1

Growth Disorders

Dr. Shefali Jaiswal

 Contents
2

 How is a cell formed?

What is growth?
What is differentiation?
What is morphogenesis?
 Growth disorders-
What is growth disorder?
Difference between growth and development.
 Classification – hypertropy, hyperplasia
hypoplasia, atrophy
agenesis
metaplasia
dysplasia
neoplasia
 3

 Growth hormone – hypopituitarism

hyperpituitarism
 Developmental disorder of orofacial structures – clefts
lip disorders
tongue
jaws
teeth
 Public health significance
 Conclusion
 References
 How is a cell formed ?
4

Growth Differentiation Morphogenesis

 Growth and differentiation continues throughout adult

life, as many cells of the body undergo constant cycle of
death , replacement and growth in response to normal or
abnormal stimuli.
 What is growth ?
5

 Growth is the process of increase in size and mass resulting from

the synthesis of specific tissue components.
 The term maybe applied to populations, individuals, organs, cells,
or even sub cellular organelles such as mitochondria.
 Types of growth in a tissue are :
1. Multiplicative
2. Auxetic
3. Accretionary
4. Combined patterns
Multipicative
6

increase in Auxetic
number of
cells by mitotic
cell divison, it results from
present in all increased size Accretionary
tissue in some of individual
stage of cells, mostly
development. incase of increase in Combined
growing intracellular patterns
skeletal tissue
muscles. components
between cells Increase in
as in bone and number of
cartilage. cells, size,
intracellular
tissue
compoments
•7
 What is differentiation
8
 It is the process where a cell develops an overt specialised function

or morphology which distinguishes it from its parent cell.

 Thus, it is the process by which genes are selectively expressed and

gene products act to produce a cell with a specialised function.

 The changes at each stage of differentiation may be minor, it can be

said to have occurred only if there has been overt change in cell
morphology.
9
 What is morphogenesis ?
10

 It is the term used to describe the highly complex process of

development of structural shape and form of organs, limbs,
facial features etc.
 It is complex process of embryological development.

 Involves cell growth and differentiation, and movement of cell

groups.
 Programmed cell death (apoptosis) removes unwanted
features.
 11

GROWTH DISORDERS
 What is growth disorder?
12

 Growth disorders are problems that prevent children from

developing normal height, weight, sexual maturity or other

features.

 Very slow or very fast growth can sometimes signal a gland

problem or disease.

 The pituitary gland makes growth hormone, which stimulates

the growth of bone and other tissues.

Difference between growth and development
13

 Growth - Growth is a positive change in size, and/or maturation,

often over a period of time.
Growth can occur as a stage of maturation or a process toward
fullness or fulfillment.
Eg: growth in height, an organism becoming mature.

 Development - the process of developing or being

developed.
Eg: development of foetus.
14
 GROWTH DISORDERS

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CELLULAR CELLULAR
NEOPLASIA
GROWTH DIFFERENTIATION

• METAPLASIA
INCREASED • CERTAIN
DYSPLASIAS
• HYPERPLASIA
• HYPERTROPY
DECREASED

• AGENESIS
• HYPOPLASIA ACQUIRED

• ATROPHY
HYPERTROPHY HYPERPLASIA

An increase in the size of the

cells, which results in An increase in number of
enlargement of organ without any parenchymal cells, which
changes in the number of cells. results in enlargement of
Occurs due to increased organ/tissue.
functional demand & hormonal
stimulation.

Causes –
Causes –
PHYSIOLOGIC -
PHYSIOLOGIC- enlargement of
uterus in pregnancy Hyperplasia of pregnant uterus
PATHOLOGIC - Hypertrophy of - Regeneration of liver.
cardiac muscle PATHOLOGIC:
smooth muscle Occurs due to excessive stimulation
of hormones & growth factors.
skeletal muscle
Eg: Endometrial hyperplasia
compensatory hypertrophy. following oestrogen excess.
17
HYPOPLASIA ATROPHY

A failure in development of the

normal size of an organ is termed
hypoplasia.
Hypoplasia is therefore the
failure in morphogensis although
closely related to atrophy in
terms of pathogensis
Shrinkage in the size of the cell
by loss of cell substance.
It represents a form of adaptive
response.

