AGE CHANGES IN ORAL TISSUES

Contents:
1. Introduction
2. age changes in tooth
- Enamel
- Dentin
- Pulp
3. Age changes in supporting tissues
- Cementum
- Periodontal Ligament
- Alveolar bone -- Maxilla and Mandible
4. Age changes in Oral mucous membrane
5. Age changes in Salivary glands
6. Age changes in Temporo mandible joint
7. Conclusion
8. Bibliography

As we get older, we all notice the effects of aging-wrinkles, graying hair & variety
of aches & pains that we didn’t have before. Our mouth is also affected by advancing
age understanding these changes are important to maintain good oral health.

INTRODUCTION:
 Aging also known as gerontology
 Aging is the time period between the birth of life and death of any living
animals and species including modern man.
 It is measured in terms of days, month, and years .
 With advancing age certain biological changes occur in the living tissues.
These changes are referred as age changes in the aging process.

General effects of aging:

  Tissue Desiccation
 Reduced elasticity
 Diminished Reparative capacity
 Altered cell permeability
 In the skin,
- Dermis and epidermis are thinned
- Keratinization and diminished
● Blood supply is decreased
● The nerve ending show degeneration
● Capillaries appear to be more fragile with age
● Bone undergoes osteoporosis with aging
- It is rarified
- Trabecular are reduced in number
- Cortical plates are thinned
- Vascularity is reduced
- Increased susceptibility to fracture
● malfunctioning of neuro endocrine system
● Decline in efficiency of the immune host defence system

It is widely accepted that the process of aging cannot be traced to a single

cause, a number of theories have been proposed to explain the changes observed
during aging.

Theories of age changes:

