENTAL DYSPLASIA.


– BENIGN CEMENTOBLASTOMA.
– CEMENTIFYING FIBROMA.
– GIGANTIFORM CEMENTOMA.
– CEMENTO- OSSEOUS DYSPLASIA.

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PERIAPICAL CEMENTAL DYSPLASIA –

• periapical osteofibroma, cementoma, periapical fibrous dysplasia, periapical fibro-


osteoma, periapical fibro-osteo-cementoma, cementoblastoma .

• was first reported by 1860 by Forget, in horse.

• Brophy in 1915 described the lesion known today as periapical cemental dysplasia
(PCD) in man.

• It is a self- limiting bone abnormality. These lesions are site specific forming at the
apices of teeth.

• They are not the result of pulpal degeneration and do not cause devitalization of
teeth. So, the associated teeth should be vital unless involved by secondary
processes.

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• The lesions which are usually multiple, are more frequent in women than
in men and are usually seen between 4th to 5th decade. The cause is
unknown
well circumscribed radio
well- circumscribed radiolucency Irregular radio opacities opacity with distinct
within radiolucent area. radiolucent margin.
OSTEOLYTIC STAGE CEMENTO BLASTIC STAGE MATURE STAGE

• Since this lesion is innocuous and self-limiting, it’s significance is in


distinguishing it especially during the radiolucent phase, from
inflammatory periapical lesions such as periapical granuloma or
cyst.
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BENIGN CEMENTOBLASTOMA (TRUE CEMENTOMA) –

• Cementoblastoma , a rare ectomesenchymal odontogenic tumor, was 1 first


described by Dewey as early as in 1927.

• These are rare neoplasms representing less than 1% of all odontogenic tumors.
And commonly ocurs in second and third decade of life.

• Greater than 75% arise in mandible, with 90% arising in molar and premolar
region. They rarely affect the primary dentition. There is no sex predilection.

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• Pain and swelling are present in about two third of the cases

• Radiographically, the tumor appears as a radio opaque mass that is fused to


one or more tooth roots and is surrounded by a thin radiolucent rim.

• The outline of the roots is usually obscured as a result of root resorption and
fusion of tumor with the tooth.

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• The histopathological presentation of the cementoblastoma closely resembles
that of osteoblastoma, with the primary distinguishing feature being tumor
fusion with the involved tooth.

• The majority of tumor consists of sheets and thick trabaeculae of mineralized


material with irregularly placed lacunae and prominent basophilic reversal
lines.

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• Cellular fibrovascular tissue is present between mineralized trabaeculae.

• Multinucleated giant cells are often present, and the mineralized trabaeculae
are frequently lined by prominent blast like cells.

• Microscopic examination of the decalcified section revealed cementum-like


tissues attached to the tooth root

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• Treatment of a cementoblastoma usually involves the surgical extraction of
the tooth with the attached calcified mass.

• Brannon et al reviewed and observed a recurrence rate of approximately


37% .

• recurrence is more likely if curettage without extraction of involved teeth is


done.

• Thus recommended treatment is complete resection of tumor with


enucleation and extraction of associated teeth followed by curettage and
peripheral osteotomy.

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CEMENTO-OSSEOUS DYSPLASIA
• most common dysplatic lesion encountered in clinical practice. It occurs in the
tooth bearing areas of the jaws and it develops in close approximation to
periodontal ligament and exhibits histopathological similarities with it.

• Based on clinical and radiographic features, it is separated into three groups


(WHO 2005)
1) focal 2) periapical and 3) Florid

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FOCAL CEMENTO OSSEOUS DYSPLASIA –

• It is characterized by single site involvement. It has a female predilection and


occur at a mean age of 38 years with predilection for 3rd to 6th decades. Can
occur in any areas of mouth but most commonly found in posterior
mandible. Most lesions are smaller than 1.5 cm in diameter.

Radiographic findings –

Radiolucent to radio opaque with a thin peripheral radiolucent rim with


well defined or irregular borders.

PERIAPICAL CEMENTO OSSEOUS DYSPLASIA –

• Common in periapical region of anterior mandible. Solitary or multiple foci


are present . Female to male predilection is 10:1 and 70% of cases are
blacks with age of 30 – 50 years .

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Radiographic findings – found as a chance radiographic finding. Radiograph
reveals well circumscribed areas of radiolucency involving the apical area of the
tooth. Later adjacent lesions fuse to form a linear pattern of radiolucency that
envelops the apices of several teeth.

Florid Cemento Osseous Dysplasia – (Chronic Diffuse Sclerosing Osteomyelitis,


Sclerotic Cemental Masses of the Jaws; Multiple Enostosis, Gigantiform
Cementomas)—

• Although may regard this as a disease of bone, others think it is of


cementum.

