Regressive changes are a variety of alterations that are not related either etiologically or either pathogenetically.

They are generally associated with the general aging process or either due to injury of tissues. But they are not due to developmental abnormalities or either due to inflammatory lesions They are the lesions of retrograde nature.

Mechanical wear and tear of tooth substance is a consequence of both physiological and pathological means. There are several mechanisms that contribute to tooth wear. They are

Abrasion : Due to friction of exogenous material forced over tooth surfaces. Eg: masticating food or the use of teeth as tools. Erosion : Due to chemical dissolution of tooth surfaces. Eg: Effects of acid from various sources or from a highly acidic diet.
Attrition: Due to tooth to tooth contact .Eg: Nightgrinding.

Defined as physiologic wearing away of a tooth as a result of tooth to tooth contact as in mastication. Occurs usually on incisal, occlusal and proximal surfaces of teeth It is physiologic rather than pathologic and it is associated with the aging process. It is seldom seen in DECIDUOUS DENTITION unless the child may suffer from dentinogenesis imperfecta or amelogenesis imperfecta.

Initially

appears as a small polished facet on a cusp tip or ridge or a slight flattening of an incisal edge.

Because of the slight mobility of the teeth in their sockets which is due to the mobility of the PDL. As age progresses and due to the continuous proximal wear, there is also shortening of the length of the dental arch as a result of the decreased mesio-distal diameter of the teeth.

AS THERE IS ONLY MINOR VARIATION IN THE HARDNESS OF TOOTH ENAMEL BETWEEN INDIVIDUALS,THERE IS NO GREATER DEGREE OF VARIATION THAT CAN BE OBSERVED CLINICALLY. MEN HAVE HIGHER DEGREE OF ATTRITION THAN WOMEN DUE TO GREATER MASTICATORY FORCE. VARIATIONS IN THE COARSENESS OF THE DIET OR OF HABITS SUCH AS CHEWING TOBACCO WHICH WOULD PREDISPOSE TO MORE OF ATTRITION. OCCUPATION:EXPOSURE TO ABRASIVE DUST IS ALSO AN IMPORTANT ETIOLOGY.

1.ADVANCED ATTRITION

COMPLETE LOSS OF ENAMEL

EXTRINSIC YELLOW OR BROWN STAINING OF THE EXPOSED DENTIN FROM FOOD OR TOBACCO 2.IF THE TOOTH PERSISTS,ATTRITION MAY PROGRESS TO THE POINT OF COMPLETE LOSS OF CUSPAL INTERDIGITATION. 3.TEETH MAY BE WORN DOWN NEARLY TO THE GINGIVA. 4.EXPOSURE OF DT AND SUBSEQUENT IRRITAION OF ODONTOBLASTIC PROCESS,THERE IS FORMATION OF SECONDARY DENTIN. 5.SUMTIMES LITTLE TENDRILS OF PULP HORN REMAIN AND ARE EXPOSED TO THE ORAL CAVITY .

 Pathological

wearing of tooth substance by abnormal mechanical process. abrasion usually occurs on the exposed root surfaces of the teeth , but under certain circumstances it maybe seen elsewhere, such as on incisal or proximal surfaces. Robinson stated that the most common cause of abrasion of root surfaces is the use of an abrasive dentrifrice.

Definition: It is the pathologic wearing away of tooth through abnormal mechanical processes. Site: Exposed root surface, sometimes on incisal or proximal surfaces.

 Although

modern dentrifices is not sufficiently abrasive to damage intact enamel severely, they can cause enough remarkable wear if the tooth brush carrying dentrifice is injudiciously used. Particularly in the horizontal than in the vertical direction. In such cases abrasion caused by a dentrifice manifests itself as a V-shaped or wedge shaped ditch on the root side of the cementoenamel junction in the teeth with some gingival recession.

 The

exposed dentin appears highly polished. The fact that abrasion was more common on the left side of the mouth for right handed people and vice versa

Other causes
Other

less common forms of abrasion maybe related to the habit of occupation of the patient The habit of opening bobby pins, holding nail tacks or pins in between their teeth. Improper usage of dental floss tooth pics. Habitual pipe smokers may develop notching of the teeth that conforms to the shape of the stem of the pipe.

 The

exposure of dentinal tubules and the consequent irritation of the odontoblastic processes stimulate the formation of secondary dentin similar to that seen in the case of attrition. Unless the form of abrasion is extremely severe and rapidly progressive one , the rate of secondary dentin formation is usually sufficient to protect the tooth against pulp exposure.