● Recently several current aging theories and there inter relationship were
reviewed.
● The theories can be grouped into four types
1. Biologic clock (programmed) type
2. Immunologic
3. DNA damage related
4. Aging related to damage of other cellular components[OCC]
 I. The clinker theory
 It is related to OCC damage
 It considers the pigments example lipofusin and ceriod accumulate with aging
 These inert substances accumulate in the non dividing cells of the heart, brain,
nerves and few other organs
 These substances interfere with the activity of involved cells
II. The falling domino theory:
 It is related to OCC damage
 It states that certain toxic substances accumulate in cells
 When one structure within a cell becomes inhibited or falls the other structures
inside the cell tend to become inhibited
 With each progressive fall the cells ability to function normally is weekend
 As aging the amount of inhibitory substances within the cells and in the inter
cellular space increases.
 Inhibited protein synthesis during aging causes gradual decline of all metabolic
and biosynthetic process.
IIII Thermal denaturation:
 It is an OCC damage theory.
 It states that low thermal denaturation immobilizes proteins. This in turn
result in disruptions and eventually death of the involved cells
IV Cellular loss theory:
 It involves DNA and OCC damage
 It considers that cell loss is one of the fundamental causes of human aging
 Dividing cells found in the skin. Mucous membranes and GIT lining have a
potential to divide 50 times and then die.
 Partially dividing cells found in the liver and kidney have the capacity to
divide in advanced age.
 Non dividing cells. Erythrocytes neurons. Cardiac and skeletal muscle are
usually lost by 75 years of age
 The cells are replaced by extra cellular fluid and CT.
  The loss of the cell can result in decreased function and shrinkage of the
involved structure .
V The enzyme/hormonal/ glycoprotein theory
 It involves OCC – damage and biologic clock components
 It considers that aging due to the reduced enzyme , hormonal and glycoprotein
activity
 Most f the deed enzyme and coenzyme activity occurs within mitochondria.
 It contrast lysosomal activity with its destructive lose of hydrolytic enzymes,
increases with aging.
 Many hormones have decrease production and efficiency with aging.
 P-glycoprotein removes toxins within cells. With aging formation of P-
glycoprotein and decreased e leads to cellular death.
VI The genetic time table/ecologic evolutionary theory:
 It states that for each species, a specific genetically determine maximum life
span exists .
 There is definite time course and direction of the alteration in the various part
of the person
 The sum total iof these changes result in the failure of the person to withstand
both external and internal stresses and death occurs
VII DNA deterioration
 It is a major DNA damage theory also includes OCC damage , immunologic
and biologic clock aspects
 One possible cause for agoing is that a cell multiplies a certain number of
times and then dies because its DNA has deteriorated
 Another poissibility is that after a given period of times the cells of DNA
repair mechanisms no longer function efgfectively
 With aging there are more DNA strand breaks.
- A decrease in DNA supercoiling
- A steady loss of methylation of DNA basis
- An increase of migratory DNA
 - A dramatic ↑ in sister chronmatin exchange
- Deterioration of the chromatin that prevents the repair enzymes from
reaching the damaged lesion.
VIII The error theory
 It has DNA – and OCC damage and biologic –clock components.
 The abnormal protein formation could be a basic cause of aging
 Error in protein formation may occur due to errors in DNA, messenger RNA ,
transfer RNA, Ribosomal RNA, or other aspects of protein formation.
IX Somatic mutation theory:
 It is a basic DNA-damage theory.
 It considers that somatic cells gradually accumulate defective genes by mutation
which causes decrease in cell function.
 If structures of older persons contain number cells containing mutations. They
function less efficiently than normal.
 When the somatic cells accumulate a specific number of mutations, senescence
and death should follow.
X The radiation theory:
 It has DNA- and OCC damage components.
 It considers that aging is caused by harmful ionizing radiation from outer
space, rocks and soil.
 Ionizing radiation produces several changes that are comparable to normal
aging.
XI The Immunologic theory:
 It has biologic - clock as well as immunologic components.
 It states that aging is caused by a progressive breakdown in the body’s
immunologic system that produces antibodies and lymphokines.
 The theory assumes that with aging the immunologic system becomes less
capable of distinguishing normal proteins from foreign proteins and therefore
normal beneficial proteins are destroyed.
 The protective antibodies and T-Lymphocytes become less and lead to infectious
and malignant diseases.
XII The nutritional theory:
 It is an OCC damage theory.
 It considers that aging can result from the buildup of nutrient metal minerals such
as copper, iron, manganese, zinc and calcium as well as toxic metals such as lead,
aluminium, cadmium, tin and titanium.
 It also considers that intake of polyunsaturated and saturated fatty acids
p0romotes aging because of lipid per oxidation and dev of obesity.
XIII The macrophage theory:
 It is an OCC damage theory.
 Metchnkoff believed that aging was related increased activity of macrophages in
the colon.
 This theory is related to the ‘waste product theory’, which stated that aging related
from the accumulation of non excreted wastes.
XIV The watch spring theory
 It is a biologic clock theory.
 It states that the human body is like a watch spring, gradually ceases to function
because its stored energy runs out.
XV The wear and tear theory
 It is a combination of DNA and OCC – damage theory.
 It is based on the finding that all inanimate objects wear out.
 It states that aging is caused by some kind of wear or damage to the various body
components either by the use of the parts (wear-tear) or by injuries to the genetic
or protein forming mechanisms.
 The injuries can occur from physical stressors such as heat, light, oxidation,
radiation, chemicals, drugs, pollutants, trauma, pressure, infection, diet and noise.
XVI The hypoxia theory:
 It states that aging is mainly the result of lowered oxygen tension in critical areas
of the body such as brain.
  The decline in oxygen tension could relate to genetic factors, environmental
traumas or both that could impair circulation and reduce oxygen flow.
XVII Stress Theory of aging:
 It is a major OCC damage theory.
 It states that stress per sec causes aging.
 The concept is that an accumulation of environmental stressors can accelerate
aging result in death.
 Evidence shows that accumulation of lipofuscin pigments in neurons is
accelerated by stress.
XVIII The cross linkage theory:
 It is major DNA and OCC damage theory.
 The chain of events starts with formation of cross linkages in proteins and nucleic
acids.
 According to this theory, with aging an increased accumulation of cross linkage
agents occur.
 The cross linking agents include glyceraldehydes, acetaldehyde, formalaldehyde,
monoldehyde, pyruvic acid, citric acid, succinic acid, lead, calcium, zinc,
aluminium, copper etc form the cross linking products.
 The concept of this theory might be the accumulation of cross-linked collagen
reduces the diameter of blood vessels which inturn impairs circulation and
eventually results in cell death.
XIX The free-radical theory:
 It is a DNA damage, OCC damage, immunologic factors and biologic-clock
mechanisms.
 The free-radical theory is steadily gaining acceptance.
 It gave tha possible explanation of primary chemical reactions involved in aging.
 Free-radicals have been called the “great white sharks of the biochemical sea of
life”.
 If they are unchecked, free-radicals can continue to create other free-radicals
from normal molecules thereby disrupting vital functions.
  In this way free-radicals can cause serious effects to cellular metabolism as a
consequence of damage to DNA, RNA, enzymes, Lipids, immune cells and cell
membranes.
 Free –radicals can propagate through hundreds of thousands of molecules and
wreak havoc before they can create another free-radical.
 Free-radicals are usually produced as unwarranted by-products of normal oxygen
metabolism and lipid per oxidation of polyunsaturated fatty acids.
 Examples of free-radicals include:
1. Hydroxyl that is produced by radiation and can be involved
in arthritis.
2. Super oxide which reacts with h2o2 to form hydroxyl radicals
and damage DNA, destroy cells inactivate enzymes.
3. Peroxides which are involved in lipid per oxidation and can
activate formation of aging pigments.
4. Hypo chloride and Alkoxyl.
Erosion:
 Chemo mechanical wearing away of tooth structures.
 Acids, fruits, juices, drinks, medicine…
 Frequent vomiting, Fizzy drinks.
 With respect to aging, this theory states that oxygen-derived free radicals
cause lipid per oxidation which in turn damage the cell membranes and
other cellular structures.

