22.Disturbances of growth (Eruption) of teeth.ppt

This ppt is useful for understanding various disturbance of tooth eruption

1. Normal eruption-broad range for both primary and
secondary
Only those grossly beyond external of normality

2. Premature eruption-dentitia
praecox
Natal teeth present at birth (eruption at birth)
Neonatal birth- erupt within 30 days of birth-
1
-
2 mandibular incisor
Clinical features
Primary - Well formed teeth, normal, somewhat mobile
Aetiology;
Primary dentition- unknown ?familial endocrinology
(thyroid, adrenals, gonads)
Permanent dentition- premature loss of deciduous teeth
Whole dentition- hyperthyroidism
Should be retained even if nursing may be difficult

3. Delayed eruption – dentitia tarda
Should be grossly overdue
Aetiology
Primary teeth - unknown. ? Systemic factors – ricketts,
cretinism, cleido-cranial dystosis or local factors eg
fibromatosis gingivae as the dense collagen will not permit
eruption
Treatment- Treat the cause
Multiple unerupted teeth
Rare. Lack of eruptive force, hormonal disturbance or
cleido-cranial dystosis
Retained deciduous teeth shed but failure of secondary
teeth to erupt (Pseudo-anodontia)
Treat the cause

4. Erupting sequestrum
Associated with teeth eruption in children
Clinical
Bone spicules overlie the crown of erupting
permanent tooth (e.g. 1
st
molar)
Sequestrates through mucosa along with
eruption of a tooth –within the soft tissue
Treatment- Nil

5. Embedded and impacted teeth
Aetiology
Embedded teeth- lack of eruptive force
Impacted teeth – physical obstruction (space, tooth germ rotation)
Clinical
Any tooth but more common are:
3
rd
molars (maxillary 22%, Mandibular 18%)
Maxillary canines(0.9)
Premolars and supernumerally
Positions
Mesial-angular (most common)
Distoangular
Vertical
Horizontal
Buccal or lingual (palatal) deflection
Complications (if untreated)
Infection (if partially erupted)
Jaw fracture
Dentigerous cyst
Tooth crown resorption

6. Ankylosed deciduous teeth
Submerged teeth
Aetiology
?trauma, infection, genetic factors
Clinical
Mandibular second molar
Root resorption –ankylosed, prevent exfoliation
Primary tooth which is firmly attached to bony socket
Occlusal surface is below that of adjacent permanent teeth
Treatment-removal
Residual apices
Irregular resorption of primary teeth may lead to residual
root fragment formation

7. Regressive tooth changes
Are not necessarily aetiologically or
pathogenetically related and are not
necessarily aetiologically or
pathogenetically related
usually associated with age related
phenomenon and injury to tissue
Lesions of retrograde nature
Not developmental, not inflammatory
Non bacterial loss of tooth substance

8. attrition
Def: Physiological ‘wearing away' of tooth
substance on occlusal, incisal and
interproximal surfaces
Aetiology
Course abrasive diet
Loss of teeth with increased wear of remaining
teeth (tooth-tooth contact eg mastication)
Exposure to dust and industrial pollution,
bruxism, xerostomia
Associated with aging process, the older, the
more attrition

9. Clinical
Localized facets on contact surfaces of teeth
Initially, only incisors, later occlusal surfaces of
molars
palatal cusps of maxillary teeth and buccal cusps
of mandibular molars
Interproximal wear may be as much as 1 cm from
3
rd
molar to 3
rd
molar
Pathological attrition occurs when position of
tooth is abnormal or forces are abnormal-bruxism
Pathological
May lead to dentinal exposure-dentinal
sclerosis-tertiary dentine formation.
Dead tracts develop after odontoblastic death
Males more than females of comparable age

10. Abrasion
Def: Pathological wearing away of tooth
substance by a foreign body independent of
occlusion (mechanical).
Clinical: depends on etiology
Etiology
Tooth brushing (cervical buccal surfaces of maxillary teeth
especially)
Partial denture (friction of clasps or denture)
Habits (pipe, etc)
Occupational (needle workers, hair-dressers, shoemakers,
musicians, ritual/social practices (asia, American Indians,
Africa)
Pathology: Same as attrition
Dentinal exposure
Dentinal sclerosis—tertiary
Dentinal formatiom

11. Erosion
Def;
superficial loss of dental hard tissue by a chemical process
unrelated to bacterial activity
aetiology:
 acidic beverage (anterior teeth)
Regurgitation of gastric acids (posterior)
Acidic saliva (increased citric acid Increased mucin
contents and low pH)
Occupational hazards (exposure to inorganic industrial
acids)
Clinical
Gingival third of buccal surfaces of incisors show shallow,
smooth scooped-out cavities
The dentine exposure leads to sensitivity

12. Reparative dentinal changes
Transparent (translucent or sclerosed)
dentine
Aetiology
Caries, attrition, abrasion, erosion, age
Pathogenesis
Chronic dentinal irritation or age leads to the
deposition of peritubular mineral salts
A harder than normal dentine is produced
Simultaneous deposition of secondary dentine in
the pulp chamber forms secondary dentinal tubuli
continuous in with primary tubuli
Dentinal tubuli are calcified and become highly
calcified

13. Dead tracts
Aetilogy
More intense irritation than that which produces
transparent dentine
Pathogenesis
Odontoblasts die
Affected dentine becomes opaque and pulpal ends of
dentinal tubuli are sealed off by atubular calcified material
New odontoblasts may differentiate to form tertiary
dentine.
Clinical
Under L/M, black zones (transmitted light) or white zones
(reflected light) are seen.