 It

is defined as the loss of tooth substance by a chemical process that does not involve known bacterial action. It occurs most frequently on the labial and buccal surfaces of the teeth, it may also occur on the proximal surface of the teeth.

 DEFINITION:

Erosion is a progressive loss of hard dental tissue by chemical processes not involving bacterial action. ETIOLOGY: extrinsic causes. intrinsic causes.

Citrus fruits intake (more than twice daily). Soft drink consumed (4-6 or more per week). Eating disorder (weekly or more often) . Sports drinks intake (weekly or more often). Bruxism habits. Excessive salivation . whole saliva un-stimulated flow rate (0.1ml/min) symptoms of history of gastro-esophageal reflux disease (GERD)

 Regurgitation

of gastric contents as in chronic vomiting and anorexia nervosa. Vomiting causes generalized abrasion on lingual surfaces.

 Broad

concavities within smooth surface enamel Cupping of occlusal surfaces (incisal grooving) with dentin exposure . Increased incisal translucency 4.Wear on non-occluding surface . Raised amalgam restoration . Clean , non-tarnished appearance of amalgams .

 Loss

of surface characteristics of enamel in young children . Preservation of enamel cuff in gingival crevice is common . Hypersensitivity . Pulp exposure in deciduous teeth .

Appearance
The

loss of tooth substance is manifested by a shallow, broad, smooth,highly polished, scooped-out depression on the enamel. Although generally confined to the gingival third of the labial surfaces of anterior teeth. The lesions , which may exhibit considerable variation in shape and size, usually involve several teeth.

 Some

erosions may progress to involve the dentin and thereby provoke a secondary dentin response similar to the case seen in abrasion and attrition. The etiology of the disease is unknown in majority of the cases. The work of McClure, Ruzika and zipkin suggested that it maybe due the citrate content in the saliva.

 It

has also been suggested that the decalfication maybe due to the local acidosis in the periodontal tissues resulting from damage due to traumatogenic occlusion.

Causes
It

is caused by obvious decalcification In cases of chronic vomiting The labial surfaces of the teeth who drink large quantities of highly acidic carbonated beverages or lemon juice or who sucks lemon or other citric fruits maybe affected.

 The

erosion by gastric acid decalcification is seen in anorexia nervosa. Dental erosion is a seen in many industries involving the use of acids.

 Treatment

of etiology-GERD-Medical

therapy Salivary hypofunction -use sugarless gum/mint chewing . Sjogrens syndrome/post therapeutic head and neck radiation -use oral pilocarpine(salagen).

Diminished the frequency and severity of the acid challenge . Enhance the defence mechanism of the body (increase in salivary flow and pellicle formation) . Enhance acid resistance, remineralization and rehardening of the tooth surface. Improve chemical protection . Decreased abrasive forces . Provide mechanical protection . Monitor stability breakdown proportionate to magnitude; duration; direction ; frequency and location of forces

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)

 It

a theory that explains the non-carious cervical lesions(NCCL). It suggests that they are caused by flexural forces; especially at the cementoenamel junction(CEJ), under goes this pattern of destruction by separating the enamel rods. As teeth flex under pressure, the arrangement of teeth touching each other, known as occlusion causes tension on one side of the tooth and compression on the side of the tooth

 This

is believed to cause V-shaped depressions on the side under tension and C-shaped depressions on the side under compression. This theory is widely disputed by some who think that these type of lesions are due to over-zealous brushing since the cervical lesions are mainly located in the premolar regions.

 Recent

studies by T.C Abrahamsen have shown that toothpaste (not the tooth brush) is abrasive enough to cause damage if the patient is too aggressive in brushing the teeth in a very hard sawing motion. Abrahamsen suggests that the term toothbrush abrasion be replaced with the term toothpaste abuse

 ETIOLOGY:

Biomechanical

forces >>> static- eg . Produced due to swallowing and clenching. >>> cyclic-eg. Force during chewing action.
CLINICAL

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

Characterized by calcification of dentinal tubules Not only due to injury but also occur due to caries or abrasion and also due to normal aging process. In ground sections when examined by transmitted light ,a translucent zone can be seen in the dentine underlying the cavity. Sclerotic dentin is impermeable to dyes & caries. The calcification is due to the calcium from the dentinal fluid. This process decreases the conductivity of the odontoblastic process and slows an advancing carious process. Sclerotic dentin is actually harder & more highly calcified than adjacent normal dentin.

