Presentation is loading. Please wait.

Presentation is loading. Please wait.

DISORDERS OF DEVELOPMENT OF TEETH

Similar presentations


Presentation on theme: "DISORDERS OF DEVELOPMENT OF TEETH"— Presentation transcript:

1 DISORDERS OF DEVELOPMENT OF TEETH

2 May be prenatal or postnatal in origin
May be inherited or acquired Causes : Abnormalities in the differentiation of the dental lamina and the tooth germs leading to anomalies in the number, the size and shape of teeth (abnormalities of morphodifferentiation) Abnormalities in the formation of the dental hard tissues leading to disturbances in tooth structure (abnormalities of histodifferention).

3 DISTURBANCES IN NUMBER OF TEETH.
ANODONTIA= Absence of teeth May be : Complete anodontia Partial anodontia (hypodontia) Pseudoanodontia : Absent teeth because of impaction or delayed eruption False anodontia : When teeth have been exfoliated or extracted

4 NUMBER (cont…) Partial anodontia is relatively common, mostly third molars, followed by second premolars and maxillary lateral incisors. Complete anodontia is rare but is often associated with hereditary ectodermal dysplasia (hypohidrotic ectodermal dysplasia).

5 NUMBER (cont…) SUPERNUMERARY TEETH.
May have a normal morphology : Supplementary teeth May be rudimentary and miniature Causes: Hereditary Syndrome associated (cleft palate or cleidocranial dysplasia) Location: Most frequently in the anterior and molar regions of the maxilla, followed by the premolar region of the mandible Permanent dentition more affected than primary ; females more affected than males.

6 SUPERNUMERARY TEETH(cont…).
Significance: Supernumerary teeth occupy space, may prevent the eruption of other teeth. May erupt into the buccal or lingual embrasure or outside the line of the dental arch May cause delayed eruption, maleruption and malalignment of other teeth Inaesthetic If between the roots of adjacent teeth, they cause diastema Resorption of adjacent teeth May develop into dentigerous cysts if unerupted

7 SUPERNUMERARY TEETH(cont…).
Mesiodens: These are supernumerary teeth occurring between central incisors Most common of all the supernumerary teeth They mostly occur between the maxillary central incisors Natal teeth: Supernumerary teeth appearing at the time of birth Very rare Not to be confused with prematurely erupted deciduous teeth and eruption cysts or false teeth Usually mandibular central incisors

8 DISTURBANCES IN SIZE OF TEETH
MICRODONTIA. May be Generalized or localized True microdontia when teeth are measurably smaller than normal (in pituitary dwarfism) Relative microdontia in comparison with a large mandible and maxilla Usually the shape is also altered Commonly seen with the maxillary lateral incisors= peg shaped laterals, followed by maxillary 3rd molars and supernumerary teeth Causes: Usually hereditary in origin Significance: Only cosmetic

9 SIZE (cont…) MACRODONTIA. May be generalized:
Absolute macrodontia as seen in pituitary gigantism Relative macrodontia when seen on a disproportionately small maxilla and mandible May also be localized: Abnormally large tooth or group of teeth Relatively uncommon condition Usually seen with mandibular 3rd molars, incisor and canine region. Hemifacial hypertrophy: The teeth on the affected side are abnormally large compared with the unaffected side

10 DISTURBANCES IN SHAPE OF TEETH.
May involve the crown, the root or both GEMINATION. Definition: This is a fusion of two teeth from a single enamel organ resulting either in: Partial cleavage leading to two crowns that share the same root and same pulp canal Complete cleavage making twinning (2 teeth from one tooth germ) The cause is unknown but trauma has been suggested as a possible cause Significance: Inaesthetic May cause crowding of teeth

11 SHAPE (cont…) FUSION. Definition:
It is the joining of two developing tooth germs, resulting in a single large tooth. The fusion process may involve the entire length of the tooth or the roots only; in that case, cementum and dentin are shared. Root canals may also be separate or shared. May also involve the crown only. The fusion must involve the dentin because, when 2 teeth are connected only by cementum, the condition is termed “concrescence” It may be impossible to differentiate fusion of normal or supernumerary teeth from germination. The cause is unknown but trauma has been suggested

12 SHAPE (cont…) CONCRESCENCE. Definition:
It is a form of fusion in which the adjacent, already formed teeth are joined by cementum. It is an acquired anomaly This may take place before or after eruption of teeth Most commonly seen in association with the maxillary second and third molars Causes: Believed to be related to trauma or overcrowding Most frequently seen in the permanent dentition where the roots develop close together Hypercementosis associated with chronic inflammation Significance: None unless one of the teeth involved requires extraction. Surgical sectioning may be required to save the other tooth.