AGE CHANGES IN ENAMEL

* Enamel is a nonvital tissue that is incapable of regeneration. It is the hardest

tissue of the body.
 The most apparent age changes in enamel is attrition or wear of the occlusal
surfaces and proximal contact points as a result of multication.
 As a result of attrition there is gradual loss of enamel over the cusps and
incisal edges of the teeth.
 The loss is extremely depends on the
 - diet of the individual
- Nature of the occlusion
- Composition of the enamel.
 This is evidenced by a loss of vertical dimension of the crown and by
flattening of the proximal contour.
 The outer enamel surfaces themselves undergo post eruptive alterations in
structure at the microscopic level.
 The surfaces of unerupted and recently erupted teeth are covered completely
with pronounced rod ends and perikymate.
 These structures begin to disappear at the points of highest contour of the
surfaces.
 This is followed by a generalized loss of the rod ends and a much slower
flattening of the perikymata.
 Finally, the perikymata disappears completely.
 The rate at which the structure is lost depends on the
- Location of the surface of the tooth &
- Location of the tooth in the mouth.
 Facial and lingual surfaces loose their structure much more rapidly than
proximal surfaces and anterior teeth loose their structure more rapidly than
posterior teeth.
 It is difficult to demonstrate age changes within the enamel microscopically.
 The enamel gradually becomes less permeable.
 Localized increased in certain elements such as nitrogen and fluorine is found
in the superficial enamel layers of older teeth.
 Teeth may darken with age it could be due to the addition of organic material
from the environment & deepening of dentin seen through the layer of
translucent enamel
 Resistance to decay may be increased with age.
 Fluoride is most beneficial in preventing caries
  As the tooth ages, the gradient of fluoride concentration from exterior to
interior is less steep.
 Hairline cracks are also seen in older teeth.
 In deciduous teeth, once the resorption has begun the permeability of enamel
decreases rapidly until it becomes practically impermeable.

Age changes in Dentin

 Dentin is a mineralized. (vital), hard tissue that forms the bulk of the tooth
covered by enamel over the crown and cementum over the root.
 It contains odontoblastic process & dt
 It is laid down throughout the life.
 Pathologic effects of dental caries, abrasion, attrition or the cutting of dentin
during operative procedures cause changes in dentin.
 These changes in dentin.
 These changes are described as
- Secondary dentin
- Dead tracts
- Sclerosis
- Reparative dentin
 The mechanism that occur in the development of secondary dentin, reparative
dentin, dead tracts and sclerosis are not yet fully understood.

Secondary Dentin
 It is a narrow band of dentin bordering the pulp and representing that dentin
formed after root completion & it is a continuation of the circumpulpal dentin.
 It contains fewer dentinal tubules than primary dentin.
 It can be differentiated from primary dentin by the sharp bending of the
dentinal tubules because of rapid laying down of dentin.
 The pattern of secondary dentin deposition varies among the different groups
of teeth.
  In molars, it is deposited in greater quantities in the floor and roof of the pulp
chamber than on the walls.
 In maxillary anterior teeth:
The greatest dentin deposition occurs on the polatal wall of the pulp chamber with
subsequent deposition in the incisal tip and remaining walls of the pulp chamber.
Dead tracts :
 When dried ground sections of dentin is observed. The odontoblast processes
disintegrate and the empty tubules are filled with air. These are called as dead
tracts.
 They appear black in transmitted light and white in reflected light.
 They may extend from the dentino-enamel and dentino-cemental junctions to
the pulp.
 These dead tracts are produced may be due to aging or trauma.
 Dead tracts are originally described by fish be called it as opaque scleroses
elentin
 Chemical analysis of opaque dead tracts have shown less organic matter and
lower percentage of calcium and phosphorous than normal dentin.
 These areas demonstrate decreased sensitivity and appear greater extent in
older teeth.
 These are often seen in areas of narrow pulp home because of the crowding of
odontoblant, and also on the cusp tips that are subjected to abrasive forces that
cause attrition.
 Dead tracts can also occur in incisor which have never erupted.
 The dead tracts involved with caries will have a leathery consistency and may
be hand excavated with minimal effort.
 The pulpal end of the dead tracts generally become occluded by sclerotic
dentin and may be covered with a patch of reparative dentin.
Sclerotic/Transparent Dentin :
 Stimuli may not always induce formation of reparative dentin but leads to
protective changes in the dentin itself.
  In cases of caries, attrition, abrasion, erosion or cavity preparation, sufficient
stimuli are generated to cause collagen fibers & apatite crystals to begin
appearing in the dentinal tubule.
 In such cases blocking of the tubules may be considered as defensive reaction
of the dentin.
 Appetite crystals are initially sporadic in a dentinal tubule but gradually fill it
with a fine meshwork of crystals.
 Gradually tubule lumen and obliterated e mineral which appears very much
like the peritubular dentin.
 When this occurs in several tubules in the same area the dentin assumes a
glossy appearance and the refractive indices of dentin in which the tubules are
occluded are equalized and such areas become transparent.
 The amount of sclerosis increases with age.
 It & most comon in the
- Apical 1/3 of the root.
- In the crown, midway between the DEJ & surfaces of pulp
- Also beneath tomes granular layer in the oerrical area of older teeth &
- Beneath slowly progressing caries
 It appears transparent or light in transmitted light and dark in reflected light.
 Teeth containing translucent dentin appears to be more brittle than other teeth.
Making them more liable to # during extraction.
Reparative Dentin/Tertiary Dentin/ Irregular Dentin :
 As a result of extensive abrasion, erosion, caries or operative procedures, the
odontoblastic processes are exposed or cut. The odontoblasts either die or if
they are alive deposits reparative dentin.
 It is believed that the origin of the new odontoblast is from undifferentiated
perivascular cells
 Both the damaged and the newly differentiated odontoblasts then begin
deposition of reparative dentin.
 This is the healing process initiated by the pulp resulting in resolution of the
inflammatory process and removal of the dead cells.
  The hard tissue thus formed is termed as reparation dentin.
 It is result of defensive activities of pulp dentin complex.
 It may or may not contain tubules. If they are present, fewer in number,
irregularly arranged wavy in their course.
 It is believed that bactenia, living or dead or their products, as well as
chemical substances from restorative materials, migrate down the tubules to
the pulp and stimulate response leading to reparative dentin formation.
 The reparative dentin is deposited in the affected area at an increased rate that
averages 1.5mm per day.
 The demarcation zone between secondary and reparative dentin and called the
calciotraumatic line.
Difference between sclerotic dentin & Tertiary dentin.
Sclerotic Dentin Tertiary Dentin
1. More calcified * Less calcified
2. Mostly age changing process * Associated with stimulus
3. More transparent * Less transparent
4. No tubules found * May or may not found (Mostly irregular
tubules)
5. Most commonly found in apical 1/3rd * Found in response to stimulus.

