1. ABNORMALITIES OF TEETH
Environmental Alterations of Teeth
Developmental Alterations of Teeth
牙齒的異常-環境與發育的影響
王文岑 高雄醫學大學 牙醫學系

2. ENVIRONMENTAL ALTERATIONS OF TEETH
Developmental tooth defects
Turner’s tooth
Hypoplasia caused by antineoplastic therapy
Fluorosis
Syphilitic hypoplasia
Postdevelopmental structure loss
Tooth wear
Internal and external resorption
Discolorations of teeth
Intrinsic stains
Extrinsic stains
Localized disturbances in eruption
Primary impaction
Ankylosis

3. Enamel development
Three stages: 1. Matrix formation: protein laid down
2. Mineralization: minerals deposition, majority of original prot. removed-- diffuse, opaque white, soft enamel
3. Maturation: final mineralization-- translucent, hard enamel
Amelogenesis imperfecta
Enamel hypoplasia

4. Enamel development No remodeling after initial formation
Timing of ameloblastic damage has a great impact on location & appearance of the defect
Development of crown : from 14th week of gestation to 12 months of age in deciduous dentition; 6 months to 15 y/o in permanent dentition
Neonatal ring on deciduous enamel and deposition with a rate of 0.023mm/day
初成形後沒有remodeling, 故受損的timing 是關鍵

5. Factors associated with enamel defects
See Box 2-2
Factors associated with enamel defects
Systemic-
1. Birth-related trauma: premature birth
2. Chemicals: antineoplastic C/T, fluoride, tetracycline
3. Chromosomal abnormalities: trisomy 21
4. Infections: chicken pox, CMV, syphilis
5. Inherited diseases: Vit.D-dependent rickets
6. Malnutrition: Vit. A deficiency
7. Metabolic disorders: hypoparathyroidism, maternal diabetes
8. Neurologic disorders: cerebral palsy

6. Factors associated with enamel defects
See Box 2-2
Factors associated with enamel defects
Local-
1.Local acute mechanical trauma
2. Electric burn
3. Irradiation
4. Local infection: periapical inflammatory disease

7. Clinical and Radiographic Features
Environmental enamel defects:
1.Hypoplasia: pits, grooves or large area of missing enamel
2. Diffuse opacities: variation in translucency, normal thickness, white opacity without clear boundary
3. Demarcated opacities: increased opacity, a sharp boundary with adjacent normal enamel, normal thickness

8. Turner’s hypoplasia, Turner’s tooth
Permanent teeth
Periapical inflammatory disease of the overlying deciduous tooth, less frequently in anterior teeth
Traumatic injury- not rare
-45% children sustain injury to their deciduous teeth, 23% permanent teeth development disturbed
Turner’s hypoplasia secondary to previous trauma

9. Turner’s teeth

10. Hypoplasia caused by antineoplastic therapy
Under 12 y/o, esp. under 5y/o
Age at treatment, forms of therapy
Chemotherapy-
Less alteration than radiation
Increased number of enamel hypoplasia and discolorations, slight smaller tooth size, radicular hypoplasia

11. Radiotherapy-
0.72 Gy related to mild defects in enamel, dentin (一般成人頭頸癌照射一次約為2Gy)
Dose, radiation field

12. Developmental radicular hypoplasia and microdontia caused by radiotherapy

13. Hypodontia, microdontia, radicular hypoplasia, enamel hypoplasia, mandibular hypoplpasia, reduced in vertical development of lower 1/3 of face
Mandibular hypoplpasia may caused by Radiation →impaired root development →reduced alveolar bone growth
Cranial radiation→ altered pituitary gland function→ growth failed

14. *Dental fluorosis 1901, Dr. Frederick S. McKay: Colorado brown stain
1909, Dr. F.L. Robertson in Bauxite, Arkansas
1930, H.V. Churchill: high concentration of fluoride of Bauxite(13.7ppm) and Colorado
1931, Dr. H. Trendley Dean: association between fluoride, dental fluorosis and prevalence of caries among children
1.0 ppm reduced caries by 50~70% and associated with low and mild mottled enamel
0.7~1.2 ppm water fluoridation was recommended after 1962, currently 0.7ppm is recommended due to increased dental fluorosis

15. Dental fluorosis
Retention of the amelogenin protein in enamel structure → hypomineralized enamel → permanent hypomaturation → increased surface and subsurface porosity → alters light reflection and create white, chalky area

16. Dental fluorosis
Critical period for clinical dental fluorosis is the 2nd and 3rd year of life, dose dependent
Caries resistant

