G DM -----------------------RNING

!By: Dr. Ram Thiramdas

TRY TO GUESS THE TOPIC?

REGRESSIVE ALTERATIONS

OF TEETH (RAOT)

• Results in Results in wear and tear wear and tear – Mostly n few – Mostly n few exceptions.exceptions.

• Impaired structures Impaired function.Impaired structures Impaired function.

• A variety of alterations in . . . . . . (E, D, P & C)

• There are not developmental abnormalities or inflammatory lesions.

Complete loss/defect in enamel leads to dentinal hypersensitivity!

RAOT- Changes seen in the teeth structure.

THERE IS NO BACTERIAL INVOLVEMENT IN RAOT!

• These regressive changes results fromThese regressive changes results from

-General -General ageing process.ageing process.

- Chronic injury - Chronic injury to the tissues.to the tissues.

Enamel

Attrition Abrasion Erosion Abfraction

Dentin Dentinal sclerosis Dead tracts Secondary dentine

Pulp Reticular atrophy of pulp Pulp calcifications

Resorption of teeth External Internal Cementum

Hypercementosis Cementicles

REGRESSIVE ALTERATIONS OF TEETH

Physiologic wearing away of a tooth as a result of tooth to

tooth contact as in mastication and occlusion.

Term- Latin verb ATTRITUM refers to the action of

rubbing against another surface.

The older a person gets, the more attrition he exhibits.

“The older a person gets, the more RAOT SEEN”

•Up to some degree it is physiological, when the

amount of tooth loss is extensive and begin to affect

the esthetic appearance and function ,the process is

considered as pathologic.

AETIOLOGY•AGEING OF AN INDIVIDUAL.

•HABITS SUCH AS CHEWING TOBACCO OR GUM.

• ABNORMAL TEETH ARRANGEMENT CAUSING TRAUMATIC OCCLUSION.

•PYSCOLOGICAL DISORDER PATIENTS.

•COARSENESS OF THE DIET.

•BRUXISM.

FACTORS:

a) Poor quality or absent enamel – eg: Fluorosis Enamel hypoplasia Dentinogenesis imperfecta

a

A.

B.

c.

b

c

b) Premature contacts - Edge-to- edge

occlusion.

c) Intraoral abrasives, erosion, grinding

habits.

CLINICAL FEATURES: Abnormalities in occlusion and chewing pattern .

Occlusal , incisal, proximal surface.

Primary & permanent dentition.

Primary dentition : Amelogenesis and Dentinogenesis

imperfecta.

M > F.

Habits.

According to Robinson there is also shortening of

dental arch due to proximal attrition.

APPEARANCE: As a small polished facet on the cusp tip or ridges or slight

flattening of an incisal edge.

Advanced Conditions: when enamel is

completely worn it appear as yellow or brown

staining of the exposed dentine. Thus there is

formation of secondary dentin to protect pulp.

Correction of abnormalities in teeth structure.

Correction of parafunctional habits.

Protection of tooth by metal or metal

ceramic crowns, where structural defects

exists.

Construction of occlusal guards in bruxism

habit if persists.

DEF : Abrasion is a pathological wearing away of tooth by some abnormal mechanical process.

•The term – Latin verb – ABRASIUM –means to scrape off and implies wear or partial removal through a mechanical process.

•Mainly on exposed root surfaces.

• Different foreign substances produce different patterns of tooth

abrasion .

• Though the etiology is varied , the pathogenesis under these different

conditions is essentially identical .

a. Tooth brush abrasion

b. Habitual abrasion

c. occupational abrasion

d. prosthetic abrasion

e. Ritual abrasion

RIGHT HAND BRUSHING LEFT HAND BRUSHING

• Most common type .• Horizontal direction . • Horizontal cervical notches on buccal surfaces of exposed

radicular cementum and dentin at the CEJ in the teeth with some gingival recession .

Foregin body abrasion

So, change your tooth brush before it turns into a sun flower.

• Pipe smokers, Tooth picks / Dental floss

•Prosthetic abrasion.

•Ritual abrasion.

•Pipe smokers

OCCUPATIONAL ABRASION

Develops when objects / instruments are habitually held between the teeth by people during work .

