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REGRESSIVE ALTERATIONS OF TEETH

Regressive changes in dental tissues are alterations that could be:


A-associated with the aging process B-Resulting from injury to dental tissues

Attrition
Definition: physiological wearing away of a tooth as a result of tooth to tooth contact in mastication. It is associated with the aging process.

Attrition
Affected tooth surfaces: occlusal,
incisal and proximal. Except in cases of malocclusion.

Affected

dentitions: primary
and permanent

1.Abnormal occlusion e.g. crowding of teeth or malposed teeth. 2.Abnormal chewing habit e.g. bruxism

3.Structural defects in teeth e.g. Amelogenesis imperfecta Dentinogenesis imperfecta

TYPES: 1.Physiological attrition tooth loss proportinate to age of individuals. 2.Pathological attrition occurs due to certain abnormalities in occlusion,chewing pattern or some structural defects.

Attrition
Clinical appearance:
Attrition is first seen as a small polished facet on the tip of cusp, or as a flattening of the incisal edge. Similar facets occur on the proximal surfaces as a result of slight mobility of teeth in sockets (resilience of periodontal ligament.)

Attrition
As the person becomes older, there is: 1- gradual reduction in cusp height, which may progress to loss of cuspal interdigitation. 2- Flattening of the occlusal plane. 3- Shortening of the length of dental arch due to proximal attrition.

The amount of attrition depends on:

1Age: more attrition is seen with aging. 2- Sex: more attrition is seen in males due to greater masticatory forces. 3- Consistency of diet: coarse diet is associated with increased attrition. 4-Habits: Such as chewing tobacco or bruxism

Secondary dentine formation: The

exposure of dentinal tubules following the wearing down of enamel result in irritation of the odontoblastic processes and formation of secondary dentine, this prevent pulp exposure through attrition.

TREATMENT
1.Correction of developmental abnormality

2.Correctionof parafunctional chewing habit.

3.Protection of tooth by metal or metal ceramic Crowns where structural defects are present.

Abrasion
Definition: It is the pathologic wearing away of tooth through abnormal mechanical processes.
Site: Exposed root surface, sometimes

on incisal or proximal surfaces.

Causes of abrasion:

1-

abrasive dentifrice, with forceful use of tooth brush in horizontal direction. This leads to V-shaped or wedge shaped ditch on root surface at the cemento-enamel junction.

Causes of abrasion
2- Habits or occupations: Opening of bobby pins or holding nails with teeth result in notching of the incisal edge of maxillary central incisors

Causes of Abrasion
3- Pipe smokers 4- Improper use of tooth picks

Secondary

dentine formation: The exposure of dentinal tubules following abrasion results in irritation of the odontoblastic processes and formation of secondary dentine, this prevent pulp exposure unless abrasion is severe and rapidly progressing.

CLINICAL FEATURES:

1.In abrasion of tooth the type and severity of surface will depend upon the duration and type of faulty habit adopted by the person. 2.Maxillary teeth are more commonly affected than the mandibular teeth. 3.Tooth brush abrasion commonly occurs in cervical region of labial surface of incisors canines and premolars 4.The produces a v shaped or wedge shaped groove on the tooth with sharp angels and highly polished dentine surface 5.Toothbrush abrasion may causes gingival recession 6.The occupational abrasion often produces a small deep well polished ditch on an incisal edge of teeth 7.Severe abrasion may cause opening of dentinal tubules and hence the patient experiences sensitivity in affected teeth due to hot and cold substance.

TREATMENT 1.Adaptance of normal brushing habits prevent abrasion.

2.Restoratine treatment helps to keep the tooth surface intact and prevent further tooth wear.

EROSION

DEFINATION Erosion is a progressive loss of hard dental tissue by chemical processes not involving bacterial action.