13 SHAPE (cont…) DILACERATION. Definition:
It is an extraordinary curving or angulation of tooth roots. Causes: Trauma during root development Hereditary factors Lack of space for development Significance: Eruption generally continues without problems Extraction may be difficult Root canal treatment may be challenging

14 SHAPE (cont…) DENS INVAGINATUS. Definition:
Also known as dens in dente, it is an uncommon tooth anomaly that represents an exaggeration or accentuation of the lingual pit. Can range from superficial (only the crown affected) to deep (crown and root involved). Permanent maxillary lateral incisors most commonly involved Any anterior tooth may be affected Bilateral involvement commonly seen Cause: Unknown Genetic factors believed to be involved in small percentages of cases

15 SHAPE (cont…) Complications:
Predisposes the tooth to early decay and subsequent pulpitis Management: Prophylactic filling of the pit is recommended to avoid these complications When pulpitis has led to nonvitality, endodontic procedures may salvage the affected tooth

16 SHAPE (cont…) DENS EVAGINATUS. Definition:
This is a relatively common developmental condition characterized by an anomalous tubercle, or cusp, often bilateral, located in the center of the occlusal surface. The premolar teeth are predominantly affected. Causes: It is unknown but race related because it has been reported almost exclusively in Asians and Native Americans.

17 SHAPE (cont…) Complications:
There can be an early exposure of an accessory pulp horn extending into the tubercle due to quick occlusal abrasion. Periapical pathology in young caries-free teeth often before completion of root development and apical closure making root canal fillings challenging Management: Grinding the opposing tooth or the tubercle to stimulate secondary dentin formation in order to prevent the periapical syndrome.

18 SHAPE (cont…) TAURODONTISM. Definition:
A taurodont tooth(bull-like tooth) is one in which the pulp chamber has a greater apico-occlusal height than in normal teeth, whith no constriction at the level of the amelo-cemental junction; the chamber extends apically well beyond the cervix. It affects multirooted teeth and is rare in primary dentition Causes: Failure of Hertwig’s sheath to invaginate at the proper horizontal level Can be seen as an isolated incident or in association with syndromes such as Down’s syndrome and Klinefelter’s syndrome. Genetic factors (high prevalence in Eskimos and Middle Eastern population) Significance: Little clinical significance, no treatment required Aesthetic concern

19 SHAPE (cont…) SUPERNUMERARY ROOTS. Definition:
These are accessory roots commonly seen in mandibular canines, premolars and molars. They are rarely seen in upper anterior teeth and mandibular incisors Significance: When extractions or root canal fillings are necessary, radiographic recognition of an extraordinary number of roots becomes important.

20 SHAPE (cont…) ENAMEL PEARLS. Definition:
These are small masses of enamel found apically to the amelocemental junction. They occur most commonly in the bifurcation or trifurcation of teeth but may appear on single-rooted premolar as well. Maxillary molars more commonly affected than mandibular Can be detected radigraphically Cause: Hertwig’s sheath remains in contact with the dentin and stimulated to differentiate into functional ameloblasts. Significance: Little clinical significance except when located in an area of periodontal disease.

21 DISTURBANCES IN STRUCTURE OF TEETH.
DISTURBANCES IN STRUCTURE OF ENAMEL. Enamel normally develops in two stages: Secretory stage: Matrix production Initial mineralization Matrix production: Synthesis and secretion of matrix proteins (amelogenins and enamelins) Initial mineralization: Appears immediately after secretion, crystals abut the plasma

22 ENAMEL DEFECTS (cont…)
Maturation stage: Withdrawal of water and proteins Concomittant increase in mineral content before the tooth erupts Defective amelogenesis can be related either to matrix formation leading to enamel hypoplasia or to mineralization and maturation stages leading to hypomineralized enamel. Enamel Hypoplasia: It is a quantitatively defective enamel, when of normal hardness Enamel hypocalcification: It is a qualitatively defective enamel when normal amounts of enamel is produced but are hypomineralized; the enamel is softer than normal.

23 ENAMEL DEFECTS (cont…)
The extent of enamel defects depends on three conditions: The intensity of the etiologic factor The duration of the factor’s presence The time at which the factor occurs during crown development. Clinical features: Defects can range from yellowish or brownish pigmentation of the enamel to extensive pits and irregularities of the surface The crown is usually smaller than normal.