• Carpenters

• Shoe makers

TAILORING

CLINICAL FEATURES:

• Appear as V shaped or wedge ditch on the root side of the

CEJ in the tooth with some gingival recession.

• Lesions are more wide than deep.

• Premolar and cuspids are more commonly affected.

• Exposure of dentinal tubules.

• Consequent irritation to odontoblast process.

• Secondary dentine formation.

• Avoidance of abnormal brushing habits. • Restorative treatment.• Patient education.

DEF:

Irreversible loss of hard dental tissues by a chemical processes

not involving bacterial action.

GERD

ETIOLOGY

EXTRINSIC- ACIDIC BEVERAGES ,

CITRIC FRUITS,

MEDICATIONS,

CARBONATED DRINKS,

FRUITS, DRINKS.

-SEEN ON LABIAL AND BUCCAL REGIONS.

INTRINSIC:

•GASTROEOSOPHAGEAL REFLEX DISEASE

(GERD) & VOMITING.

•SEEN ON LINGUAL AND PALATAL SURFACES.

SALIVA AS A MODIFYING FACTOR FOR EROSION

1) Salivary PH

2) Buffering capacity

3) Flow rate of saliva

NEUTRALISES ACIDS IN THE ORAL CAVITY

•MINERAL IONS IN THE SALIVA HELPS IN THE REMINERALIZATION PROCESS.

CLINICAL FEATURES

Broad concavities with in the smooth surface enamel.

Cupping of occlusal surface (incisal grooving) with dentine exposure.

Increased incisal translucency.

Wear on non occluding surface.

Raised amalgam restorations.

Hypersensitivity- trigger to secondary dentin formation.

Pulp exposure in deciduous teeth.

PERIMOLYSIS:

Erosion of dental structures due toexposure to gastric secretions is termed as perimolysis

EROSION

TREATMENT

•Identification of the etiology is the first step in the management of erosion.

•Gerd- general physician.

•Salivary hypofunction- sugarless

chewing gums.

-Use of straw for cool drinks.

- Acidic drinks should be drunk quickly rather

than sipped.

- A patient with alcholism should be treated in

rehabiltation program.

Grippo – 1991

It is pathologic loss of enamel and dentine caused by

biomechanical loading force.

Loss of tooth surface at the cervical areas of teeth

caused by tensile and compressive forces during tooth

flexure.

Studies need to prove the hypothetical phenomenon.

Crack on a wall

Yet to be proved!

ETIOLOGY

•FORCES PRODUCES DURING SWALLOWING, TONGUE THRUSTING AND CLENCHING OF THE TEETH .

•FORCES PRODUCES DURING CHEWING.

•INDIVIDUALS WITH OPEN BITE DEEP BITE

Deep narrow V – shaped notch. Affects the buccal / cervical areas of

teeth. Often affects a single tooth with

adjacent tooth unaffected. Most commonly affects bicuspids and

molars.

CLINICAL FEATURES

•Identification and correction of aetiological agent.

•Restoration helps to keep the tooth surface intact and prevents furthur tooth wear.

TREATMENT

Characterized by calcification of dentinal tubules.

Cause: Results due to injury to the dentinal tubules.

DC.

Abrasion.

Aging process.

-

Appearance:

Translucent zone in transmitted light

(refractive index)

Seen in

- Apical third of root

- In crown midway between DEJ & surface of

pulp.

- Dentine underlying the cavity.

-The exact mechanism of dentinal sclerosis or

the deposition of calcium salts in the tubules is

not understood.

- Sclerotic dentin is more calcified than

reperative dentin.

Sclerosed dentin (1)

Dead tracts (2)

secondary dentin (3)

TRANSLUCENT DENTIN (1)

More mineralised

Source of Ca salts:Dental lymphsaliva

Result:Decreased conductivity of odontoblastic

process.Slows the advancing carious process.

Dye cant penetrate through the sclerotic dentine.

Dead tracts are empty dentinal tubules filled with air. These

appear dark in ground section of dentin under transmitted

light and white under reflected light.

The dead tracts are formed due to degeneration of

odontoblastic process in the dentinal tubules. This occurs

due to exposure of dentin following attrition, abrasion or

erosion.