17. Syphilitic hypoplasia
Congenital syphilis
Hutchinson’s incisors & mulberry molars

18. POSTDEVELOPMENTAL LOSS OF TOOTH STRUCTURE
Begin from enamel surface (tooth wear):
Attrition, abrasion, erosion, abfraction
Begin from dentin, cemental surface: internal or external resorption

19. Attrition
Tooth to tooth contact during occlusion and mastication, some are physiologic
Accelerated by: poor quality or absent enamel, premature contact, intraoral abrasives, erosion, grinding habits
Incisal, occlusal and interproximal surfaces

20. Abrasion
Pathologic loss of tooth structure or restoration secondary to the action of an external agent (ex. Toothbrush, hair grips, toothpicks, chewing tobacco, biting thread, dental flossing…)
Toothbrush abrasion: horizontal buccal cervical notches of exposed radicular cementum and dentin with smooth surface.
Greater on prominent teeth ( canines, premolars , and teeth adjacent to edentulous area) and side of the arch opposite to the dominant hand
Demastication- when tooth wear is accelerated by chewing an abrasive substance between opposing teeth (both attrition and abrasion)

21. Abrasion

22. Improper use of hair grips
Abrasion
Long-term use of tobacco pipe

23. Erosion
Chemical process, exposure to acidic foods or drinks, medications (chewable Vit. C, aspirin), involuntary regurgitation (ex. esophagitis, pregnancy), voluntary regurgitation (ex. psychologic problems, bulimia)
Perimolysis- dental erosion from gastric secretion
Facial surface of maxillary anteriors affected-dietary source
Posterior teeth extensive loss of occlusal surface, and palatal surface concave dentin surrounded by an elevated enamel rim- regurgitation of gastric secretion
上顎前牙的腐蝕可能是食物因素而起, 而舌側及咬合面的腐蝕則可能是內生性的, 如胃液逆流而來。

24. concave dentin surrounded by an elevated enamel rim
Erosion
concave dentin surrounded by an elevated enamel rim

25. Erosion
A bulimia patient

26. Abfraction
Repeated tooth flexure caused by occlusal stresses (tensile stress)
→ concentrate at the cervical fulcrum
→ may produce disruption in the chemical bonds of enamel crystal
→cracked enamel can be lost or removed by erosion or abrasion
Wedge-shaped cervical defects, deep, narrow V-shaped, not allow toothbrush to contact base; if the defect, often affect a single tooth
Almost exclusively on facial surface and more often in bruxism, higher in mandibular dentition

27. Abfraction

28. Treatment and prognosis of tooth wear
Resolve pain and sensitivity
Identify the cause of tooth structure loss
Protection

29. INTERNAL & EXTERNAL RESORPTION
Internal resorption- by cells located in pulp, rare
Follows injury to pulp tissues, physical trauma or caries, continue as long as vital pulp remains, may result in communication of the pulp and PDL
External resorption- by cells in PDL, common

30. Factors associated with external resorption

31. Clinical and Radiographic Features
Internal resorption-
Inflammatory resorption- dentin replaced by inflamed granulation tissue
Pink tooth of Mummery: internal resorption involved coronal pulp Balloonlike enlargement of the canal
Replacement, or metaplastic absorption- pulpal dentinal walls are replaced by bone or cementum-like bone

32. Clinical and Radiographic Features
External resorption-
Moth-eaten loss of tooth structure, less well-defined and variation in density in radiography
Most involved apical or midportions of root, occasionally, begin from cervical (invasive cervical resorption)

33. Histopathologic Feature
Increased cellularity, vascularity and collagenization
Numerous multinucleated dentinoclasts
Inflammatory cells infiltration

34. Treatment and prognosis
Internal resorption-
Removal of all soft tissue from site of resorption
Endodontic treatment before perforation in internal resorption
Placement of calcium hydroxide paste for remineralization
Surgical exposure and restoration
Extraction
External resorption-
Identification and elimination the accelerating factor

35. ENVIRONMENTAL DISCOLORATION OF TEETH
Extrinsic- surface accumulation of exogenous pigment
Intrinsic-secondary to endogenous factors that result in discoloration of underlying dentin

36. Extrinsic stains
Bacterial- Chromogenic bacteria, green, black-brown, orange coloration Frequently in children, labial surface of maxillary ant. in gingival third
Iron- formation of ferric sulfide
Tobacco
Food and beverage- chlorophyll
Gingival hemorrhage- Hb. breakdown to biliverdin
Restorative material – ex. Amalgam
Medications- iron, iodine, silver nitrate, chlorhexidine, stannous fluoride