24 ENAMEL DEFECTS (cont…)
Localized causes: Local infections or trauma related to the deciduous predecessor resulting in damage to the ameloblasts of permanent successor. Such teeth are often called Turner teeth. Radiotherapy Idiopathic

25 ENAMEL DEFECTS (cont…)
General causes: Environmental/Systemic factors: Can be either Prenatal:- Infections, e.g. rubella, syphilis Maternal disease Excess fluoride ions Neonatal: -Haemolytic disease of the newborn Hypocalcaemia Premature birth/ Prolonged labour

26 ENAMEL DEFECTS (cont…)
Postnatal: Severe childhood infections especially the viral exanthema Chronic diseases in childhood e.g. congenital heart disease, gastrointestinal and endocrine diseases Nutritional deficiencies e.g. vit D Cancer chemotherapy Excess fluoride ions

27 ENAMEL DEFECTS (cont…)
For systemic factors to have an effect on the developing permanent teeth, they must generally occur after birth and before the age of 6 years. Genetic factors: Only teeth affected- Amelogenesis imperfecta Teeth affected in association with generalized defects- Ectodermal dysplasia syndromes Down’s syndrome (Trisomy 21)

28 ENAMEL DEFECTS (cont…)
ENAMEL OPACITIES. Definition: These are white spots seen in smooth surface enamel, some of which become brown-stained after eruption. They are most common in children aged 12-14years Both deciduous and permanent dentitions are affected. Maxillary permanent central incisors most frequently involved Causes: Unknown but are thought to be due to local rather than systemic factors The prevalence is less in areas with 1 PPM of fluoride in the drinking water The opaque spots are hypomineralized.

29 ENAMEL DEFECTS (cont…)
CHRONOLOGICAL HYPOPLASIAS. Most enamel hypoplasias due to environmental causes are of this type. They are time related disturbances. E.g. Any serious nutritional deficiency or systemic disease occurring during the time of formation of teeth. The disturbance occurring in utero, at or soon after birth may affect the incisal edges of the permanent central incisors and the occlusal surfaces of the first permanent molars, in addition to the deciduous teeth.

30 ENAMEL DEFECTS (cont…)
CONGENITAL SYPHILIS. Affects permanent incisors and first molars Affected incisors (Hutchinson’s incisors) are tapered incisally and notched centrally on the incisal edge Affected molars (Mulberry molars) show a lobulated occlusal surface.

31 ENAMEL DEFECTS (cont…)
FLUORIDE IONS. Ingestion of drinking water containing fluoride at levels greater than 1 PPM during the time the crowns are being formed may result in enamel hypoplasia or hypocalcification= Fluorosis. Clinical features: Mild to moderate fluorosis: Ranges from white enamel spots to mottled brown-and-white discolorations Severe fluorosis: Pitted, irregular, discolored enamel Are cosmetically objectionable.

32 ENAMEL DEFECTS (cont…)
AMELOGENESIS IMPERFECTA. Definition: It is an inherited developmental abnormality of enamel. Affects both dentitions. Classification: 2 main types Hypoplastic: Defective matrix formation Hypocalcified: Matrix formation is normal but calcification is abnormal Causes: Genetic factors Autosomal dominant Autosomal recessive X-linked patterns

33 ENAMEL DEFECTS (cont…)
Clinical manifestations: The defects range from pits and grooves in one patient to complete absence (aplasia) in another Abnormal contour and absent interproximal contact points may be evident Fractures and wears due to gross attrition appear readily in the hypocalcified type, exposing the dentine Sometimes, in the smooth form, teeth have sharp, needle-like cusps Color varies from white opaque to yellow to brown

34 ENAMEL DEFECTS (cont…)
Teeth tend to darken with age due to exogenous staining The teeth are not caries prone Radiographic features: Enamel appears reduced in bulk, often showing a thin layer over occlusal and interproximal surfaces Dentin and pulp chambers appear normal Treatment: Full crown coverage for aesthetic concerns

35 DISTURBANCES IN STRUCTURE OF DENTINE.
DENTINOGENESIS IMPERFECTA. Definition: Dentinogenesis imperfecta is an autosomal-dominant trait affecting the dentine, with variable expressivity. Affects both dentitions. Classification: 3 types Type 1: Dentin abnormality occurs in patients with concurrent osteogenesis imperfecta Primary teeth more affected than permanent teeth Type 2: Only dentin abnormalities and no bone diseases Type 3: Similar to type 2 but with multiple pulp exposures, periapical radioluscencies, variable radiographic appearances.