Age changes in Dental pulp

 The dental pulp is specialized, well vascularized connective tissue, entirely
enclosed in dentininal walls.
 It is responsible for the vitality of dentin and the entire tooth.
 It has a shape that confors the respective tooth and the total volume of pulp
organ of all permanent teeth is 0.38cc and the mean value of single tooth if
0.02cc
 In younger teeth.
 The pulp and pulp chamber is wider and as advances due to secondary dentin
deposition, pulp chamber and root pulp gradually reduces in size.
Cell changes :
 The cells are fewer in number in the aging pulp.
  They decrease in size and number of cytoplasmic organelle.
 The fibroblast exhibits less periniclear cutoplasm
 The intercellular organelles are reduces in number and size (Oral path, oral
Medicine oral 1991)
Age-related changes of the dental pulp are
1. Compromised circulation and innerration
2. Fat droplet deposition
3. Vacuolization of the oxontoblasts.
4. Reticular atrophy
5. Fibrosis of the pulp
6. Hyaline degeneration
7. Fat replacement
8. Pulp cysts
9. Mucoid degeneration
10. Calcifications
11. Metaplasia.
Compromised circulation and innerravtion
 With aging the apical deposition of the secondary dentin and cementum
increases
 This tends to narrow the originally wide-open root apex.
 Hence the blood supply, lymphatic, nerve supply to the pulp and
compromised.
 In extreme old age the complete that the blood, lymphatic and nerve supply to
the pulp and almost completely shut off.
 Blood vessels to the aged pulp undergo arteriosclerotic changes, resulting in a
diminished blood supply to the pulp cells.
 The arterial intima thickens and adventitia calcifies
 The pulpal nerve shows progressive mineralization of the nerve sheath and
nerve itself.
Fat droplet deposition
 The first observable change within the pulp is fat droplet deposition.
  According to histologic fine etroplets of fatty deposits are found in the
odonoblasts, nuclei of pulp cells and walls of pulp tissue capillaries.
Vacuolization of the odontoblasts :
 The odonotoblastic cells are pushed apart and separated from the dentin wall
by the apparent pressure of an intercellular accumulation of tissue fluid.
Reticular Atrophy :
 It is considered as an artifact by some authors
 Histologically, the tissue has a netlike appearance which is apparently related
to an abundance of intercellular fluid and a reduction in the number of pulp
cells.
Fibrosis of pulp :
 As the pulp ages there is a great decrease in the number of cells. (Fibroblasts,
odonoblasts, mesenchymat cells )
 Increase in the no of collagenous fibers
 The cell density of the pulp decreases.
 The odontoblasts that remain smaller and more flattened.
 The number of cells and size of the pulp decreases with age & remaining
pulpal space is filled with fibers.
 In addition the number of blood capillaries, lymphaties and nerve decrease.
 The reticular fibers also increase with aging
 In time the pulpal nerves become less sensitive this is why the aged teeth are
painless.
 Reduction in cellular, fibrous tissue accumulation
 Decrease in circulatory and nervous elements
 There is first and decrease and then a reduction in the acid-
mucopolysaccharides.
 Eventually nothing remains in the pulp except fibrous tissue.
 This stage is called fibrosis (Fibrous degeneration of the pulp)
Hyaline Degeneration :
 It is an intimidate stage in the formation of pulp calcification.
  The pulp has only on blood circulatory system and no collateral circulation.
 Minor circulatory disturbances can often result in hyalinization of areas of the
pulpal tissue.
 Hyalinization denotes change in the microscopic appearance of a tissue, it is
due to change within the intercellular fibers of connective tissue.
 It is usually sequcla of tong standing fibrous degeneration.
 In time this hyaline material and the spaces formed by the shrinlcage fill with
fat. This is the stage of fat replacement.
Fat replacement :
 Under the light microscope in ordinary was sections, fat replacement appears
as cercular spaces in the tissues.
 Some investigators considered it as artifact.
 According to stewart, he isolated monoglycerides, diglycerides,
phospholipids, lipoproteins, cholesterol and cholesterol esters.
 Calcifications commonly occure in these fat deposits and can lead to
formation of pulp stoals.
Pulp cysts : (Pseudocysts)
 Also called as pulp atrophy
 They are apparent spaces that are filled with fluid and surrounded by fibrous
connective tissue.
 They are the result of localized pulp atrophy with accompanying shrinkage of
the pulp tissue.
 Etiology of pulp calcifications not known but calcifications way fund around
egeuerating cells, blood thromi connective tissue, and nerve fibers.
Mucoid degeneration :
 Mucoid lies in the interstitial spaces between the cells and the reticulum.
 It is the normal constituent of pulp.
 With aging, mucoid increases and simultaneously the level of acid
polysaccharides decreases,
 Under pathologic conditions masses of mucoid can accumulate with the pulp
  Together with mucoid, degenerative changes including a complete loss of
embryonic connective tissue structure occurs.
Calcifications :
Pulp Stone / Denticles :
 Pulp stones or denticles are nodular, calcified masses appearing n either or
both the coronal or root portions of the pulp organ.
 They have been seen functional as well as embeded unerupted teeth.
Classification :
I. According to their structure
1. True denticles.
2. False
3. Diffuse clacifications.