Causes –
PHYSIOLOGIC:
Causes – Normal process of aging in some tissues,
which could be due to endocrine stimulation
Cerebellum caused by mutation in & arteriosclerosis.
the Reelin gene Eg: Atrophy of lymphoid tissue.
Tooth - Turner's hypoplasia PATHOLOGIC:
Starvation atrophy- carbohydrate/fat
Mandible in congenital Ischemic atrophy- atrophic kidney
hypothyroidism
Disuse atrophy- atrophy of pancrease
Optic nerve in optic nerve Neuropathic atrophy- poliomyelitis
hypoplasia Endocrine atrophy- hypopituitarism
Pressure atrophy- erosion of spine
Idiopathic atrophy- testicular atrophy
19

HYPOPLASIA
AGENESIS

The failure of an organ to develop

during embryonic growth and development due to the
absence of primordial tissue.

Causes –
Agenesis of the corpus callosum
Renal agenesis
Phocomelia
Penile agenesis
Müllerian agenesis
Agenesis of the gallbladder
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 METAPLASIA

 META-Transformation

 PLASIA-Growth

 It is a reversible change of one type of epithelial or mesenchymal

cells, usually in response to persistant abnormal stimulus which

in turn may change into a malignant cell.
 CLASSIFICATION
METAPLASIA

EPITHELIAL MESENCHYMAL
METAPLASIA METAPLASIA

Squamous metaplasia Columnar metaplasia

Eg: respiratory epithelium Osseous metaplasia
Eg: Intestinal metaplasia
of chronic smokers, in healed chronic gastric Cartilaginous
vitamin A deficiency. ulcer metaplasia
 EPITHELIAL METAPLASIA

 The most common type.

Metaplastic change can either be patchy or diffuse

Leads to alterations in the epithelium.

Deprivation of protective mucous secretion.

More prone to infection.

 MESENCHYMAL METAPLASIA
 Less often there is transformation of one type of

mesenchymal tissue to another.

 OSSEOUS - Formation of bone in fibrous tissue, cartilage

& myxoid tissue.

Eg: In arterial wall in old people.

 CARTILAGENOUS - In healing of fractures, where there

is undue mobility.
 DYSPLASIA

 Disordered cellular development often accompanied with

metaplasia & hyperplasia (ATYPICAL HYPERPLASIA).

 Occurs most often in epithelial cells, which is characterised

by cellular proliferation & cytologic changes.

CAUSES CHANGES

-Increased number of
-Occurs due to chronic layers of epithelial cells.
irritation or prolonged -Disorderly arranged
inflammation. cells.
-Loss of basal polarity.
-On removal of stimulus, -Cellular & nuclear
the changes may pleomorphism.
disappear. -Increased
nucleocytoplasmic ratio.
-In majority of cases -Nuclear
dysplasia progresses into hyperchromatism.
carcinoma in situ or -Increased mitotic
invasive cancer. activity.
 NEOPLASIA
28

 The word neoplasia means new growth

 The term tumour is often used to denote a neoplasm although a

tumour was originally defined as a swelling associated with

inflammation which is less precise.
 29

 Neoplasia is characterised by abnormal, uncoordinated and

excessive cell growth.

 Persists after initiating stimulus has been withdrawn.

 Associated with genetic alterations.

 Neoplastic cells influence behaviour of normal cells by the

production of hormones and growth factors.

 NEOPLASMS
30

 A neoplasm is an abnormal mass of tissue, the growth of which

exceeds and is uncoordinated with that of normal tissue and

persist in the same excessive manner after cessation of the stimuli
which evoke the change. (Willis)
 CLASSIFICATION
31

 According to –

1. Region or organ involved and the gross appearance.

eg: bone tumor and brain tumor

2. Histogenesis – eg: epithelial tumor and connective tissue tumor

3. Histological – well and poorly differentiated or anaplastic tumor.

4. Behaviour – bengin and malignant

 32

 Neoplasms results from uncontrolled growth and often disordered

differentiation which is excessive and purposeless.

 The growth of neoplasm continues in an autonomus manner and

in the absence of normal stimuli.

 Many neoplasms cease to proliferate only on the death of the

patient as there is no oxygen and nutritents.

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 Causes
34

 The causes of neoplasia are complex.

 The risk of an animal developing a tumour is often related to a

combination of events:

 Exposure to a carcinogen.
 A carcinogen is any agent causing normal cells to become neoplastic.