36 DENTINE (cont…) DENTINE (cont…)
Clinical features: In both dentitions, the teeth exhibit an unusual transluscent, opalescent appearance Color variation from yellow-brown to gray to violet Entire crown appears discolored because of the abnormal underlying dentin Enamel fractures easily, resulting in rapid wear Overall tooth morphology unusual due to excessive constriction at the cemento-enamel junction, giving the crown a tylip or bell shape Roots are shortened and blunted Teeth do not exhibit any greater susceptibility to caries

37 DENTINE DEFECTS (cont…)
Radiographic features: Type 1 and 2 exhibit identical features such as: Opacification of dental pulp because of continued deposition of abnormal dentin Short roots Bell-shaped crowns Type 3: Dentin appears thin Pulp chambers and root canals extremely large giving the appearance of thin dentin shells=shell teeth

38 DENTINE DEFECTS (cont…)
Histological features: Dentin contains fewer but larger and irregular dentinal tubules Dentin poorly calcified with occasional cellular inclusions Dentin is softer and has a greater water and inorganic content Enamel appears normal Dentino-enamel junction is smooth instead of scalloped. Treatment: Full-crown coverage (protection against tooth wear and aesthetic concern)

39 DENTINE DEFECTS (cont…)
DENTIN DYSPLASIA. Definition: It is an autosomal-dominant trait that affects dentin. This is a rare condition subdivided into type I (radicular type) and a more rare type II (coronal type) Both dentitions are affected Similarities with dentinogenesis imperfecta: Early obliteration of pulp chambers and root canals by atypical dentin Differencies from dentinogenesis imperfecta: The teeth are normal in color No tendency for the enamel to chip off No rapid attrition Altered, retarded, deficient root formation with radioluscent areas at the apices of some teeth.

40 DENTINE DEFECTS (cont…)
Clinical features: Teeth of normal color with no attrition Looseness, malposition, early loss of teeth due to retarded root formation and lack of supporting bone Radiographic features: Type I: Roots appear extremely short Pulps almost completely obliterated Residual fragments of pulp tissue appear typically as horizontal lucencies Periapical lucencies (chronic abscesses, granulomas, cysts)

41 DENTINE DEFECTS (cont…)
Type II: Deciduous teeth radiographically similar to type I Permanent teeth exhibit enlarged pulp chambers that have been described as thistle tube appearance Histological features: The enamel and immediately subjacent dentin appear normal Deeper layers of dentin show atypical tubular patterns and irregular organization Treatment: The treatment is directed toward retention of teeth for as long as possible The prognosis is poor due to short roots and periapical lesions.

42 DENTINE DEFECTS (cont…)
REGIONAL ODONTODYSPLASIA=Ghost teeth Definition: It is a dental abnormality that involves the hard tissues derived from both the epithelial (enamel) and mesenchymal (dentin, cementum and pulp) components of the tooth-forming apparatus. Several teeth in a quadrant or region are affected Both mandible and maxilla can be affected Permanent teeth more affected than deciduous Maxillary anteriors mostly affected

43 DENTINE DEFECTS (cont…)
Clinical features: The teeth exhibit short roots, open apical foramina and enlarged pulp chambers Eruption of the affected teeth is delayed or does not occur Teeth have irregular shape Hypoplastic and irregularly mineralized enamel Radiographic features: Wide, open apices Pulp stones Reduced radiopacity of the teeth Loss of distinction between the enamel and dentine described as a “ghostly” appearance.

44 DISTURBANCES IN STRUCTURE OF CEMENTUM.
The coronal 1/3 of the cement consists of acellular cementum (primary) whereas the apical 2/3 consists of cellular cementum (secondary). The cellular cementum continues to be formed throughout the life of the tooth. Thickness varies between individuals, generally increases with age to compensate for occlusal wear.

45 CEMENTUM DEFECTS (cont…)
HYPERCEMENTOSIS. Definition: This is an abnormally increased cementogenesis Aetiology: Some cases are idiopathic Others may be associated with certain conditions like: Periapical inflammation (generalized thickening or localized knob-like enlargement) Mechanical stimulation Functionless and unerupted teeth Paget’s disease of bone Hypercementosis may be associated with root ankylosis Significance: The tooth extraction can be laborious

46 CEMENTUM DEFECTS (cont…)
HYPOCEMENTOSIS. Hypoplasia and aplasia of cementum are uncommon Hypocementum is associated with: Cleidocranial dysplasia in which there is lack of cellular cementum Hypophosphatasia characterized by: Reduced serum alkaline phosphatase level, Deformities of extremities similar to those of rickets, Failure of calcification of the calvarium Clinical complications: Premature loss of some or all deciduous and permanent teeth due to poor periodontal attachment and abnormal dentine formation.