37. Intrinsic stains Amelogenesis imperfecta Dentinogenesis imperfecta
Dental fluorosis
Erythropoietic porphyria –
autosomatic recessive disorder of porphyrin metabolism, increased synthesis and excretion of porphyrins and their related precursors
Porphyrin deposition in teeth, reddish-brown coloration, red fluorescence when exposed to a Wood’s UV light
Present both in dentin and enamel in deciduous teeth, but only dentin affected in permanent teeth

38. Erythropoietic porphyria
Hyperbilirubinemia

39. Ochronosis-alkaptonuria, blue-black discoloration
Intrinsic stains
Hyperbilirubinemia- bilirubin, breakdown product of RBC, jaundance (yellow-green discoloration), erythroblastosis fetalis, biliary atresia
Biliverdin deposition, green discoloration of teeth (chlorodontia)
Ochronosis-alkaptonuria, blue-black discoloration
Trauma- coronal discoloration, pulp necrosis
Localized RBC breakdown

40. Intrinsic stains Medications-
Tetracycline (bright yellow to dark brown), chlortetracycline (gray-brown), oxytetracycline (yellow) , minocycline hydrochloride
Time of administration dose, duration
Avoid from pregnancy up to 8 yrs of age

41. Minocycline hydrochloride
Tx for Acne
Blue-gray from incisal 3/4, to dark green or black in roots, also affect developed teeth
Skin, nail, sclera, conjunctiva, thyroid, bone discoloration in susceptible individuals
Stained alveolar bone

42. Treatment and prognosis
Extrinsic stains- polishing
Intrinsic stains- bleaching, bonded restoration, crowns

43. LOCALIZED DISTURBANCES IN ERUPTION
PRIMARY IMPACTION- Teeth cease to eruption before emergence
ANKYLOSIS -Cease of eruption after emergence and anatomic fusion of tooth cementum or dentin with alveolar bone

44. Impaction
3rd molars, maxillary canines, mandibular premolars, mandibular canines, maxillary premolars, maxillary central incisors, maxillary lateral incisors, and mandibular second molars; usually angulated or diverted
Factors associated with impaction:
Crowding and deficient maxillofacial development
Overlying cysts or tumors
Trauma
Reconstructive surgery
Thickened overlying bone or soft tissue
A host of systemic disorders, diseases or syndromes

45. Eruption sequestrum Classification :
Partially erupted or full bony impaction
according to angulation: Mesioangular, distoangular, vertical, horizontal or inverted
Eruption sequestrum

46. Treatment and Prognosis
Choice of treatment:
Long-term observation
Orthodontically assisted eruption
Transplantation
Surgical removal
The risks associated with nonintervention:
Crowding dentition
Resorption and worsening of the periodontal status of adjacent teeth
Development of pathologic conditions, ex infections, cysts or tumors

47. The risks associated with intervention:
Transient or permanent sensory loss
Alveolitis
Trismus
Infection
Fracture
TMJ injury
Periodontal injury
Injury to adjacent teeth

48. ANKYLOSIS
Infraocclusion, secondary retention, submergence, reimpaction, reinclusion

49. ANKYLOSIS Clinical And Radiographic Features
Pathogenesis is unknown, may be secondary to many factors and result in PDL barrier deficiency.
May occur at any age, any tooth
Most affect 8~9yr-old children and D , E , D , E
PDL absent
Occlusal, periodontal problems, impaction of the underlying teeth
Treatment and Prognosis
Variable : extraction, orthodontics, segmental osteotomy

50. DEVELOPMENTAL ALTERATIONS OF TEETH
NUMBER Hypodontia
Hyperdontia
SIZE Microdontia Macrodontia
STRUCTURE Amelogenesis imperfecta Dentinogenesis imperfecta
Dentin dysplasia I & II Regional odontodysplasia
SHAPE Gemination, Fusion, Concrescence Accessary cusps
Dense in dente Ectopic Enamel
Taurodontism
Dilaceration Hypercementosis
Supernumerary roots

51. Missing teeth Ectodermal dysplasia orofaciodigital syndrome
% , excluding 3rd molars, female predominance
Hypodontia: missing one or more teeth
Oligodontia: missing 6 or more teeth
Anodontia: total missing
8 > 5 > 2 > 1
Deciduous mandibular incisors
Gene mutation, ex: PAX9, MSX1, AXIN2 gene, He-Zhao deficiency, maps to chromosome 10q11.2
AXIN2 mutation: associated with the development of adenomatous polyps of colon, and colorectal carcinoma
Ectodermal dysplasia
orofaciodigital syndrome % 4