• This disease exhibits a strong predilection for middle- aged, black females.
The age ranged from 26 to 59 with a mean of 42 years.

• The lesion shows marked tendency for bilateral often symmetric .

52
• in some it causes intermittent, dull pain. expansion of the involved bone occurs
but expansion is rarely sufficient to produce facial swelling. Fluid containing
bone cavities (cysts) are also found.

• Radiographic findings –

• The typical lesion of osseous dysplasia shows radiodense masses with


surrounding halos of radiolucency. In some cases, the lesions seem to
originate around the roots of teeth .

• As the dense material grows, it may attach to the roots of teeth. These
observations are taken as evidence that the material is cementum.

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Histopathological findings –

• All 3 lesions demonstrate similar histopathologic features. The tissues contain


fragments of cellular mesenchymal tissue composed of spindle- shaped
fibroblasts and collagen fibers with numerous small blood vessels .

• within this fibrous connective tissue is a mixture of woven bone, lamellar


bone, and cementum like particles forming a relatively acellular cemento-
osseous material.

• Sclerosis and calcification, are the hallmark of progression .

• Aging increased the risk of necrosis and secondary infection, primarily because
of ischemia of the affected tissues.

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Treatment –

• Uncomplicated osseous dysplasia requires no treatment therefore, teeth


should not be extracted without good reason.

• Traumatic ulceration of overlying mucosa due to exposure of sclerotic masses


also predisposes to infection.

• Antibiotics followed by saucerization of bone are indicated in such cases.

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FAMILIAL GIGANTIFORM CEMENTOMA

• It is a disorder of the gnathic bone that ultimately leads to the formation of


massive sclerotic masses of disorganized mineralized matter.

• It is an autosomal dominant disorder that demonstrates a high penetrance and


variable expressibility, predilection for Caucasian population.

• clinically it causes Gnathic enlargement, facial deformity, malocclusion,


impactions.

• The affected bone in final stages is very sensitive to inflammatory stimuli and
becomes necrotic with minimum stimuli.

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Radiographic findings –

• Most patients develop radiographic alterations during first decade initial


features resemble cemento-osseous dysplasia, appearing as multiple
radiolucencies in periapical areas. Mature lesion is predominantly radio
opaque with thin radiolucent rim.

• Histologically, familial gigantiform cementoma shows same spectrum of


changes as cemento-osseous dysplasia and both cannot be distinguished
microscopically.

• Treatment involves extensive resection of altered bone and reconstruction of


facial skeleton and associated soft tissues.

57
CEMENTIFYING FIBROMA

• It is a true neoplasm with significant growth potential it resemble focal cemento


osseous dysplasia radiographically and to a lesser extent histopathologically.

Hisotological features –

• well demarcated from surrounding bone with fibrous capsule.

• Tumor mass contain fibrous tissue and hard tissue is formed by trabeculae of
osteoid and bone or poorly cellular spherules that resemble cementum.

• The cemental spherules contain peripheral brush borders that blend in to adjacent
connective tissue.

58
Radiological features –

• The appearance is variable and depends on the amount of bone (cementum)


produced.

• Those tumors with little calcified material are radiolucent. Those with much
calcified matrix are radiodense.

• Intermediate degrees of radiolucency-radiodensity may be seen. The border of


the tumor is usually sharply circumscribed.

Treatment –

• As it is well circumscribed enucleation can be done with relative ease recurrence


and malignant transformations are rare.

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CONCLUSION
• Cementum is probably the least understood of all dental tissues.

• But this does not lessen its role in the periodontal attachment apparatus.

• With the development of newer concepts of regenerative cementogenesis, the


need for us to better understand this basic tissue is very much essential.

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REFERENCES
• CARRANZA’S CLINICAL PERIODONTOLOGY-10’TH EDITION.

• SHAFERS TEXT BOOK OF ORAL PATHOLOGY – 6’TH EDITION.

• ORAL AND MAXILLOFACIAL PATHOLOGY 3’RD EDITON

• CEMENTUM INVOLVED IN PERIODONTAL DISEASE: A REVIEW OF ITS FEATURES


AND CLINICAL MANAGEMENT 1979, JOURNAL OF DENTISTRY,7,3,185-193.

• THE PERIODONTALLY-INVOLVED ROOT SURFACE, J CLIN PERIODONIOL 1993: 20:


402-410

• PERIODONTITIS WITH HYPERCEMENTOSIS: REPORT OF A CASE AND DISCUSSION OF


POSSIBLE AETIOLOGIC FACTORS, AUSTRALIAN DENTAL JOURNAL 2012; 57: 511–514.
• PERIAPICAL CEMENTAI DYSPLASIA AND PERIODONTAL DISEASE A CASE REPORT
WITH REVIEW OF THE LITERATURE J PERIODONTAL2010,55,3,181-197.

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