47 DISTURBANCES IN STRUCTURE OF THE PULP.
PULP CALCIFICATION. It is a common phenomenon that occurs with increasing age for no apparent reason There appears to be no relation to inflammation, trauma or systemic disease May be of microscopic size or large enough to be detected radiographically Calcifications may be diffuse (linear) or nodular (pulp stones) Linear calcifications are typically found in root canals, pulp stones in pulp chambers Can be true denticles when composed predominantly by dentin or false denticles when they represent foci of dystrophic calcifications Are referred to as attached pulp stones when incorporated into dentine or free pulp stones when surrounded by pulpal tissue Clinical significance: None but can be problematic during endodontic therapy

48 OTHER DISORDERS OF TEETH

49 DISORDERS OF ERUPTION AND SHEDDING OF TEETH.
PREMATURE ERUPTION, NATAL AND NEONATAL TEETH. Natal teeth are slightly more common than neonatal teeth They are seen in +/- 1 in 3000 live births Almost always one or two central incisors are involved The mandible is four time more involved than the maxilla Aetiology: Normal tooth germ developing in a superficial position in a superficial position in the jaw Prognosis: They are either lost spontaneously Can be extracted to prevent them being inhaled or ulcerate the tongue or the mother’s nipple If left in the jaw, the roots may sometimes continue to develop and the teeth become firm.

50 ERUPTION AND SHEDDING (cont…)
2.RETARDED ERUPTION. Can be associated with: Endocrinopathies (e.g. hypothyroidism) Prematurity Nutritional deficiencies Down’s syndrome Both dentitions can be affected Other causes involved: Idiopathic migration Traumatic displacement of tooth germs Abnormally large crowns Cleidocranial dysplasia causing delayed eruption and multiple and impacted supernumerary teeth.

51 ERUPTION AND SHEDDING (cont…)
3.PREMATURE LOSS. Usually it is the result of either dental caries and its sequelae or chronic periodontal disease Occasionally associated with:-Hypophasphatasia -Prepubertal periodontitis -Hereditary palmar-plantar hyperkeratosis 4.PERSISTANCE OF DECIDUOUS TEETH. Usually associated with the failure of eruption of the permanent successors Persistance of the entire deciduous dentition is uncommon ( cleidocranial dysplasia when eruption of permanent teeth is impeded)

52 ERUPTION AND SHEDDING (cont…)
5. IMPACTION OF TEETH. Definition: An impacted tooth is one which remains unerupted or only partly erupted, in the jaw beyond the time it should normally be fully erupted. One or several teeth may be affected The condition may be symmetrical Rarely seen in primary dentition Teeth most frequently involved are: Third molars Mandibular premolars Maxillary canines

53 ERUPTION AND SHEDDING (cont…)
Aetiology: Local factors: Abnormal position of the tooth germ Lack of space for the teeth Supernumerary teeth Cysts and tumours Systemic factors: Cleidocranial dysplasia (multiple impacted teeth) Possible complications: Resorption of the impacted tooth or adjacent erupted teeth Development of dentigerous cysts and odontogenic tumours

54 ERUPTION AND SHEDDING (cont…)
REIMPACTION OF TEETH (Infraocclusion, Submerged teeth). Definition: It is a situation in which previously erupted tooth becomes submerged in the tissues. The deciduous second molar most commonly affected Mandible two times more affected than maxilla Clinical features. Deficient development of the alveolar process around the reimpacted tooth which may become completely covered by oral mucosa The roots are usually partly resorbed and ankylosed to the bone.

55 NON-BACTERIAL LOSS OF TOOTH STRUCTURE.

56 TOOTH WEAR ATTRITION. Definition:
This is a loss of tooth substance as a result of tooth-to-tooth contact. It is an age-related process and varies from one individual to another. It may be physiological or pathological in origin Chronology: Incisal edges of the incisors are worn first Occlusal surfaces of the molars Palatal cusps of the maxillary teeth and buccal cusps of mandibular teeth.

57 TOOTH WEAR (cont…) When the dentine becomes exposed, it generally becomes discoloured brown. The patient may complain of hypersensitive dentine. Men generally show more severe attrition than women Aetiology: Abnormal occlusion Bruxism and habits such as tobacco and betel chewing Abnormal tooth structure Abrasive property of food

58 TOOTH WEAR (cont…) ABRASION. Definition:
It is a pathological wearing away of tooth substance as a result of an abnormal use of abrasive substances orally or abnormal use of abrasive substances orally. -The location and pattern are directly dependaent on the cause -The gingival 1/3, incisal edges and proximal surfaces are more affected

59 TOOTH WEAR (cont…) Aetiology:
Tooth brush abrasion (left side more involved in righthanded and vice versa) Pipe smoking Chewing tobacco and various foreign substances (sand, stones) Use of abrasive dentifrice Occupational abrasion( holding objects between or against teeth during work like thread or nails) Ritual abrasion

60 TOOTH WEAR (cont…) EROSION.
Definition: This is loss of tooth structure from a non-bacterial chemical process Aetiology: External or internal acids such as: Excessive intake of acidic beverages Sucking citrus fruits (lemons) Occupational erosion (e.g. battery manufacturing) Chronic alcoholism Idiopathic erosion (acidic saliva) The patient may complain of hypersensitive dentine.