 Environmental co-carcinogens;

 Predisposing host factors.

 35

 In few cases there is a known aetiological agent.

eg: the Feline Leukaemia virus.

 In the majority of neoplasias the cause is unknown or only

partially explained.

 They appear to be extrinsic and intrinsic causal factors involved.

Extrinsic Causes Intrinsic Causes
36
-Diet
Excess fat.
-Physical agents Cell changes or modulate organ
susceptibility.
UV light Eg: Aflatoxin in pigs/mice.
Ionising radiation -Hormones
-Tumour viruses prolonged hormonal stimulation of a tissue.
DNA viruses Eg: the mammary gland, uterus and testes.
RNA viruses -Genetic
Eg:Lymphoma clusters in dogs, pigs and
-Chemical carcinogens cattle.
Aromatic hydrocarbons -Age
Nitrosamines Common in old-age.
Duration of exposure to a carcinogen.
Changes in the tissues, promoting abnormal
cells to grow.
Chromosomal deletions.
 Growth of Tumours
37

 There are several features and factors associated with growth of

primary tumours:

 Mode of growth

 Rate of growth

 Degree of differentiation

 Vascularity
 Mode of Growth
38

 Benign tumours

 Remain localised
 Grow by expansion into available space or by compression of
tissues.
 Cause adverse effects if near vital structures.
 Malignant tumours

 Do not remain localised

 Local growth is by infiltration and super-population of adjacent
tissues.
 Invasion causes destruction of local normal tissue.
 Rate of Growth
39

 Rate of growth is based on:

 Proportion of cells in cell cycle in comparison to those that have

differentiated and entered G0.

 Death rate of cells in the tumour.

 Where proliferation exceeds cell death then the primary tumour

increases rapidly in size.

 A high rate of apoptosis is often seen in tumours.

 This is often independent of tumour blood supply.

 40

 Adequacy of supply of oxygen and nutrients to tumour cells.

 This often depends on the neoplastic cells inducing a

supporting stroma, containing capillaries, in and around
the tumour.

 Doubling time of tumours is an important measure.

 30 doubling cycles can yield 109 cells i.e. 1g of tissue.

 Degree of Differentiation
41

 Benign tumours are usually well-differentiated; malignant ones

are not.

 Degree of differentiation is inversely proportional to growth.

 Well-differentiated tumours induce adequate supporting stroma

which supports tumour cell growth.

 Malignant tumours often outgrow stromal development and

consequently necrose.
 Vascularity
42

 Secretion of angiogenesis factors allow tumours to develop a

vascular stromal support.
 These angiogenesis factors are often growth factors.
 E.g. fibroblast growth factor (FGF).

 Failure to maintain adequate oxygen and nutrient supply results

in either
 Necrosis, or
 Slower degeneration with dystrophic calcification
Growth Hormone
 Growth hormone (somatotropic hormone or somatotropin) is a

small protein molecule that contains 191 amino acids in a single

chain and has a molecular weight of 22,000.

 It causes growth of almost all tissues of the body that are capable

of growing.

 It promotes increased sizes of the cells and increased mitosis,

with development of greater numbers of cells and specific

differentiation of cells such as bone growth cells and early muscle
cells.
IMPORTANCE OF GROWTH HORMONE -
(1) increased rate of protein synthesis in most cells of the body;
(2) increased mobilization of fatty acids from adipose tissue,
increased free fatty acids in the blood, and increased use of fatty
acids for energy;
(3) decreased rate of glucose utilization throughout the body.

 growth hormone enhances body protein, uses up fat stores, and

conserves carbohydrates.
 Hypopituitarism/Pituitary Dwarfism
46

 Results due to reduced secretion of pituitary hormone that occurs due to

pituitary adenoma which compresses the pituitary gland.
 Total absence of all pituitary secretions is known as
Panhypopituitarism.
 Clinical features-

Short stature of individual,

Hypocalcemia,
Males – loss of libido, females - amenorrhea
Delay in maturation of the skeleton
Skull and facial bones are small
 47

 Oral manifestations-

o Failure in development of maxilla and mandible leading to severe

malocclusion.

o Lack of condylar growth and short ramus

o Tooth eruption is delayed and so is shedding of deciduous teeth.

 Hyperpituitarism
49

 Results from hyperfunction of anterior lobe of pituitary gland.