ETIOLOGY
Extrinsic causes: 1.citrus fruits intake (more than twice daily) 2.soft drink consumed (4-6 or more per week) 3.eating disorder (weekly or more often) 4.sports drinks intake (weekly or more often) 5.bruxism habits 6.excessive saliavation 7.whole saliva unstimulated flow rate (0.1ml/min) 8.symptoms of history of gasoesophageal reflux disease (GERD)

Causes: Acids from: external sources (work environment eg. Battery manufacturing or excessive use of citrous fluids in diet).

or internal sources (regurgitation of gastric contents as in chronic vomiting and anorexia nervosa). Vomiting causes generalized abrasion on lingual surfaces.

CLINICAL FEATURES
1.Broad concavities within smooth surface enamel 2.Cupping of occlusal surfaces (incisal grooving) with dentin exposure 3.Increased incisal transluscency 4.Wear on non-occluding surface 5.Raised amalgum restoration 6.Clean,non-tarnished appearance of amalgams 7.Loss of surface characteristics of enamel in young children 8.Preservation of enamel cuff in gingival crevice is comman 9.Hypersensitivity 10.Puip exposure in deciduous teeth

TREATMENT
1.Treatment of etiology-GERD-Medical therapy 2.Salivary hypofunction -use sugarless gum/mint chewing 3.Sjogrens syndrome/post therapeutic head and neck radiation -use oral pilocarpine(salagen)

PROTOCOL FOR PREVENTION


1.Diminished the frequency and severity of the acid challenge 2.Enhance the defence mechanism of the body (increase in salivary flow and pellicle formation) 3.Enhance acid resistance,remineralization and rehardening of the tooth surface 4.Improve chemical protection 5.Decreased abrasive forces 6.Provide mechanical protection 7.Monitor stability

ABFRACTION
(coined by GRIPPO in 1991) DEFN loss of tooth surface at the cervical areas of teeth caused by tensile and compressive forces during tooth flexure.(Hypothetical phenomenon) ETIOLOGY 1.Biomechanical forcesa.static- eg.Produced due to swallowing and clenching. b.cyclic-eg.Force during chewing action 2.The breakdown proprtinate to magnitude; duration; direction;frequence and location of forces.

C/F 1.Affects buccal or lingual cervical areas of teeth.(Gingival 1/3rd) 2.Deep narrow v shaped lesions. 3.Commanaly affects single teeth with excursive inferences or eccentric occlusal loads.

DENTINAL SCLEROSIS /TRANPERANT DENTIN INTRODUCTION: is a condition characterised by calcification of detinal tubulels of the tooth. ETIOLOGY: Injury to dentin by caries. Aging process Abrasion or erosion of tooth. Sclerotic dentin found under slowly progressive caries. MECHANISM Exact mechanism unknown. Calcium salts deposition from fluid Dental lymph within tubules | Increased mineralization | Decreased conductivity of odontoblstic process.

IMPORTANCE It reduces permiability of dentin and prolongs pulp vitality. Sclerosis decrease conductivity of tubules. HISTOLOGICAL FEATURE It presents as a translucent zone in teeth without seen by transmitted light because difference in R.I. of sclerotic or calcified dentinal tubules. DEAD TRACTS Seen in G.S. as dark zone by transmitted and white zone by reflected light. Optical phenominon ;due to difference in R.I. of affected and normal tubals.

Dentinal sclerosis (translucent dentine)


Definition: Regressive alterations characterized by calcification of dentinal tubules. Causes: 1- Normal age change in dentine. 2-Injury of dentine by caries or abrasion

Microscopicappearance:
by transmitted light, a ground section of shallow

caries shows a translucent zone of dentine underlying the caries cavity. This is due to difference in refractive indices between calcified dentinal tubules and adjacent normal ones.

Significance: Increased mineralization or sclerosis: 1Decreases conductivity of dentine. 2Slows the advancing caries process.

Secondary dentine
Definition: Dentine having irregular morphologic pattern formed physiologically in response to stimuli associated with aging process, or pathologicaly as a result of stimulation of dentinal tubules and odontoplastic processes from caries, attrition, abrasion, erosion tooth fracture and cavity preparation.