61 TOOTH WEAR (cont…) Resorption.
It can be physiological like the resorption of deciduous teeth or microscopic areas of superficial resorption of the roots of permanent teeth. When the resorption is sufficient to be diagnosed radiologically it is always pathological It is not a continuous process, osteoclasts are not always present. There are 2 types: External resorption and internal resorption

62 TOOTH WEAR (cont…) Pathological external resorption may be associated with: Periapical inflammation Mechanical stimulation (excessive force in orthodontic treatment) Neoplasms or cysts Unerupted teeth Transplanted or replanted teet Idiopathic resorption Pathological internal resorption is usually associated with pulpitis.

63 DISCOLORATION OF TEETH.
Normal variation in the color of teeth must be distinguished from pathological discoloration. Aetiology: Surface deposits (Extrinsic stains) Changes in the structure or thickness of the dental hard tissues Diffusion of pigments into the dental hard tissues after their formation Incorporation of pigments into the dental hard tissues during their formation

64 DISCOLORATION OF TEETH (cont…).
Extrinsic stains: Substances in the diet Habitual chewing of betel nut or tobacco Tobacco smoking Medications Chromogenic bacteria

65 DISCOLORATION OF TEETH (cont…).
Changes in the structure or thickness of dental tissues Enamel hypoplasia, fluorosis Amelogenesis imperfecta Enamel opacities Enamel caries Dentinogenesis imperfecta Dentinal dysplasia type II Age changes in dental tisúes

66 DISCOLORATION OF TEETH (cont…).
DIFFUSION OF PIGMENTS INTO DENTAL TISSÚES AFTER THEIR FORMATION. Extrinsic stains Endodontic materials Products of pulp necrosis (Lysis of necrotic tissue and red blood cells) PIGMENTS INCORPORATED DURING FORMATION OF DENTAL TISSUES. Bile pigments (Rhesus incompatibility); the color appears yellowish-brown Porphyrins; the color appears pinkish-brown Tetracyclins; the color appears yellowish at eruption then darker and browner

67 REIMPLANTATION OF TEETH.
Definition: It is an avulsed tooth following traumatism that is returned to its own socket. Clinical features: Usually, the pulp and soft tissues attached to the root degenerate due to traumatic injury of the blood supply Sometimes the resorption is rapid but other times it is slowly progressive up to years Resorption is largely a function of the length of time the tooth has been out of the jaw.

68 ROOT FRACTURE. The outcome of an intra-alveolar fracture of a root depends on: Presence or absence of infection The vitality of the pulp The position of the fragments The degree of communition The location of the fracture The mobility of the coronal fragment

69 ROOT FRACTURE (cont…). Healing process: It may occur in 3 patterns
The roots fragments become united totally, or in part, by calcified repair tissue resembling bone and/or cementum The fractured surfaces of each fragment become rounded off and clothed by cementum but are not united by calcified tissue. Fibrous tissue fills the space. The fractured surfaces of each fragment become rounded off and clothed by cementum but the fragments are widely separated. Alveolar bone fills the space. The pulp chamber in either fragment may become obliterated by calcified tissue.

70 AGE CHANGES IN TEETH. These include changes in morphology associated with tooth wear especially attrition and changes in structure and composition of the dental hard tissues. Enamel. Tends to become more brittle and less permeable (ionic exchange) It darken with age (absorption of organic material) Dentine. Continued formation of secondary dentine leading to reduction in size or obliteration of the pulp chamber. Dentinal sclerosis associated with continued production of peritubular dentine resulting in root brittleness that may fracture during extraction The dentinal sclerosis is also associated with increasing translucency that can be used in forensic dentistry as one method of age estimation.

71 AGE CHANGES (cont…) Cementum.
Gradual increase in thickness to compensate for interproximal and occlusal attrition The amount of secondary cementum can also be used for age estimation Pulp. The volume gradually decreases due to continued production of secondary dentine Decreased vascularity, reduction in cellularity and increase in collagen fibres may impair the response to injury and its healing potential. Prevalence of pulp stones and diffuse calcification increase.

72 ODONTOMAS AND ODONTOGENIC
TUMOURS.

73 A. ODONTOMAS. Definition:
It is a non-neoplastic, developmental anomally or malformation that contains fully formed enamel and dentine. It can be considered as dental hamartomas containing the calcified dental tissues. Are the most common odontogenic tumours. There are 2 types: Compound odontomas: Numerous miniature or rudimentary teeth Complex odontomas: Amorphous conglomerations of hard tissues

74 ODONTOMAS (cont…). Clinical features:
Lesions of children and young adults (2nd decade of life) Maxilla affected slightly more often than mandible Compound odontomas have a tendency to occur in the anterior jaws Complex odontomas in the posterior jaws No gender predilection Associated with a retained deciduous tooth, an impacted tooth and alveolar swelling Generally no symptoms.