 Types –

Gigantism – increase in levels before the epiphysis of the

long bones are closed.

Acromegaly – increase occurs later in life after epiphysis

closure.
 50

Gigantism – generalized overgrowth of tissue in childhood.

 Underdeveloped genitals.

 Increase in size of calvarium.

Acromegaly – hands and legs become large, with clubbing of the

toes and fingers.
 Bone overgrowth and thickening of the soft tissue cause coarse
facial appearance.
 51

Oral manifestations-

 Increased tooth size

 Mandibular condyle is prominent

 Palatal vault is flattened

 Prognathism

 Macroglossia

 Lips are thick

Developmental disorders of
orofacial structures
 55

 A developmental defect characterized by the failure of fusion of

facial processes.

• 6 th and 7th week - upper lip

• 8 th week - palate (Anterior to posterior)

• Maxillary process - cleft palate

Orofacial Clefts
 Etiology

 Genetic abnormalities

 Inherited

 Spontaneous mutation

 Environmental factors

 Nutritional Deficiency

 Cigarette smoking

 Drugs, radiation

 Amniotic bands
 Cleft Lip and Palate

 Most common among the facial clefts.

 Cleft is a division or separation of parts of the lip or palate that is

formed during the early months of development of the foetus.

 Clefts may be unilateral or bilateral.

 They can vary in severity.

 3-8% of clefts are associated with syndromes

Unilateral incomplete cleft lip
Bilateral Complete Cleft Lip
 Frequency of occurrence

 Isolated Cleft Lip : 25%

 Isolated Cleft Palate : 30%
 Cleft Lip + Cleft Palate : 45%

 CL ± CP : more common in males.

 For isolated CL , M : F = 1.5 : 1

 For CL + CP, M : F = 2 : 1

 Isolated CP is more common in females.

 Location

 Cleft Lip is more commonly unilateral (80%)

 70% of cleft lips on left side.

 Complete Cleft lip extends upward into nostril.

 Cleft palate may involve hard and soft palate or soft palate alone.

 Cleft or Bifid Uvula is more common.

Complete cleft palate
Bifid uvula
Submucous palatal cleft
 Pierre Robin Syndrome

Triad of :
 Mandibular micrognathia
 Glossoptosis
 Cleft Palate.
 Problems associated with clefts

 Esthetic disfigurement

 Difficulty in breathing ,feeding and speech

 Malocclusion.

 Psychosocial problems.

 Recurrent upper respiratory tract infections.

 Developmental disorders of Lips

 Lip Pits:

Para median Lip Pits

Commissural Lip Pits

 Double Lip
Paramedian
Lip Pits
• Rare
• Autosomal dominant inheritance
• Persistence of lateral sulci on embryonic
mandibular arch
• Bilateral symmetric fistulas on either side
of the midline
• Appearance varies from subtle
depressions to prominent humps.
• Pits can extend to a depth of 1.5 cm and
may express salivary secretions
• Seen in Van der Woude syndrome with
CL±CP
• Surgical excision for cosmetic reasons
Commissural Lip
Pit
• Small mucosal invaginations at corners of the
mouth on vermilion border.
• Failure in the normal fusion of maxillary and
mandibular processes during development
• Seen in 12-20 % of adult population.
• Males > Females
• Unilateral / Bilateral
• May be associated with preauricular pits
• No treatment required

70
Double Lip
 Rare
 Redundant fold of tissue on
the mucosal side of the lip.
 May be Congenital or
acquired( from trauma or
oral habits such as lip
sucking)
 More common in upper lip
 Sometimes both lips affected
 Seen on smiling.
 Feature of Ascher’s
syndrome
 Ascher’s syndrome

Triad of :

 Double lip

 Blepharochalasis

 Nontoxic enlargement of thyroid gland

 73

Developmental disorders of tongue

 Macroglossia
 Microglossia
 Ankyloglossia
 Lingual Thyroid
 Median Rhomboid glossitis
 Benign Migratory glossitis
 Hairy Tongue
 Bifid tongue
 Fissured tongue
 Lingual Varices
Macroglossia

 Congenital:
• Haemangioma
• Lymphangioma
• Cretinism
• Down syndrome
• Beckwith Weidemann
Syndrome
• Neurofibromatosis
• Hemi hyperplasia
 Causes

 Acquired:
• Amyloidosis
• Myxoedema
• Acromegaly
• Angioedema
• Carcinoma and other tumours
• Edentulous state
Microglossia

 Oromandibular- limb hypogenisis syndrome

 Frequently Seen along with hypoplasia of mandible
Ankyloglossia

 Anomaly characterized by
short thick lingual frenum
resulting in restriction in
tongue movement.