Physiologic

Microscopic appearance:

secondary

Pathological

similar to primary dentine but with fewer dentinal tubules.

dentine:

secondary

irregular, few tortuous dentinal tubules. Some odontoblasts may be entrapped in the rapidly formed tissue, so it is called osteodentine.

dentine:

CLINICAL FEATURES 1.Not significant 2.Descreased in tooth sensitivity 3.Delayed pulpal involvement as it acts as insulating layer of calcified tissue 4. Found in both dentition; anterior > Molar (Bevelander and Benzer)

ROENTGENOGRAPHIC FEATURES 1.Found in pulp horn areas particularly also on proximal wall of teeth with proximal caries. 2. Decreased size of pulp chamber and root canal. HISTOLOGICAL FEATURES 1.Same as 1* dentin but demarcated by deep staining as exhibit different tinctorial reaction. 2.Fewer tubules with irregular course Inconspicuous if not completely absent . 3.Formed at rapid rate and odontoblast may entrapped ,resembles to bone;then termed as Osteodentin. 4.Rate of formation insignificant-:

RETICULAR(ATROPHY OF PULP 1.More discrete vacuolization of pulpal tissue and cells as age changes. HISTOLOGICAL FEATURES-: 1.Large vacuolated spaces in pulp with decrease in cellular element disappearance of odontoblast 2.According to most investigators conditions an artifact Purely and not in vivo

PULP CALCIFICATION In includes morphological form 1.CELL CHANGES 2.FIBROSIS 3.PULP STONES/DENTICLES 4.DIFFUSE CALCIFICATION ETIOLOGY CLINICAL SIGNIFICANCE

1.CELL CHANGES 1.Decrease size an no. of cytoplasmic organells 2.Pulpal fibrocytes/fibroblast have abundant rough surface cytoplasmic reticulam ;golgi bodies and numerous mitochondri with well developed cristae. 3.Ffibroblas exhibite less perinuclear cytoplasmic processes. 2.FIBROSIS 1.Acumulation of diffuse fibrillar componetns and bundles of collagen fibre. 2.Fibrous bundles arranged longitudinally in radicular and diffuse on coronal pulp. 3.Increase fibre in pulp organ is generalised. 4.Vascular changes occur in pulp organ. 5.Atherosclerotic plaque apprars in pulpal vessels. 6.Calcifications in walls of blood vessels near apical foramen. 7.Outer diameter increaed as increase in collagen fibre in medial and adventitious layer.

PULP STONES / DENTICALS


1.Nodular calcified masses appearing and coronal portions of pulp organ. 2.Asymptomatic unless impinges nerves or lod vessels. 3.According to structure C/as a.true b.false according to relation to dentin a.free b.attached c.embedded 4.Eventually fill substantial part of pulp chamber.

LOCAL METABOLIC DYSFUNTION

TRAUMA

HYLINISATION OF INJURED CELLS

VASCULAR DAMAGE (TROMBOSIS) VESSEL WALL DAMAGE

TROMBOSIS

MINERALISATION (NIDUS FORMATION) GROWTH WITH TIME

PULP STONES

5.TRUE DENTICALS Localised masses of calcified tissue resembles dentin as tubular structure(sec. dention) tubules are irregular and few in no. more comman in pulp chamber than root canals 6.FALSE DENTICALS Localized masses of calcified tissue unlike true dentine not exhibit dentinal tubules concentric layers or lamellae deposited around a central nidus.

4.DIFFUSE CALCIFICATIONS 1.Appears as irregular calcific deposits in pulp tissue,collagenous fibrous bundles in blood vessels. 2.Persits as fine calcified spicules and may develop to large masses. 3.Found in root canals surrounding blood vessels 4.Also K/as calcific degeneration EITIOLOGY 1.unknown,increases with age. 2.No relation with local or systemic diseases or gender 3.Micro organisms high % of pulp stones yeild pure growth of steptococcus in culture 4.Operating procedures +restorative materials---pulp stones incidence increase CLINICAL SIGNIFICANCE 1.Mild to severe pulpal neuralgia,excruciating pain resembles tic doulerex (trigeminal neuralgia) 2.Difficulty in pulp extirpation during RCT.