Dead tracts develop in the region of cusp or incisal edge due

to death of odontoblasts as a result of overcrowding.

DEAD TRACTS

-Formed in response to normal or abnormal stimulus after

complete formation of tooth.

a) Physiological secondary dentin :

•Formed after root completion and eruption of teeth.

•It is regular, uniform layer of dentin around the pulp

chamber which is laid down throughout the life.

• This type of secondary dentin is produced more slowly

than primary dentin.

•Physiological secondary dentin is similar to primary

dentin and is seperated by deep stained resting line.

Primary dentin Secondary dentin

Contour line

b) Reparative secondary dentin/ Tertiary dentin /

reactive dentin•Result of irritation, abrasion, erosion or operative

procedures.

•These processes cause degeneration of a large number of

odontoblasts. But, few odontoblasts survive and form dentin.

•The degenerated cells are replaced by the undifferentiated

cells of cell rich zone of the pulp.

CLINICAL FEATURES: No significant clinical features are there

to identify the secondary dentin formation.

There is decrease in the sensitivity due to secondary dentin formation.

THIS TYPE OF DENTIN FORMS ADDITIONAL INSULATING LAYER IN TOOTH.

Change in the direction of the dentinal tubules as they pass from primary (b) to secondary ( a) dentin

R/F: Seen in in pulp horn areas as well as on the proximal wall of teeth

with proximal caries.

Seen on routine radiographic investigations.

H/P Secondary dentine is rapidly formed at a rapid rate and

odontoblasts may become entrapped producing a superficial

resemblance to bone – osteodentine. Some times, irregular dentine and mixed dentine are seen.

REGRESSIVE CHANGES OR DEGENERATIVE CHANGES OF PULP

Reticular atrophy of pulp Pulp calcification

DEPOSITION OF CALCIFIED MASSES WITHIN THE PULP FOR NO APPARENT REASON S IS CALLED PULP CALCIFICATIONS.

Characterized by presence of large vacuolated spaces in the pulp, with

a reduction in the number of cellular elements.

Associated with degeneration and disappearance of the odontoblasts.

It is seen in elderly people, as the age changes. There is no clinical

significance

It can be produced by improper fixation of the tooth and pulp after

extraction followed by histological sectioning.

Most investigators feel it as artifact but not degenerative change.

CLASSIFICATION-DENTICLES-PULP STONES-DIFFUSE CALCIFICATION.

DENTICLES•Denticles are small masses of tubular dentin formed within the pulp near the furcation area of the tooth.

•They are believed to form as a result of epithelio-mesenchymal interaction within the developing pulp.

PULP STONESTRUE PULP STONES:

•Localized mass of calcified tissue that resemble dentine because of their tubular structure.

•Resemble secondary dentine, because of few dentinal tubules and irregular arrangement. •Site : More common in pulp chambers than root canals.

True denticles -- Depending on attachment 2 types

Attached denticles– attach to the dentinal wall.

Free denticles- Not attached to the dentinal wall.

False denticles: Don’t exhibit dentinal tubules They are larger than true denticles Nodules appear to be made up of concentric layers

or lamellae deposited around the nidus Free Attached typeo Interstitial denticle

Free PULP STONE

Attached PULPSTONES

Embedded PULP STONES

PULP STONES

DIFFUSE DENTICLES / CALCIFIC

DEGENERATION:

Seen in Root canals.

Pattern of calcification is in amorphous, unrecognized linear strands or columnar paralleling the blood vessel and nerves of the pulp.

CONDITIOS WHERE PULP STONES ARE SEEN ARE

-DENTIGEROUS IMPERFECTA

-DENTIN DYSPLASIA

-REGIONAL ODONTODYSPLASIA

ETIOLOGY Local metabolic dysfunction

Trauma

Hyalinization of injured cells Vascular damage

Fibrosis Mineralization (Nidus formation)

Growth with time Pulp stone

Types: External resorption Internal resorptionINTERNAL RESORPTION:

(Chronic perforating hyperplasia of pulp, Internal granuloma, Odontoclastoma, Pink tooth of mummery.)

Characteristic feature: Unusual form of tooth resorption that begins centrally with in the

tooth associated with peculiar inflammatory hyperplasia of pulp. Cause pulpal inflammation / unknown.