 Severe case tongue fused to

floor of mouth

 Frenum some time attached

to tip of the tongue

 Ankyloglossia

 Seen in 2-5 % of the

population

 Males > Females

 May be partial or complete

 May cause speech defects.

 Surgery if the anomaly is

severe
Lingual Thyroid-origin

 Failure of primitive thyroid

gland to descend into the

neck during development.

 About 10 % of both men and

women may show thyroid

tissue if biopsy is taken from
posterior part of tongue.
Lingual Thyroid-Clinical features

 Symptomatic and clinically

evident lingual thyroid seen

less commonly.

 4 - 7 times more common in

females

 May cause dyspnoea,

dysphonia, dysphagia
Median Rhomboid glossitis
Benign Migratory glossitis
 Hairy Tongue

 Accumulation of keratin on the filiform papillae may be

due to increased production of keratin or decrease in the
normal keratin desquamation
 Fissured Tongue

 Multiple grooves and furrows on the surface of the tongue

 Strong association noted between geographic tongue
 Seen some time in Melkersson Rosenthal syndrome
Lingual Varices

 Abnormally dilated and

tortuous veins

 Seen in 2/3rds of people

older than 60 years of

age(indicating age related
degeneration )

 Asymptomatic
 Developmental disorders of the jaws

 Exostoses and Tori

 Hemifacial atrophy

 Hemifacial hypertrophy

 Condylar hypertrophy

 Coronoid hypertrophy

 Mandibular aplasia
Mandibular Torus
Palatine Torus
Hemifacial Atrophy
Hemifacial hypertrophy
Condylar hypertrophy
Coronoid hypertrophy
Mandibular aplasia
Developmental Anomalies of Teeth
Development of teeth
96
Developmental Anomalies:- are the malformation or defects resulting
from disturbance of growth & developmental anomalies.

a)Congenital anomalies:- present at birth or during intra

uterine life

b)Hereditary anomalies:- inherited from the parents to

the offspring

c)Acquired anomalies:- due to some pathological

environment condition

d)Hamartomatous:- Hamartamatous change in tissue

e)Idiopathic anomalies:- Unknown etiology

 Developmental disturbance in the
number of teeth:
I. Anodontia:
It is the congenital absence of teeth in oral cavity
Classification/types:
i. Complete/ Total anodontia
ii. Partial anodontia
- Hypodontia
- Oligodontia
iii. Pseudo anodontia
iv. False anodontia
 True Anodontia Hypodontia Oligodontia

Definition • congenital • absence of one or • lack of development

absence of all few teeth of six or more teeth
teeth in oral
cavity
Etiology • Hereditary • Hereditary • Hereditary
• Ricket or Syphilis, • Associated with
• German measles Rieger’s syndrome,
during pregnancy Chondroectodermal
Radiation dysplasia
overdose • High dose radiation

Clinical features • Associated with • females > male • Rare in primary

Hereditary • Rare in deciduous dentition
Ectodermal dentition (<1%) • Multiple missing
Dysplasia • drifting teeth
• Involve both • drifting
dentition

Treatment • Prosthetic • Prosthetic & • Prosthetic &

rehabilitation orthodontic orthodontic
rehabilitation rehabilitation.
 Hyperdontia/ Supernumerary
(according to location)
MESIODENS PARAMOLAR DISTOMOLAR

• located at or near the • supernumerary molar, • located distal to third

midline
• usually small and molar
• may occur singly or rudimentary • teeth are smaller than
paired, erupted or
impacted or even • situated buccally or normal second and third
inverted lingually to one of the molar

• a small tooth with cone maxillary molars or • crown morphology is

shaped crown and short interproximally highly abnormal.
root

• cause retarded eruption,

displacement or
resorption of adjacent
 According to shape
CONICAL SUPPLEMENTAL TUBERCULATE

• small peg-shaped conical • duplication of teeth in • Possesses more than one

tooth and is most the normal series & is cusp or tubercle

common type found at the end of tooth • described as barrel-

• usually present as series shaped.

mesiodens . • common in primary

dentition.
 Odontome
 abnormal proliferation of cells of the enamel organ result in an
odontogenic tumor, commonly referred to as an odontoma.

 form as a result of continued budding of the primary or permanent

tooth germ in which case an odontoma replaces the normal tooth.