Resorption of teeth
Physiological resorption occurs in the roots of deciduous teeth due to pressure from successors. In deciduous teeth, a period of resorption is followed by repair. Occasionally excessive repair tissue deposited during the resting

phases of resorption results in fusion of the roots with adjacent bone, preventing shedding.

Types of resorption:
External: Occurs on the external surface of root or crown due to tissue reaction in the pericoronal or

periodontal tissues. Internal: Occurs on the inside of the tooth due to pulpal reaction

Mechanism: Resorption occurs by the action of osteoclasts activated by pressure. Osteoclasts are derived from fusion of blood monocytes. They are multinucleated cells with ruffled border. Osteoclast are seen lying in lacunae in hard tissue.

Causes of external resorption

Periapical periodontitis: A long standing periapical granuloma may cause root resorption. This appears in x-rays as a slight raggedness or blunting in the root apex.

EXTERNAL RESORPTION a.Periapical inflammation 1.resorption of calcifid tissue same as bone. 2.trauma or pulpal infection periapical granuloma resoption of root apex;as resoption more in vascular areas. 3.tooth filled/ RC treated if periapical inflammation persists resopton of root altimately leaving only RC filling progecting through shortenrd root.

Causes of resorption: Tumours & cysts

Malignant tumours causes root resorption, but benign tumors causes root displacement. Cysts cause root resorption by pressure though displacement is more common.

b.Tumours and cyst


1.Resorption of tumour same as cyst aspressure phenomenon . 2.Both Benign and malignant causes resoption of root.although Benign likely produces displacement than actual destruction (epithelial invading jaws) 3.Neoplastic cells adjacent and within ragged resoption lacunae on root surface tumours 4.Displacement of teeth more comman than resoption Cyst 5.Pulp infection apical periodontal cyst connective tissue stimulation Osteoclast formation resoption begins comman reaction for periodontal > Dentigerous Premordial , Fissural cyst.

d.Excessive mechanical or occlusal foces


1.During ortho T/t ; multipal root resorption seen irrespective of manner of T/t i.e type of appliance, duration and degree of force exerted. 2.Systemic predisposing factor like hypothyroidism. 3.Pressure on supporting bone-- destruction of bone-- small lacunae often appears on surface of cementum extend into dentin early tooth resorption. e.Impacted teeth 1.Impacted /Embeded tooth resoption of crown or both crown and root. 2.Initiatd in ceown limited epithelial destruction allow CT to come in contact with crown and resorption process initiated. 3.Mandi. 3rd molar > Maxi. 3rd molar >Maxi. Cuspid . 4.Impacted supernumerary teeth perticularly mesiodence undergoes resorption.

Causes of external resorption


Excessive mechanical or occlusal forces: e.g. Orthodontic treatment.

Causes of external resorption


Trauma: trauma causes injury or necrosis of the periodontal ligament leading to root resorption. Trauma may result from a single event or as a result of malocclusion.

Causes of external resorption: Impacted teeth


Resorption may affect crown or root of impacted teeth. This is related to partial loss of the protective effect of the periodontal ligament or reduced enamel epithelium. Impacted teeth may cause resorption of roots of adjacent teeth

Causes of external resorption


Reimplanted or transplanted teeth: These are non-vital teeth that undergo root resorption. The resorped root is replaced by bone producing ankylosis.

f.Idiopathic resorption
1.In normal adults root of permanent teeth undergoes resorption; this phenomenon termed as Idiopathic resorption. 2.Maxi. Bicuspids most comman ; Mandi. Incisors and molar least. 3.Resorption related to one or more systemic disorders; most obvious is Endocrine disturbances. 4.Multipal idiopathic resorption (very rare) 5.Resorption at CEJ or nearer to root apex in patient who are medically normal but past history of ortho T/t or Radiation.

Internal resorption (chronic perforating pulp hyperplasia, pink spot


Definition: unsual form of tooth

resorption that begins in the dentine of the pulpal walls in the pulp chamber or root canal.

also called as Chronic perforating hyperplasia of pulp or internal granuloma or orthoclastoma or Pink tooth of mummmery.

Pathological resorption of tooth which is started from pupal surface is called as INTERNAL RESORPTION.