II According to their location in relation to dentinal wall.
1. Free denticles.
2. Attached denticles.
3. Embeded denticles.
True Denticles :
 They are comparatively rare consists or irregular kind of dentin with traces of
dentinal tubules and odontoblasts.
 Usually found close to apical foramen but also seen in the walls or bottom of
the pulp chamber
 The epithelial remnants induce the cells of the pulp (Tlertwigs epithelial root
sheath)
 Ry pulp Stone –
1. Long burs E narrow shank i.e. Goose neck, Lone neck.
2. Canal probes
3. EDTA
4. R.C. Prep.
5. Ultrasound.
 To differentialte in to odontoblasts, which then form the dentin masses called
true pulp stones.
False Denticles :
 False denticles are calcified structures in the pulp cavity that do not show the
structure of dentin.
 They consist of concentric layers (Lamellas) of calcified material and cells.
 The Cells are derived from degenerated hyalinized pulp tissue.
 Calcification of thrombi in blood vessel (Phleboliths) may also serve as cause
for (development) origin for false denticles.
Diffuse calcifications :
 They are fine, irregular and fibrillar calcific deposits in the pulp tissue.
 They usually found in the root canal and less often in the coronal area.
 They can begin in the wall of a blood vessel, in connective tissue, surrounding
a nerve or following the course of blood ressels and nerves
 They can start as fine spicules, or by fowon they can develop into larger
bodies.
 They increase with advencing age
 Pathologic changes can occur if they grow and exert pressure on the nerve
bundles and if they cause pressure on the blood ressles.
Free Denticles :
 They lie unattached in the pulp tissue and not connected to the walls.
 Most free denticles are fake denticles.
Attached Denticls :
 They are attached to the walls of the pulp cavity and are usually false
denticles.
Embede Denticls :
 They are embeded within dentin.
 They are originally free, lying close to the dentin surface.
 The continuous growth of dentin caused them to become entrapped with its
structure.
 With advancing age, denticles decrease in size and number.
 They can also be found in functionless, erupted and impacted teeth.
Metaplasia :
 Metaplasia is the change from one tissue type in to another.
 Mesenchymal cells, which from either odontoblasts or fibroblasts probably
change into cementroblasts or osteoblasts.
 This is not true metaplasia.
Age changes in cemetum
 Cementum is the avascular, mineralized, hard dental tissue covering the
anatomic roots of human teeth
 It was first demonstrated microscopically in 1835 by two pupils of purkinje.
 It begins at the cervical portion of the tooth at the CEI and continues to the
apex.
 Two types of cementum can be differentiated
1) Cellular cementum – Seen in the apical 1/3 of the root (Thickest – 150-
200 mm)
2) Acellular cementum – CEJ to the apix (thicl ness 20-50 mm)
 Cementum is subjected to the masticatory forces and stress.
 Most visible age changes in cementum is increase in thickness and hardness of
cementum and decrease in cellular components
 Cementum increases in thickness by appositional growth
 This process occure throughout the life of the tooth.
 The deposition of cellular cementum and much thicker than the acellular
cementum, which lease to gradual constriction of apical foramen.
 It is more resistance to resorption than bone.
Hypercementosis :
 Abnormal thickening of cementum and called hypercementom
 It may be diffuse or circumscribed.
 If overgrowth improves the functional quality of the cementum, it is termed a
sphyertrophy it is found in teeth that are exposed to greatest stress.
 If overgrowth occurs in nonfunctional teeth, it is termed as pherplasia.
 Cementum resorption occur after trauma or encessive occlusal forces.
  Cellular elements of cementum exhibits age changes, the degenerative change
affect tooth occleus and othe cytoplasmic constituents.
 The neclear change involves conctensation of the chromatin ferminating
finally in fragmentation and lysis of the nuclear material.
 In the cytoplasm the organella are decreased and alteration in cell organization
may result in vacuolization.
 Finally the cell undergoes autolysis.
 With aglng the surface of the cementum becomes more irregular, less
permeable.
 Hypercementosis is seen in
- Periapical inflammatory conditions.
- Periapical cementoma
- Systemic diseases-paget’s disecese, Acromegaly, Gigantism.
Age changes in periodontal ligament.
 The periodontium is a specialized connective tissue organ covered by
epithelium attached between the cementum of the tooth and lamina dura of the
alveolar bone.
 It varies in thickness i.e. 0.15-0.38 mm.
 It is thinnest in the middle region of the root and it is thin in functionless and
embeded teeth.
 It is wide in teeth that are under excessive occlusal stresses.
Changes observed in periodontal ligament are,
- Greater number of elastic fibers
- Decreases in vascularity and mitotic activity,
- Fibroplasia and the number of collagen fibers and
- Mucopolysaccharides.
- Increases in arteriosclerotic changes.
- Cementicles
- Excementosis.
Age changes in Alveolar bone.
  It is that bone of the jaws containing the soclcets which surrounds and
supports the roots of teeth.
 It is living hard calcified bony structure, forming the dental socket walls in
which tooth or teeth are held by the periodontal fibers.
 The alveolar body structure is also subjected to mosticatory forces and
prossures.
 Remodelling of alveolar bone takes place with advancing age in order resist