52. Hypodontia

53. Ectodermal dysplasia
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

54. Supernumerary teeth, hyperdontia
Mesiodens
4th molar
Paramolar
Distomolar, distodens
deciduous - lat. incisors
86% single supernumerary
multiple & impaction
cleidocranial dysostosis
Gardner’s syndrome

55. Mesiodens The most common in supernumerary.
Premaxillary area , usually between upper central incisors
Cone-shaped crown & short root
One or two in number

56. Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

57. Cleidocranial dysostosis
1.Skull: flat appearance, sutures remain open
2.Jaws: underdeveloped, high narrow palate
3.Teeth: prolonged retained deciduous teeth,
delayed eruption of permanent teeth
4.Clavicles: complete or partial absent

58. Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

59. Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

60. Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

61. Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

63. 3.multiple epidermoid cysts or sebaceous cysts of the skin
Gardner’s syndrome
1.multiple polyposis of the large intestine
2.osteoma of the bone
3.multiple epidermoid cysts or sebaceous cysts of the skin
4.desmoid tumors
5.impacted supernumerary & permanent teeth

64. Predeciduous dentition
Neonatal teeth: within 30 days
Natal teeth: newborns
Most are prematurely erupted deciduous teeth
Removal only if mobile and at risk of aspiration

66. Microdontia True: 1.General -pituitary dwarfism
2. Single -peg lat., 3rd molar
Relative microdontia

67. Macrodontia True macrodontia : 1. Generalized-pituitary gigantism
2. Localized- single, hemifacial hypertrophy
Relative macrodontia: small jaw, child

69. Gemination, Fusion, Concrescence

70. Gemination single tooth germ division tooth no.: normal
single root & root canal + 2 complete or incomplete separated crowns
tooth no.: normal
twinning

71. Fusion Union of 2 separate tooth germs
Contact of tooth germ before calcified
Confluent of the dentin
Complete- form a single tooth
Incomplete- after calcified begins
Tooth no. : less one

72. Fusion after root formation Cementun united
Concrescence
Fusion after root formation
Cementun united
Traumatic injury or crowding
Pre-extraction x-ray check

73. Talon cusp Eagle’s talon
Lingual projection from the cingulum area of ant. teeth
Most contain a pulp horn
Both in deciduous & permanent dentition

74. Dens evaginatus
( central tubercle, occlusal tuberculated premolar; Leong’s premolar; evaginated odontome; occlusal enamel pearl )
An accessory cusp or a globule of enamel on central groove or buccal cusp of premolars or molars; unilateral or bilateral.
15% in Asians, rare in whites

75. Dens evaginatus
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

76. Shovel-shaped incisors

77. Tooth within a tooth, incidence 5%
Dens in dente
(Dens invaginatus; Dilated composite odontome)
Tooth within a tooth, incidence 5%
Invagination of the enamel organ into dental papilla before calcification
Coronal type: 3 types
maxillary lateral incisors are common

78. Dens invaginatus, coronal type II

79. Dens invaginatus Radicular type Hertwig’s sheath invagination
Food deposition→ caries → pulp infection
Restorated as soon as possible

80. Bi- or trifurcation near the apex
Taurodontism
“Bull-like “ teeth
Bi- or trifurcation near the apex
Pulp chamber : greater apico-occlusal height and no constriction at the cervical of the tooth

81. Syndromes associated with taurodontism

82. Hypercementosis

83. Supernumerary roots Any tooth may develop accessary roots
No tx required, but critical important in endodontic procedure

84. Dilaceration
Angulation, sharp bend of root or crown
Trauma during tooth is forming
Pre-extraction x-ray check

85. Amelogenesis imperfecta
(Hereditary enamel dysplasia; Hereditary brown enamel; Hereditary brown opalescent teeth)
Defects in--
Formative stage→hypoplastic type → defective formation of matrix
Calcification stage →hypocalified → defective mineralization of formed matrix
Maturation stage → hypomaturation → enamel crystallites remain immature
Genes mutation : AMELX, ENAM, MMP-20, KLK4, DLX3

86. Amelogenesis imperfecta

87. 1.Hypoplastic type
Thin enamel with pitted, rough or smooth & glossy surface; yellowish to brown
undersized, squared crown, lack of contact
flat occlusal surface & low cusps, attrition

88. Hypoplastic type
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

89. Hypoplastic type

90. 2.Hypomaturation
normal thickness of enamel, but mottled surface; cloudy white, yellow or brown, opaque in color
softer than normal
same density as dentin

91. Hypomaturation type
Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

92. 3.Hypocalcified type
normal thickness of enamel, density less than dentin
normal size & shape when erupt, abrade or fracture away rapidly
permeability increase, darkened & stained
4.Hypomaturation-hypocalcified
with taurodontism