Etiology:-
 seen in association with cleft lip & palate , cleidocranial dysplasia
& Gardner syndrome
 develop as a consequence of proliferation of epithelial cells from
dental lamina
Clinical features:
 Prevalence: 1-3%
 male=female (in primary dentition)
but male >female (in permanent dentition
 cause of crowding type of malocclusion
 directly or indirectly responsible for increased caries incidence &
periodontal problems
 Dentigerous cyst may sometimes develop from an impacted
supernumerary tooth
 Developmental disturbance in size
of teeth:
The size of teeth depends upon both proliferative and secretary
activities of the cell.
Variation in the size of teeth are as a result of factors affecting the
growth of tooth germ at cap and bell stage.

Types:
i. Microdontia

ii. Macrodontia
 MICRODONTIA MACRODONTIA

TYPES True generalized: True generalized

occurs in pituitary all the teeth are larger than
dwarfism, Down's normal
syndrome and congenital associated with pituitary
heart disease. gigantism
Relative generalized:
are present in jaws that are Relative generalized:
somewhat larger than teeth are normal or slightly
normal. larger than normal
exhibits spacing between but present in smaller jaw
the teeth.
Localized: Localized: one or more
involves only single tooth large teeth exist
occurs with congenital
heart diseases,
Down's syndrome and
progeria.
TREATMENT Crown & bridge prosthetic Orthodontic Rehabilitation
can be provided for esthetic
rehabilitation of such teeth.
 Developmental disturbance in Shape
of teeth
 Gemination
 Fusion
 Concrescence
 Dilaceration
 Taurodontism
 Dens-in-dente (Dens Invaginatus)
 Dens Evaginatus
 Talon cusp
 Supernumerary roots:
 Gemination Fusion

Definition • Counting the bifid crown as • Incomplete attempt of two tooth buds to
one tooth, normal no of teeth fuse into one
are present & anomalous
tooth has only one root canal

Etiology • tooth bud divides • Pressure produced by physical force

results in formation of tooth Hereditary tendency
with bifid crown &
• common root and root canal.

Clinical • normal no. of teeth present • two crowns joined by enamel or dentin
features • tooth has two crown one root • complete/ incomplete

Clinical • Spacing or diastema

complicatio • Crowding of teeth
n • Esthetic problems
• Periodontal complication
Treatment • Crown and bridge • Surgical division
• Crowns or bridges fabrication for esthetic
purpose
 Concresence Dilaceration

Definition Union of two or more adjoining teeth by abnormal angulation or bend

cementum alone without in the root or less frequently
confluence of dentin the crown of a tooth.

Etiology •Traumatic injury • Trauma to calcified

•Crowding of the teeth portion
•Hypercementosis associated with Chronic • Secondary to an adjacent
inflammation cyst, tumor, or
odontogenic hamartoma.

Clinical features • Not much significant clinically •Maxillary lateral incisor

Radiograph needed for diagnosis mostly affected
angulation may be present
anywhere
Clinical • Radiograph before extraction • care should be taken
significance attempted extraction may cause removal during extraction of such
of 2 teeth teeth

Treatment • No treatment if patient is •Small deviation no

asymptomatic treatment
Extraction if interferes with eruption of •Larger deviation may need
succeeding tooth hemisection or extraction
 Taurodontism Talons Cusp

Definition • Abnormally large crown in • cusp like structure

expense of root projecting from the
cingulum area or
cementoenamel junction of
anterior teeth
Etiology • Heriditary , Error in • outward folding of inner
enamel epithelial cells
Hertwig’s epithelial root • Ass. With Rubunstein-
sheath Taybi Syndrome