and compensate the forces of mastication.
 Bone deposition and resortion are intermittent process
 The lining of alveolus is fairly smooth in youngsters
 With age the socket becomes rougher and in histologic section, it shows
ragged outline.
 Osteoperosis decreased vasularity and reduction if metabolic rate and healing
capacity.
 When teeth are lost, gradually the alveolar process undergoes resorption
creating facial profile of edentulous person whose chin and nose appreximate
because of decreased facial hight.
Age change in Mandible and Maxilla :
 Histologically, mandible is more porous, due to an increase in the vascular
spaces,
 The lacuane are decreased in no.
 The glycoptotein material in the lacunal is altered.
 No, of osteocytes are reduced.
 Fewer but langer canalifuli in the bone.
 The walls of the bl. Ressels are thicker
 Reduction in no of canaliculi
 Diffuse calcification in many canals in juction (Collagen materia shows
increase crosslinging)
 Corticle plates at ten angle of mandible becomes thinner.
Age Changes in angle of mandible :
A+birth : The angle of mandible is obtuse (1750C)
: The body of mand becomes clongated
A+childhood : To provide space for the additional teeth the angle becomes less obtuse i.e.
1400
In the adult : The ramus becomes almost verticle in divection angle 110-1200
In old age : With less of teeth, the alveolar process is resorbed and the reman becomes
oblique, angle of maned measured 1400
Age changes in Oral mucous memberane.
 The surface of the oral cavity is known as oral mucous membrane.
 The oral miuosio may be divided in to three major types.
1. Masticatory mucosa
- Gingiva and hard palate
2. Linig or reflecting mucoses
- Lip, Cheek, vestibular fornix, alveolar mucosa floor of mouth and soft
palate
3. Specialized mucosa
- Dorsum of the tongue and taste bunds.
Gingiva :
 It is a specialized keratinized epithelial oral mucosa surrounding the neck of
the tooth.
 It is clinically described as masticatory macosa.
 Changes have been identified with aging :
- Diminished keratinization in both men and women.
- A reduced or unchanged amount of stippling.
- Increased width of attached gingiva with constant location of the
mucogingival junction throughout adult life.
- Decreased connective tissue cellularity.
- A greater amount of intercellular substances
- Reduced oxygen consumption
- An increase or no change in the mitotic index of gingival epithelium in
aged humans has been reported.
Dentogingival Junction :
 It represents a unique auatomic feature concerned with attachment of the
gingiva to the tooth
 With age there is progressive apical migration of dentogingival junction.
 Once the tooth erupts in to the oral cavity the junctional epithelium of the DGJ
extends to the CEJ.
 At the age of 12, the gingiva is located on the enamel
 At the age of 25 the gingiva is attached closed to the cemento-enamel
junction.
 At the age of 50, slight occlual wear and slight slight recession
 At the age of 70, moderate attrition and slight to mocterate recession.
Age changes in other areas of the oral mucosa.
 Atrophy acid thinning of the oral epithelium
 An increased keratinization of lip and cheek mucosa,
 Atrophy of the connective tissue with loss of elasticity.
 A decrease in the number of protein-bound hexoses and mucoproteins.
 Increase in the number of mast cells.
Masticatory efficiency :
 Reduction in matsticatory efficiency in aged individulas is due to the result of
unreplaced missing teeth, loose teeth, poorly fitting dentures or an
unvoillingness to wear dentures
 Reduced masticatory efficiency leads to poor chewing habits and the
possibility of associated digestive disturbances.
 Avitaminosis is relatively common in aged person
 An inadequate intake at vitamins, calcium, iron and potassium is particularly
important to geriatric patients.
Age changes in salivary glands :
 The salivary glands are exocrine glands whose secretions flow in to the oral
cavity.
 Types
 1. Major salivary glands.
- Parotid glad
- Submandibular gland
- Sublingual Gland
2. Minor salivary glands
- Labial and buccal glands, palatine glands, glossopalatinc glands, lineal
glands.
- The most important function of salivary gland is production of saliva
which provides the primary natural protection for the teeth and soft tissues
of oral cavity and it assists in mastication, deglutition and digestion of
food.
Changes in salivary glands, are
- Gradual replacement of parenchyma with fatty tissue
- Reduction in salivary flow with age leads to dryness and incidence of
dental caries.
- Increase in the viscosity of saliva
- Recent studies have shown that the flow of saliva in aged person in
reduced during resting condition but the quality and composition of saliva
remains same in young and aged individuals.
Age changes in Temporomandibular joint.
Temperomandibular joint is most unique and non-weight laearing joint in human
body associated with facial skeleton-working through out the life of a person.
As age advances certain changes are observed in TMT they are, - Decrease in synovial
fluid
- Degeneration of the fibrous covering of the articulating surfaces and disc.
- Loss of elasticity in the articulate cartilage surface erosions
Questions :
1. Clinical significaue of pulp stone in eudodontics.
 INFLAMMATION
CONTENTS :
 Introduction
 The agents causing inflammation cells inv. In infl
 Signs of inflammation
 Classification of inflammation
 Acute inflammation
 Chronic inflammation
 Clinical implications
 Conclusion
 Bibiligoraphy