SECONDARY DENTIN DEPOSITION PULP CHAMBER REDUCED ODONTOBLASTIC CELL CROWDING APOPTOSIS MINERALIZATION ODONTOBLASTIC PROCESS SCLEROSIS OF DENTINAL TUBULES

SCLEROTIC DENTIN

SYNONYMS :
TRANSPARENT DENTIN TRANSLUCENT DENTIN

TOOTH INSULT (DENTIN)

NORMAL TOOTH (DENTIN)

RAPID DEATH OF ODONTOBLAST GROUND SECTION

TUBULES FILLED WITH AIR

BLACK COLOR

DEAD TRACTS

Dead tracts is seen in dentin in ground sections alone. In transmitted light it is manifested as a dark zone. In reflected light it is seen as white zone. This optical phenomenen is dur to the differences in the refractive indices of the affected & normal tubules Unlike sclerotic dentin they are not calcified and so they are permeable to the penetration of dyes.

Formed and deposited in response to nomal or slightly abnormal stimulus after the completion of tooth formation.There is a considerable variation between primary and secondary dentin.

DEVELOPMENT :
EMBRYONIC INTERACTION FORMED BEFORE ROOT
COMPLETION PHYSIOLOGIC STIMULUS AFTER ROOT COMPLETE & TOOTH OCCLUSION

RATE OF FORMATION :
FAST

SLOWER THAN PRIMARY DENTIN

LESS & IRREGULAR

TUBULE PATTERN :
MORE & REGULAR NOT UNIFORM

PATTERN OF

It is a regular , uniform layer of dentin around the pulp chamber. Laid down throughout the life as a result of physiological factors. It is produced more slowly than primary dentin.

Dentin that forms around the pulp chambers due to attrition or irritation This gradual traumatic process stimulates the development of natural protective measures,such as secondary dentin.

No significant clinical change but there is evident decrease in tooth sensitivity when secondary dentin formation is extensive. It forms an additional insulating layer of calcified tissue between the pulp and the progressing external agent.Thus it delays the eventual pulp involvement. It may also occur in deciduous dentition. The anterior teeth exhibit a higher incidence of secondary dentin formation than the molar teeth.

It can be seen in the dental radiograph if its area of occurrence is not overcrowded by any other calcified tissues. It can be noted particularly in the pulp horn areas as well as on the proximal walls of teeth with proximal caries.

oPhysiologic secondary dentin is similar to primary dentin and may be rather well demarcated by a deeply staining resting line oReparative secondary dentin is usually irregular in nature. They consist of only a few tubules that are tortuous. Sometimes this secondary dentine is formed at a higher rate entrapping the odontoblasts which produces a superficial resemblance to bone.they are known as OSTEODENTIN.

Occurs in many circumstances other than normal process (shedding of teeth). Root resorption also occurs in permanent teeth due to variety of stimuli.

EXTERNAL

INTERNAL

Periapical inflammation Reimplantation of teeth Tumors and cysts Excessive mechanical or occlusal forces Impaction of teeth Idiopathic

Idiopathic

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

 Results

in severe resorption of tooth. In transplanted developing teeth , vascular supply may be re-established , hence its vitality is maintained. Tooth root is resorbed and replaced by bone resulting in ANKYLOSIS.

 Malignant

tumours causes root resorption But benign tumors causes root displacement. Cysts cause root resorption by pressure though displacement is more common. It is basically a pressure phenomenon forming basis of orthodontic practice.

 Epithelial

tumors including jaws Neoplastic cells are found adjacent and within ragged resorption lacunae on root surface. Pulp infection apical periodontal cyst connective tissue stimulation Osteoclast formation resorption begins . Common reaction for periodontal cysts Dentigerous, Primordial or Fissural cyst.

During ortho T/t ; multipal root resorption seen irrespective of manner of T/t . Type of appliance. Duration and degree of force exerted. Systemic predisposing factor like hypothyroidism. Pressure on supporting bone-- destruction of bone-- small lacunae often appears on surface of cementum extend into dentin early tooth resorption. Minor resorption are repaired by deposition of bone , so orthodontic pressure is relieved.

Impacted or embedded teeth undergo resorption of crown or both crown and root. Initiated in crown limited epithelial destruction allow connective tissue to come in contact with crown and resorption process initiated. Mandibular 3rd molar > Maxillary 3rd molar >Maxillary Cuspid . Impacted supernumerary teeth perticularly mesiodence undergoes resorption.