Type • Hypotaurodontism
• Mesotaurodontism
• Hypertaurodontism
Clinical Features • Commanly affects • Commanly affect max.
permanent molars lateral incisors
• unilateral/bilateral • Pulp horn may project
from the cusp
Radiographic features • pulp chamber is large
• Lacking cervical
constricton
• Furcation more apically
Treatment • No special treatmnet • Sealant application in the
 Dens in Dente
(Dens invaginatus)
Definition an invagination in the surface of crown
before calcification
Etiology • increased localized external
pressure, focal growth retardation &
focal growth stimulation of the
tooth bud
Clinical Feature • max. parmanent lateral incisor mostly
affected
Types:
i.Coronal: invagination in coronal portion
ii. Radicular: invagination on the root
portion
Depending upon the extent to the
invagination towards the pulp:
-Mild: confined to crown
-Intermediate: below CEJ (tooth within
tooth)
-Extreme: Extend till root
Known as “dilated odontomes”
Dens Evaginatus
(Occlusal enamel pearl)
Appears clinically as an
accessory cusp or globules of
enamel on occlusal surface,
between buccal and lingual
cusps of premolar
• Proliferation &
envagination of an area of
inner enamel epithelium
• premolar and molar teeth
• consists of all three dental
tissues, i.e. enamel,
dentine and cementum
• appears as a tubercle of
enamel on occlusal surface
of the affected tooth.
 Dens in Dente
Clinical significance • vulnerable to caries soon
after the tooth erupts
• may develop pulpitis, pulp
necrosis, periapical cysts
or abscesses etc.
Radiographic feature • Pear shaped invagination of •
enamel and dentin
Treatment • Early detection &
restoration.
• Endodontic treatment
Extraction if severely
involved
Dens Evaginatus
• Displacement of teeth
with pulp exposure and
subsequent infection
may present, following
occlusal wear or fracture.
Tuberculated appearance
of occlusal surface.
• No treatment unless
symptomatic.
• minor occlusal reduction
• Endodontic treatment if
pulp exposed
 Supernumerary roots ( Radix
entomolaris)
 Development of increased number of roots compared to normal.

Clinical features:-

 Common in permanent dentition

 Commonly affects molars particularly 3rd molars

 Appears as slender outgrowths at the center of furcation area of molar

teeth.
Clinical significance:-

 During endodontic therapy due consideration has to be given to the

presence of such tooth

 During extraction if one of these roots may be broken off & if

unrecognized & allowed to remain in the alveolus, may be the

source of future infection.
 Developmental Disturbances In
Structure of teeth:

I. Amelogenesis Imperfecta

II. Dentinogenesis Imperfecta

 I. Amelogenesis imperfecta -
Amelogenesis imperfecta is a group of hereditary disorders characterized by
alteration of the quantity and quality of enamel in humans and is frequently
associated with a significant dental disease .

Classification of Amelogenesis Imperfecta According to Witkop (1989)

TYPE I
Hypoplastic
IA Hypoplastic, pitted autosomal dominant
IB Hypoplastic , local autosomal dominant
IC Hypoplastic, local autosomal recessive

ID Hypoplastic, smooth, autosomal dominant

IE Hypoplastic, smooth X-linked dominant

IF Hypoplastic, rough autosomal dominant

IG enamel agenesis, autosomal resessive

Type II Hypomaturation

IIA Hypomaturation,pigmented autosomal recessive

IIB Hypomaturation, X-linked recessive

IIC Snow-capped teeth, autosomal dominant

TypeIII Hypocalcified

IIIA Autosomal dominant

IIIB recessive
Type IV Hypomaturation- hypoplastic with taurodontism

IVA Hypomaturation – hypoplastic with

taurodontism, autosomal dominant

IVB Hypoplastic- hypomaturation with

taurodontism, autosomal dominant
Clinical features:

i. Hypoplastic:

ii. Hypomaturation:
iii. Hypoclacified:

iv. Hypomaturation hypoplastic

with taurodontism:
 II. Dentinogenesis Imperfecta

Dentinogenesis Imperfecta is a hereditary developmental

disturbance of the dentin that may be seen alone or in conjunction
with the systemic hereditary disorder of the bone, osteogenesis
imperfecta.

Classification
1. Dentinogenesis imperfecta 1
2. Dentinogenesis imperfecta 2
i. Dentinogenesis imperfect 1:
(dentinogenesis imperfecta without osteogenensis imperfect)
Etiology: mutation in DSPP gene encoding dentin phosphoprotein
and dentin sialoprotein

ii. Dentinogenesis imperfecta 2:

(Shields type III, Brandywine type dentinogenesis imperfect)
The crown of deciduous and permanent teeth wear rapidly after
eruption and multiple root exposure may occur.
 Dentin is amber and smooth.
 Dentin dysplasia

 Dentin dysplasia is an autosomal dominant inherited disorder

characterised by defective dentin formation and abnormal pulpal
morphology. The condition is also known as root-less teeth.