Two main patterns Inflammatory resorption Replacement or metaplastic resorption.

INFLAMMATORY RESORPTION:

Resorbed dentin is replaced by inflamed granulation tissue. Site – cervical zone Resorption continues as long as vital pulp remains Coronal pulp – necrotic and apical pulp – vital

Appear as uniform , well circumscribed symmetric

radiolucent enlargement in the pulp chamber or canal

.

Involvement of coronal pulp - pink tooth of

mummery as the vascular resorptive process approaches the surface.

When the root surface is perforated, it is impossible to determine whether the lesion began externally or internally.

REPLACEMENT INTERNAL RESORPTION:Here portion of pulpal dentinal wall are resorbed and replaced with bone or

cementum like boneR/F : Enlargement of the canal that is filled with bone or cementum like bone

will be less radiolucent than the surrounding dentin.

So the central zone appears partially obliterated. The out line of destruction is less defined than that seen in inflammatory resorption.

H/F: Variable degree of resorption of the inner or pulpal

surface of the dentine and proliferation of pulp tissue filling the defect.

Lacunae shows - odontoclasts or osteoclasts so called as odontoclastoma.

Ch. Inflammatory cells are present. Lacunae like areas in the dentin or osteodentin Enamel is also resorbed when the internal resorption

occurs in the crown portion.

Resorption begins on the external surface of teethETIOLOGY: Periapical inflammation Reimplantation of teeth Tumors and cysts Excessive mechanical or occlusal forces Impaction of teeth Dental trauma Hormonal imbalance Intra coronal bleaching of pulp less teeth Local involvement of herpes zoster Paget's disease of bone PDL treatment

CHARACTERISTIC FEATURE : Non neoplastic condition in which excessive cementum is deposited

in continuation with normal radicular cementum.ETIOLOGY: Local factors Systemic factors Idiopathic factorsConditions which favor the deposition of excessive amount of cementum Accerlated elongation of tooth Inflammation around the tooth Tooth repair Ostitis deformans or pagets disease of bone

Accerlated elongation of tooth: Loss of antagonist hyperplasia of cementum ( to

maintain the normal width of periodontal ligament) Site : apex of the tooth

Inflammation at the apex of a tooth root: Cause – pulpal infection Cementum is laid down on the root surface at some distance

above the apex as the cementoblasts are induced by inflammatory reaction

Deposition of cementum doesn’t occur immediately adjacent to the area of inflammation since the cementoblasts and their precursors in this area have been lost as a result of the inflammatory process

Tooth repair:

Occlusal trauma - mild root resorption which is repaired by secondary

cementum

Root fracture repaired by deposition of cementum between the tooth

fragments and the periphery

Cemental tear, detachment of strip of cementum from the root due to

trauma are repaired by cementum growing in to and filling the defect

Ostitis deformans/ pagets disease:

Generalized skeletal disease characterized by deposition of excess

amount of secondary cementum on the roots of the teeth and by

apparent disappearance of laminadura.

Generalized hyper cementosis is suggestive of osteitis deformans

Spike formation: Characterized by the occurrence of small spikes or out

growths of cementum on the root surface.Cause : Excessive occlusal trauma May occur due to deposition of irregular cementum in focal

groups of periodontal ligament fibers Exact mechanism not known

C/F: No significant clinical signs and symptoms When these teeth are extracted roots appear larger in

diameter than normal and present round apices

R/F: Thickening and apparent blunting of roots by loss in their

typical sharpened or spiked appearance. It is impossible to distinguish it from dentine so diagnosis

is made on shape or out line of root.

o Cementicles are small foci of calcified tissue which are not true cementum but lie free in the periodontal ligament of the lateral & apical root areas.

o These represent the areas of dystrophic calcifications.

o Cementicles are round globules of calcium salts which arise from focal calcifiction of connective tissue between sharpeys bundles with no apparent central nidus.

•There is small spicules of cementum torn from the root surface known as cemental tears, if lying free in the periodontal ligament may resemble cementicles

•Cementicals appear through calcification of thrombosed capillaries in the pdl.

•Clusters of cemeticles at the apices of teeth may be called CEMENTOMA

•No clinical significance.

Few questions to analyse,

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ThaNk Q

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