75 ODONTOMAS (cont…). Radiographic features: 1.Compound odontomas:
Appear as numerous tiny teeth in a single focus The focus is typically in a tooth-bearing area, between roots or over the crown of an impacted tooth As many as 200 such structures have been observed in a single lesion 2.Complex odontomas: Appear in the same regions but as amorphous, opaque mass.

76 ODONTOMAS (cont…). Histological features:
Normal-appearing enamel, dentin, cementum, and pulp may be seen in these lesions Prominent enamel matrix and the associated enamel organ are often seen before final maturation of hard tissue. Differential diagnosis: Other opaque jaw lesions such as: -Focal sclerosing osteitis -Osteoma -Periapical cemental dysplasia -Ossifying fibroma -Cementoblastoma Usually compound odontomas are self-diagnostic and complex odontomas present a solid opacification in relationship to teeth.

77 B. ODONTOGENIC TUMOURS. Odontogenic tumours are lesions derived from the epithelial and/or mesenchymal remnants of the tooth-forming apparatus. Are therefore found exclusively in the mandible and the maxilla The etiology and pathogenesis are unknown Clinically asymptomatic but may cause jaw expansion, movement of teeth, root resorption and bone loss. Differential diagnosis can be based on age, location, radiographic appearance Range from benign to malignant tumors.

78 ODONTOGENIC TUMOURS (cont…)
EPITHELIAL TUMOURS. AMELOBLASTOMA. Definition: This is a benign but locally invasive neoplasm derived from odontogenic epithelium. It is the commonest of the odontogenic tumours. Accounts for approximately 1% of all oral tumours -More common in black Americans and West Africans (6% or more of oral tumours)

79 AMELOBLASTOMA(cont…)
Clinical features: Can occur in children or the elderly but In industrialized countries, usually in fourth or fifth decades of life In developing countries, about years earlier About 80% occur in the mandible of which 70% arise in molar region and ascending ramus, 20% in the premolar region and 10% in the incisor region. In the maxilla, most also occur in the molar region, 15% involving the antrum The tumour is slow-growing but locally invasive It is asymptomatic in early stages and can be discovered as an incidental finding

80 AMELOBLASTOMA(cont…)
As the tumour enlarges, there is facial deformity and expansion of the jaw bone The enlargement is initially bony hard, non-tender, ovoid or fusiform in outline In advanced cases, egg-shell crackling may be elicited due to thinning of the overlying bone In late features, there is perforation of bone and extension of the tumour into soft tissues. In maxilla, it can expand into the sinus and beyond Teeth may become loosened, pain is rarely a feature In rare cases, pulmonary metastases may occur

81 AMELOBLASTOMA(cont…)
Malignant variants of ameloblastoma may rarely be encountered: -Malignant ameloblastomas: well differentiated -Ameloblastic carcinomas: less microscopic differentiation with cytologic atypia and mitotic figures. Metastases appear usually in the lung, followed by regional lymphnodes, the skull, liver, spleen, kidney and skin.

82 AMELOBLASTOMA(cont…)
Radiographic features: Appears most commonly as a multilocular radiolucency but may also be unilocular Roots of teeth involved show varying degrees of resorption The margins are well defined and sclerotic May become associated with an unerupted tooth, particularly an impacted third molar and mimic the appearance of a dentigerous cyst At an early stage, can be mistaken for an odontogenic cyst

83 AMELOBLASTOMA(cont…)
Histological features: There are 2 types: The follicular and the plexiform patterns. a.Follicular pattern: The tumour epithelium is arranged into more or less discrete, round islands or follicles, resembling the enamel organ of the developing tooth germ The follicles consist of a central mass of loosely connected, angular cells resembling the stellate reticulum of the normal enamel organ, surrounded by a layer of cuboidal or columnar cells resembling ameloblasts The nuclei are stimulated away from the basal ends of the cells= reversed polarity The follicles are separated by varying amounts of fibrous connective tissue

84 AMELOBLASTOMA(cont…)
Microcyst formation is common that may coalesce to form larger areas of cystic change within the tumour Sometimes, small areas of squamous metaplasia may occur and then the tumour is called acanthomatous ameloblastoma b.Plexiform pattern: The tumour epithelium is arranged as a tangled network of anastomosing strands and irregular masses each of which shows the same cell layers as for foliicular pattern Each strand or mass is bounded by columnar or cuboidal cells resembling ameloblasts The central area is occupied by stellate reticulum-like cells Cystic formation is common, caused by stromal degeneration