14. Formation of new dentine
Dentine is classified as
Primary dentine
Dentine formed during odontogenesis
Secondary dentine (regular)
Formed after formation of teeth in response to
slight irritation during normal biological processes.
Secondary dentine increases with age
Incisors
Formed especially on palatal walls of pulpal chambers,
molars and premolars – more on roof, floor and
cervical areas of pulpal chamber
Histologically
Secondary dentine contains fewer and narrower
tubules with wavy appearance and a dark line is found
at the junction btw primary and secondary dentine.

15. Tertiary dentine
Forms in response to intense pulp irritation
It is located exclusively adjacent to area of
irritation
Dentinal tubuli
are irregular
contain vascular inclusions
A higher mineral content and can also be structureless
(hyaline tertiary dentine) or contain cellular teriary dentine
Synonymus to irregular dentine, reparative dentine,
irritational dentine
Osteodentine
rapid formed dentine with entrapped odontoblasts producing
a superficial resemblance to bone

16. Regressive changes of the
pulpTakes place during the formation of
tertiary dentine and with increased age.
Not associated with symptoms although
pulp may react slightly to thermal
stimulation
Classification
Fatty degeneration - vacuolation of odontoblasts
Fibrous degeneration – increased amount of
fibrous tissue (ageing)
Pulpal calcification – 2 types

17. Pulpal calcifications (types)
Diffuse calcifications
In root canals
Resemble dystrophic calcifications
Usually amorphous, linear, unorganized strands
or columns paralleling blood vessels and nerves
Pulpal stones or denticles
Discrete pulp stones (pulp nodules)
Aetiology
Unknown.
Incidence increases with age
Also in unerupted teeth
Doubtful whether pulpal diseases plays a role.

18. Types of pulpal stones
True pulpal stones
Common
Localized, small (0.5mm) masses of calcified tissue
Resembles dentine
The tubuli are irregular and few in number
Attached denticles are continuous with the dentinal walls
Free denticles lie unattached within pulpal tissue
False pulpal stones
Masses of calcified material containing no dentinal tubule
Consists of concentric layers deposited around a central nidus
of cells
May be free or attached
Often fills large portion of the pulp cavity
Clinical
Doutfull that pulpal stones cause pain
Mechanical obstruction during root canal treatment may be a
problem

19. Resorption of teeth
Physiologic resorption
Roots of primary teeth during shedding/exfoliation
normal
Pathological resorption
All other forms of resorption
External resorption (due to tissue reaction in the
periodontal or pericoronal tissue
i) Periapical inflammation
Aetiology: persistent periapical inflammation
Pathogenesis: osteoclastic reactivation
Radiology
- early: slight raggedness of apex with blunting
- later: severe shortening of the root. Teeth rarely
exfoliate, root canal filling material projects out of
shortened root.

20. ii) Re-implanted teeth
Aetiology
Re-implantation or transplantation is invariably
associated with loss of vitality
Pathogenesis
Osteoclasts
Re-implanted teeth ankylose
Roots are resorped and replaced by bone
In exceptional cases pulpal cavities of re-same as
above implanted teeth develop vascular supply and
may maintain vitality
Radiology-same as above

21. iii) Tumours and cysts
Aetiology
Pressure (benign, slow expansion) or tissue
destruction
Malignant – rapid growth
Pathogenesis
Osteoclasts differentiate from cells in fibrous
capsule btw tumour and tooth
Bengn lesions are more likely to cause tooth
displacement than resorption

22. Iv) Excessive mechanical or occlusal forces
Aetiology
Orthodontics
Tooth loss with increased occlusal forces
Pathogenesis
Activation of osteoclasts resorb bone more readily
than cementum
Small cavities in cementum are usually repaired.
With application of excessive forces, resorption of
teeth may be pronounced
Radiology: Mild shortening of roots, rarely up to
80% of length

23. Impacted teeth
Aetiology
Disruption of reduced enamel epithelium continuity
produces contact between connective tissue and
enamel
Pathogenesis
Pressure. Osteoclast activation
Connective tissue contact with enamel
Radiology
60% of impacted teeth which undergo resorption
are canines
Impacted teeth may cause resorption of adjacent
teeth without being resorbed themselves
Idiopathic
In normal adults with mo obvious cause
Aetiology - ? Endocrine
Radiology: maxillary bicuspids, maxillary and
mandibular incisors.

24. Internal resorption
Aetiology
?hyperplasia of granulation tissue in pulp
Clinical
Pink area on crown
Any single tooth pulp chamber may also be affected
Radiology
Identified on routine radiographs
Difficult to decide whether resorption began externally or
internally when root perforation has occurred
Histology
Osteoclasts in pulpal lacunae resorb intermittently
Pulpal tissue occupies resorbed cavity
Chronic inflammation present
Treatment
Endodontic
After perforation, root extraction

25. Hypercementosis
Deposition of excessive amounts of secondary
cementum on root surface
Involves entire root area or may be focally
Etiology
Accelerated elongation of tooth
Inflammation
Tooth repair
Osteitis deformans
Paget’s disease
idiopathic
Clinical-symptomless
Treatment-nill or treat the underlying
condition