 Types
-Type I
Radicular dentin dysplasia.
-Type II
Coronal dentin dysplasia.
 Type I :Radicular dentine dysplasia

 In Type I , the roots of teeth

are shorter than normal and the
affected teeth often exhibit severe
mobility and they may exfoliate prematurely.

 Radiographic Features:
Type 1 : Roots are short, blunt and conical
In deciduous teeth, pulp chambers
and root canals are completely obliterated
in permanent they may be crescent shaped.
 Type II : Coronal dentin displasia
 In Type II , the deciduous dentition exhibit an “amber- grey”
color with some translucent or opalescent appearance.
 Radiographic Features:
 Type II: The pulp chamber of the deciduous teeth becomes
obliterated. While in permanent teeth, large pulp chamber is
seen in coronal portion. Pulp stones may be found.
 Regional odontodysplasia
(ghost teeth)
Localized disorder of the tissue of dental origin resulting in
characteristically bizarre clinical and radiographic appearances.

Etiology
 A somatic mutation affecting dental lamina in the area
 activation of latent viruses
 local circulatory disorders
 Pharmacotherapy during pregnancy
 Neural disorder
 Rh incompatibility or failure of migration and differentiation of
neural crest cells
Clinical features
 Typically yellow discoloured.
 Enamel and dentin soft on probing.
 Rough surface texture.
 Permanent anterior commonly affected.
 predominant in maxilla.
 Drifting and over eruption of
 adjacent or opposing teeth.
 PUBLIC HEALTH SIGNIFICANCE
126

 Every year, close to 35,000 babies are born with cleft lips or
palates in India.
 There are over 10 lakh cases untreated.
 More than half do not receive any treatment because they do not
know a cleft can be fully corrected.
 Widespread superstition along with social taboos complex the
problem.
 92% of patients' families cannot afford the cost of surgery.
 30% of them are not aware that the condition can be corrected.
 5% are afraid of surgery.
 127

 Smile train and the Trinity care foundation with National Health
Mission and Government of Karnataka for the treatment of clefts.
 CONCLUSION
128

 The way growth disorders are viewed and managed in different cultures
varies widely.
 They are complex conditions and even well-educated people find them
difficult to understand, but when families are very poor and lacking in
basic education, and health system is starved of resources, traditional
beliefs, folk remedies and prejudice combine to make the lives of
children and adults difficult .
 Disorders have excellent outcome if, diagnosed as early as possible and
surgical repair is carried out.
 Documentation of disorders at hospitals, schools and camps should be
given priority.
 Research on genetics and advance treatment methods should inspire
dental professional to ascertain this relationship.
 REFERENCES
129

 Shafer’s textbook of oral pathology 6th edition. R Rajendran, B

Shivapathasundaram.
 Shobha Tandon. Textbook of pedodontics. 2nd edition.
 Textbook of oral medicine and radiology. Ghom.
 Robins and Cotran. Pathologic basics of diseases. 8th edition
 Harsh Mohan. Textbook of pathology. 3rd edition.
 Mc Gee, Isaacson and Wright. Oxford textbook of pathology.
Principles of pathology volume-1.
 Anderson’s pathology 10th edition.
 Y. Bhende’s. general pathology. 5th edition.
 130

 Robert britton’s. General and systematic pathology edited by

J.C.E. Underwood.
 Daniel M. Laskin. Oral and maxillofacial surgery. Volume-1.
 Contemporary oral and maxillofacial surgery. James R. Hupp,
Edward Ellis, Myron R. Tucker.
 http://www.virtualmedstudent.com
 http://www.emsa.ca.gov
 http://em.wikipedia.org
131
132
Difference between disorder and disease
133

 Disorder - a functional abnormality or disturbance.

Eg: genetic disorder - Huntington's disease

 Disease - a particular abnormal condition, a disorder of a

structure or function, that affects part or all of an organism. It is
associated with specific symptoms and signs.
Eg: chronic diseases - tuberculosis