85 AMELOBLASTOMA(cont…)
Pathogenesis: Originates within the mandible or maxilla from epithelium involved in the formation of teeth Potential epithelial sources: - Enamel organ -Odontogenic rests (rests of Mallassez, rests of Serres) -Reduced enamel epithelium -Epithelial lining of odontogenic cysts (e.g. dentigerous cyst) -Basal layer of oral epithelium The trigger for neoplastic transformation totally unknown

86 AMELOBLASTOMA(cont…)
Differential diagnosis: Odontogenic tumours (calcifying epithelial odontogenic tumour) Odontogenic cysts (dentigerous cyst, odontogenic keratcyst) Benign non-odontogenic lesions (central giant cell granuloma, ossifying fibroma) Management: Surgical resection with a margin of normal bone Simple curettage is associated with high recurrence rate (50-90%) Good follow-up since recurrence can appear years later.

87 ODONTOGENIC MYXOMA. Definition:
This is a benign but locally invasive and aggressive neoplasm. It is a mesenchymal lesion that mimics microscopically the dental pulp or follicular connective tissue. Clinical features: -Age extends from 10 to 50 years with a mean of about 30 years -No gender predilection -Mandible and maxilla equally affected

88 ODONTOGENIC MYXOMA (cont…)
Radiographic features: The lesion is always lucent, the pattern may be variable May appear as a well –circumscribed or a diffuse lesion Often multilocular and has a honey-comb or a soap-bubble appearances Cortical expansion or perforation and root displacement or resorption may be seen Histologic features: Stellate, fibroblast-like cells with long anastomosing processes, separated by abundant connective tissue=glucosaminoglucans Some cases contain a few strands of odontogenic epithelium Variant amount of collagen may be present making it difficult to distinguish between myxoid change in a fibroma and fibrous change in a myxoma hence the terms myxofibroma and fibromyxoma.

89 ODONTOGENIC MYXOMA (cont…)
Differential diagnosis: Same as for ameloblastoma Management: Surgical excision for complete removal but the locally invasive growth makes it difficult and predisposes to local recurrence Prognosis is good.

90 CEMENTOBLASTOMA. CEMENTOBLASTOMA. Definition:
It is also known as true cementoma and it is a rare benign neoplasm of cementoblast origin. Clinical features: Occurs predominantly in the 2nd and 3rd decades of life, typically before 25 years of age No gender predilection Mandible more affected than maxilla Posterior region more involved than anterior Intimately associated with the root of a tooth The tooth involved is vital It is slowly enlarging May cause cortical expansion and occasionally low-grade intermittent pain.

91 CEMENTOBLASTOMA (cont…).
Radiographic features: Opaque lesion replacing the root of the tooth Usually surrounded by a radiolucent ring representing the periodontal ligament space and the advancing front of the tumour The root usually shows resorption Histologic features: Appears as a dense mass of mineralized cementum-like material Intervening well-vascularized soft issue containing numerous, large and hyperchromatic cementoblasts

92 CEMENTOBLASTOMA (cont…).
Differential diagnosis: Odontomas Osteoblastomas Focal sclerosing osteomyelitis Hypercementosis Treatment: Surgical excision for complete removal Sacrifice the tooth because of the intimate association between the root and the tumour Prognosis: Good, recurrence not seen

93 OTHER ODONTOGENIC TUMOURS
Epithelial tumours: -Calcifying epithelial odontogenic tumour -Adenomatoid odontogenic tumour -Squamous odontogenic tumour -Clear cell odontogenic tumour

94 Mesenchymal tumours: -Central odontogenic fibroma -Cementifying fibroma -Periapical cementoosseous dysplasia Mixed tumours (epithelial and mesenchymal): -Ameloblastic fibroma and Ameloblastic fibroodontoma

95 References Hamilton B.G.Robinson, Arthur S.Miller (1993), Colby, Kerr and Robinson’s Color Atlas of Oral Pathology, 4th edition, J.B. Lippincott Company, pp.35-50;53-67; Joseph A.Regezi, DDS,MS; James J.Sciubba, DMD,PHD; Richard C,K,Jordan, DDS, Msc, Phd, FRCD (C) (1999),Oral Pathology, 4th Edition, Saunders, pp ; Soames J.V. and Southan J.C. (1999), Oral Pathology, Third Edition, Oxford, pp 1-17; 37-48; 59;


Download ppt "DISORDERS OF DEVELOPMENT OF TEETH"

Similar presentations


Ads by Google