Introduction
 Inflammation is principal safe guarol against any type of injury or infection. If the
inflammation is impaered, it will lead to serious consequences to the human body
infns would go unchecked wounds would never heal pujured orgaus remain
permanent restring saerce .
 The word inflammation is derived from the state of being inflamed. To inflame
means to “set a fire,” or burning which conjurs up the color red a sense of heat and
often pain.
 The word comes to us by way of middle English (Enflamme),
From middle French (enflamm) &
From Latin (Enflammare)

 Definition :
Inflammation is defined as the local response of living mammalian tissues to injury due
to any agent.
In is a body defense reaction in order to eliminated or limit the spread of injurious agent
as well as to remove the consequent necrosed cells and tissues.
 The unigas feature of the infl process in the react of bl ressel’s leading to
accumulation of the fluid and leucoeytes in entrarascular tissues.
 The agents causing inflammation
1. Phycical agents like heat, cold, radiation, mechanical trauma
2. Chemical agents like organic and inorganic poisons
3. Infective agents like bacteria, viruses and their toixns.
4. Immunologic agents like cell-mediated and antigen-antibody reactions.
Thus, the inflammation is distinct from infection. Inflammation is a protective
response by the boyd while the infection in incasion of harmful micrbess in to they
body and their resultat illeffects by toxins.

 Signs of Inflammation
The Roman writer Celsus in 1st century A.D. named the famous four cardinal sings of
inflammation as
1. rubor (redness);
2. tumor (swelling);
3. color (heat) ; &
4. dolor (pain);
Late Virchow added fifth sign to there i.e.,
5. functio laesa class of function
These sings are the results of vascular alterations in the area of injury.
These sings are the results of vascular alteration in the area of injury.
 Reddness and heat are due to the ed bl flow wich in turn result in vasodilatation of
vessels.
 Swelling is due to infiltration of cells and fluid from blood ressels to the interstitial
space. It is the result of alterations in vascular permeability. The release of toxins
from the bacteria, hormones and cellular elements.
 Loss of function :
Due to above change, the affected tissue is unable to be normal function
 Types of inflammation
 There are four types of inflammation
 Based on duration (severity)
1. Acute inflammation
2. Chronic inflammation
3. Subacute inflammation
 Acute inflammation ;
 It is of short duration (seconds/min) lasting for minutes, several 4-6hrs rapid in a set
hrs or few days (3-5days)and represetns the early body reaction and is usually
followed by reair.
 It also refers to be specific type of response involving an execrativereaction during
which fluid, serum proteins and white blood cells leave the blood stream and enter the
area of injury.
 It may become chronic if the injurious agent is persistent.
 The main features of acute inflammations are
1. accumulation of fluid and plama at the affected site.
2. Intravascular activation of platelets and
3. Polymorphonclear neutrophils as inflammatory cells.
Chronic inflammation :
 It is of longer duration (and occurs either after the causative agent of acute
inflammation persists for long time or the stimulus is such that it induces chronic
inflammation for the beginning .)
 The characteristic feature of chronic inflammantion is presence of chronic
inflammatiory cells such as lymphocytes, plasma cells and macrophage.
Subacute inflammation
 It is a mixed one and difficult to judge under microscope.
 It consists of mixed cells, with very few neutrophils and most of monocytes and
lymphocytes
 Transition period, few days to few weeks.
Granulomatous inflammation :
Granuloma is defined as a circumscribed, ting lesion, about 1 mm in diameter, composed
predominantly of collection of modified macrophages. Called epitheloid cells and
rimmed at the periphery by lymphoid cells.
Graunlomatous inflammation is typical of reaction to poorly oligestible agents elicited by
tuberculosis, leprosy, fungal infections, schistosomiasis, foreign particles etc.,
Granulomatus inft is a distinctive pattern of chronic inflamatory reactron characterized by
focal accumalation of activated macrophages. With often with often develop as epithelial-
like (epithelioid) appearance.
It is encountered in limited number of immundogically mediated, infechbus and some
noninfectious conditions.
Acute inflammation
The changes in acute inflammation can be described under the following two headings. :
I vascular events
II Cellular events.