93. Hypocalcified type

94. Tricho-dento-osseous syndrome
Hypoplastic-Hypomaturation type

95. Dentinogenesis imperfecta
(Hereditary opalescent dentin)
Classification of DI : (Shields)
Type I : DI + OI (osteogenesis imperfecta) COL1A1,
COL1A2
Type II : Isolated DI. (1/8000) DSPP
Type III: DI of the Brandywine type * DSPP
A racial isolate in Maryland,
DI + multiple pulp exposures in deciduous teeth

96. Osteosclerosis imperfecta
Blue sclera
M Greenwood, J G Meechan,:General medicine and surgery for dental practitioners Part 8: Musculoskeletal system. British Dental Journal 2003 (195) ,

97. Clinical features type I : deciduous severe than permanent teeth;
type II: equally affected;
type III: both dentitions affected.
Gray to brownish violet or yellowish brown color, with translucent or opalescent hue.
Enamel lost early through fracture, esp. on the incisal & occlusal surface, and dentin attrition rapidly.
Caries rate is not increased.

98. Dentinogenesis imperfecta

99. Dentinogenesis imperfecta
Histology:
1.pulp chamber obliterated with dentin
2.flatten D-E junction
3.atypical granular dentin, enlarged tubles, poor calcification
water contents: 50% above normal

100. Radiographic features
Partial or total obliteration of the pulp chamber & root canal by continued formation of dentin, in both dentitions.
Short and blunted roots
Normal cementum, PDL & supporting bone

101. Shell teeth Initial reported in the Brandywine population
Normal thickness of enamel associated with extremely thin dentin and dramatically enlarged pulps (due to insufficent and deffective dentin formation)
Short roots.

102. Kaohsiung Medical University, Oral Pathology and image Diagnosis Dept.

103. Dentin dysplasia
Hereditary, autosomal dominant. Normal enamel but atypical dentin formation with abnormal pulp morphology
Type I (radicular type): “Rootless teeth”
Type II (coronal) DSPP (dentin sialophosphoprotein) gene mutation

104. Type I (radicular type)
Radiographically:
deciduous teeth affected more severely, little or no pulp, short or absent roots.
If disorganization late---normal pulp chambers, with a large pulp stone.
periapical lesions (R-L) no obvious cause.
Histologic features
Normal coronal enamel& dentin.
In root: tubular dentin and atypical osteodentin surrounded with normal dentin --- appearance of “ Lava flowing around boulders”.

105. Dentin dysplasia, type I

106. Type II (coronal)
Normal root length in both dentitions.
Primary dentition similar to DI:
bulbous crowns, cervical constriction
thin roots , early obliterated pulp.
Permanent teeth : normal coloration, thistle tube-shaped or flame-shaped pulp chamber with pulp stones.

107. Dentin dysplasia, type II (coronal)

108. “Lava flowing around boulders”.
Dentin dysplasia
Large pulp stones

109. Regional odontodysplasia
(odontodysplasia; odontogenic dysplasia; odontogenesis imperfecta; ghost teeth)
One or several teeth in a localized area
Maxi. > Mand.; both dentitions
most in ant. area
Delayed or total failure eruption
Irregular appearance
Defective mineralization

110. Radiographic features
1. Radiodensity ↓, “ghost appearance”
2. Large pulp, thin enamel & dentin
Histologic features
1. Dentin↓
2.Widening of the predentin layer,
3. Interglobular dentin and an irregular tubular pattern of dentin ↑
4.Calcification of the reduced enamel epi.

111. Odontogenic epithelium Enameloid conglomerates
Regional odontodysplasia

112. ENVIRONMENTAL ALTERATIONS OF TEETH
Summary
ENVIRONMENTAL ALTERATIONS OF TEETH
Developmental tooth defects
Turner’s tooth
Hypoplasia caused by antineoplastic therapy
Fluorosis
Syphilitic hypoplasia
Postdevelopmental structure loss
Tooth wear
Internal and external resorption
Discolorations of teeth
Intrinsic stains
Extrinsic stains
Localized disturbances in eruption
Primary impaction
Ankylosis

113. DEVELOPMENTAL ALTERATIONS OF TEETH
Summary
DEVELOPMENTAL ALTERATIONS OF TEETH
NUMBER Hypodontia
Hyperdontia
SIZE Microdontia Macrodontia
STRUCTURE Amelogenesis imperfecta Dentinogenesis imperfecta
Dentin dysplasia I & II Regional odontodysplasia
SHAPE Gemination, Fusion, Concrescence Accessary cusps
Dense in dente Ectopic Enamel
Taurodontism
Dilaceration Hypercementosis
Supernumerary roots