PATHOGENESIS
Suddan trauma/ Injury to tooth | Intrapulpal haemorrage | Organisation of clot | Formation of hyperplastic granulation | compression of odontoblast cells | cessation of dentin formation | Stimulation of dentinoclast cells | resorption of dentin | Invasion of hyperplastic pulpal tissue into resorped spaces of dentin

CLINICAL FEATURE
1.Involves either crown or root portion. 2.Any tooth may involved but usually single tooth affected. 3.In advanced cases , involvement of coronal dentin ; so tooth appear pink. 4.No colour change if root is involved. 5.Affected tooth may remains vital untill pulp necrosis due to # of tooth or due to its perforation. HISTOPAHOLOGY 1.Multipal irregular / smooth areas of resorption in pulpal surface of dentin. 2.A hyperplastic , highly vascular pulp tissue projecting into spaces of dentin which are created by resorption. 3.Multiple multinucleated dentinoclast are found near resorption front of dentin.

Internal resorption
Cause: it is initiated by an inflammatory hyperplasia of the pulp, possibly as a result of vascular changes.

-As crown resorption progresses, a pink-hued area of crown may be seen representing the hyperplastic vascular pulp.

Histologically
Vascular connective tissue replaces the pulp with osteoclasts bordering the affected dentine or enamel. Chronic inflammatory cell infiltration and increased vascularity of the pulp. Areas of irregular bone formation may be seen.

ROENTGENOGRAPHIC FEATURE
1.Round / ovoid radiolucent area in central portion of involving toot associated with pulp not with external surface. 2.If left untreated compleate perforation is not uncomman.

TREATMENT
1.Extirpation of pulp tissue and conventional endo therapy. 2.When perforated extraction is only T/t.

Hypercementosis
Definition: This is a regressive change

of teeth characterized by the excessive deposition of secondary cementum on root surface.

INTRO
Also K/as CEMENTUM HYPERPLASIA. increases thickness of cementm on root surface of tooth due to excessive cementogenesis C/as Hypercementosis.

ETIOLOGY
1.Periapical inflammation. 2.Tooth repaire. 3.Functionless or unerrupted tooth. 4.Pagets disease of bone. 5.Accelerated tooth elongation.

C/F 1.Involved tooth is asymptomatic. 2.No increase or decrease in tooth sensitivity to percussion unless periapical inflamation 3.When extracted root appears longer in diameter than normal and with rounded apices. H/F 1.Excessive cellular cementum deposited over layer of Acellular cementum . 2.Entire root and apical region involved. 3.Cementum arranged in concentric layers around root. 4.Cementum shows numerous resting lines in deep hemotoxyphilic line || to root.

R/F
Excessive cemental thickening with typical bulbous appearance of roots.

T/t
-no t/t as condition is itself innocous -if inflammation of pulpal origin-t/t is necessary -extraction due to hypercementosis is contraindicated -excellent prognosis.

Localized hypercementosis occurs in:

Periapical periodontitis: at the center of inflammation (tooth apex) resorption is seen. Further away, coronally, cementum is laid by cementoblasts.

2-Accelerated elongation of tooth due to loss of its antagonist 3- in cases of root fracture, cementum tears are repaired by deposition of new cementum

4- Pagets disease of bone

CEMENTICLES 1.Cementicles are small foci of calcified tissue not necessary true cementum which lie free in periodontal ligament of later and apical root area 2.Idiopathic condition represents as areas of dystrophic calcifications 3.Degenerative changes Calcifications of nests of epithelial rests of mallesez in PDL enlarge by further deposition of calcim salts in adjacent CT continous periperal calcificationeventual union of cementicles,inclusion of Root cementum or alveolar bone.

4.Circular lamellated structural pattern. 5.Imparts rough globular outline to root surface . 6.Focal calcification of CT betn Sharpeys fibre cementicals ;ncentral nidus 7.Arises from calcification of thrombosed capillaries in PDL (pleboliths) 8.Too small to see roentgenographically;seldom >0.2,0.3 mm in diameter. 9.Clusture of cementicles termed as cementoma and has no clinical significance

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