 Without

any obvious cause . Takes place in 4 or more teeth , judged by radigraphic examination. More resorption takes place in maxillary bicuspid than mandibular incisors and molars. 75% teeth exhibit resorption showed loss of less than 4 mm of root apex , resorption may related to endocrine disturbances.

 Chronic

perforating pulp hyperplasia, pink spot or pink tooth mummery or internal granuloma. Definition: Unusual form of tooth resorption that begins in the dentine of the pulpal walls in the pulp chamber or root canal Pathological resorption of tooth which is started from pulpal surface is called as INTERNAL RESORPTION.

 Sudden

trauma. Injury to tooth . Intra-pulpal haemorrhage . Organisation of clot . Formation of hyperplastic granulation . compression of odontoblast cells . cessation of dentin formation . Stimulation of odontoclast cells . resorption of dentin . Invasion of hyperplastic pulpal tissue into resorped spaces of dentin.

 Multiple

irregular . Smooth areas of resorption in pulpal surface of dentin. A hyperplastic ,highly vascular pulp tissue projecting into spaces of dentin which are created by resorption. Multiple multinucleated odontoclast are found near resorption front of dentin.

 Involves

either crown or root portion. Any tooth may involved but usually single tooth affected. In advanced cases , involvement of coronal dentin ; so tooth appear pink. No colour change if root is involved. Affected tooth may remains vital until pulp necrosis of tooth or due to its perforation. As crown resorption progresses, a pink-hued area of crown may be seen representing the hyperplastic vascular pulp.

 Round

/ ovoid radiolucent area in central portion of involving toot associated with pulp not with external surface. If left untreated complete perforation is not uncommon. TREATMENT::: Root canal treatment.

 It

maybe regarded as a regressive change of teeth characterised by the deposition of excessive amounts of secondary cementum on root surfaces. This most commonly involves nearly the entire root area, although in some instances the cementum formation is focal.

Etiology

a)
b) c)

d)
e)

Reasons that may favour the deposition of excess cementum Accelerated elongation of tooth Inflamation of the tooth Tooth repair Osteosis deformans Sometimes unknown

 Acceleration

in the elongation of a tooth owing to loss of an antagonist is accompanied by hyperplasia of the cementum, apparently as a result of the inherent tendency for maintenance of the normal width of the periodontal ligament. This hypercementosis is most prominent at the apex of the root.

CLINICAL FEATURES:

Involved tooth is asymptomatic. No increase or decrease in tooth sensitivity to percussion unless periapical inflamation . When extracted root appears longer in diameter than normal and with rounded apices.

HISTOLOGIC FEATURES:

Excessive cellular cementum deposited over layer of Acellular cementum . Entire root and apical region involved. Cementum arranged in concentric layers around root. Cementum shows numerous resting lines in deep hemotoxyphilic line to root.

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

Cementicles are small foci of calcified tissue not necessary true cementum which lie free in periodontal ligament of later and apical root area. Idiopathic condition represents as areas of dystrophic calcifications 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.

Circular lamellated structural pattern. Imparts rough globular outline to root surface Focal calcification of connective tissue between Sharpeys fibre cementicals ;central nidus. Arises from calcification of thrombosed capillaries in PDL (pleboliths) . Too small to see roentgenographically;seldom >0.2,0.3 mm in diameter. Clusture of cementicles termed as cementoma and has no clinical significance

 Nodular

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

 According

to relation to dentin as:

free attached embedded . These eventually fill substantial part of pulp chamber.

 TRUE

DENTICALS: Localised masses of calcified tissue resembles dentin as tubular structure(sec. dentin) tubules are irregular and few in no. more common in pulp chamber than root canals .
FALSE

DENTICALS: Localized masses of calcified tissue unlike true dentine not exhibit dentinal tubules concentric layers or lamellae deposited around a central nidus.

 Appears

as irregular calcific deposits in pulp tissue,collagenous fibrous bundles in blood vessels. Persits as fine calcified spicules and may develop to large masses. Found in root canals surrounding blood vessels .Also K/as calcific degeneration

 Unknown

, increases with age. No relation with local or systemic diseases or gender . Micro organisms high % of pulp stones yield pure growth of streptococcus in culture Operating procedures + restorative materials---pulp stones incidence increases

 Mild

to severe pulpal neuralgia,excruciating pain resembles tic doulerex (trigeminal neuralgia) . Difficulty in pulp extirpation during RCT.