I Vascular events.
 Alteration in the microvasculature (arteriole,) capillaries and venules) is the earliest
response to tissue injury
 These alterations include.
A. Hacmodynamic changes
B. Changes in vascular permeability.

A. Haemodynamic changes :
 The earliest feature of inflammatory response results from changes in the vascular
flow and calibre of small blood vessels in the injured tissue.
 The sequence of these changes are in the following orgen
1. Transient Vasoconstriction
It is the immidiate vascular response
With mild form of injury, the blood flow may be re-established in 3-5 seconds
While with sever injury the vasoconstriction may last for about 5 minutes
2. Persistent progressive vasodilatation :
 Which involves mainly the asterioles but to a lesser extent affects venulcs and
capillaries
 This change is obrious within half an hour of injury.
  Vasodilatation results in increased blood volume in microvasculature bed which is
responsible for redness and warmth at the site of acute infl
3. Increased hydrostatic pressure.
 Progressive vasodilatation, in turn may elevate the local hydrostatic pressure resulting
in franudution of fluid in the extra vascular space. This is responsible for swelling at
the Local site of acute inflammation
4. Slowing or stasis : of blow
Slowing or is attributed to increased permeability of microvasulature that results in
increased conc of red cells and thus raised blood viscosity Bl flow condition is termed
as stasil as the stasis develops.
5. Lcukocytic margination : L . principally the neutrophils marginatc
 Leukocytic margination or peripheral orientation of leukocytes (mainly neutrophils).
Along the vascular endothelium.
 The Leukocytes stick to the vascular endothelium briefly, and then move and migrate
through the gaps betweent he endothelial cells in to the extracellular space.
 This process in known as EMIGRATION.
The hemodynamic changes are best demanstrated by the Lewis experiment
 Lewis induced the changes in the skin of inner aspect of forearm by firm stroking
with a blunt point. The reaction so elicited is known as triple response or red line
response (consisting of the following) they are as following

i. Red line :
Appears within few seconds following stroking and results from local
vasodilatation of capillaries and venules.
ii. Flare :
Is the bright reddish appearance or flush surrounding the red line and results from
vasodilatation of the abjacent arterioles
iii. Wheal
 Is the swelling or ocdema of the surrounding skin occuring due to trandsuctionof
fluid in to the extravascular space. These features, thus elicit the classical sings of
infl i.e., redness heat, swelling and pain.
B. Increased vascular permeability
[Vascular Leakage]
 In the earliest phase of infel ? vasodilation and ed bl. Flow increase intravaseular
hydrostatic pr., resulting in ed filteration of fluid from the capillaries. This fluid
contains little protein. It is called as transudate.
 Increase in permeability of the vessel wall leads to the escape in to the interstitium of
protein rich fluid termed excavate.
 This net increase of extravascular fluid is called edema.
The appearance of inflammatory oedema due to increased vascular permeability is
explained on the basis of starling’s hypothesis.
The normal circumstances, the fluid balance is maintained by two opoisng sets of forces.
i) Forces that cause outward movement of fluid from microcirculation are intra-
vascular hydrostatic pressure and osmotic pressure of interstitial fluid
ii) Forces that cause inward movement of interstifial fluid in to circulation are
intravascular osmotic pressure and hydrostatic pressure of interstitial fluid.
Whatever little fluid is left in the interstitial compartment is drained away by lymphatics
and thus no cdena results normally.
However in inflammed tissues, the endothclial lining of micro-vasculature becomes more
leaky.
Mechanism of vascular permeability : can be explaised by four mechamim
 There are four mechanism explained the leak ness of nonpermeable endothelial layer
of microvasculature
a) contraction of endothelial cells . V gap formation
 This is the most common mechanism of increase leak ness that affects venules.
 While capillanes and arteriole remain unaffected
 The endothelial cells develop temporary gaps between then due to : their contraction
and separation of intercelluler jns resulting in vascular leak ness.
 It is mediated by the release of histamine, bradykinin and other chemical mediators
Leukotricnss neuropetide
 The respones begins immediately aftex injury, is usually reversible, and is short
duration (15-30min) Example of such immediate treasient known as leakage its mild
thermal injury of skin of forearm
ii) Retraction of endothelial cells
 There is strutural re-organization of the cytoskeletion of endothelial cells. That causes
reversible retarction at the intercellular junctions.
 It also affects venules and is mediated by cytokines such as IL-I and tumor necrosis
factor (TNF), I-r
 The onset of response takes 4-6 hrs after injury and lasts for 2-4 hrs/more
iii) Direct injury to endothelial cells.
 Causes cell necrosis and appearance of physical gaps at the sites of detached
endothelial cells.
 The process of thrombosis is initiated at the site of damaged endothelial cells.
 The change affects all the levels of microvasculature [venules, capillaries &
arteniols ]
 The increased permeability may either appear immidietly after injury (Immidiate
susrained Leakage) or it may accur after a delay of 2-12 hours.
[delayed prolonged leakage]
Example for
i. Immediate sustained leakage are severe bacterial infections
ii. Delayed prolonged leakage may occur following moderate thermal injury and
radiation injury.
iv) Endothelial injury mediated by leukoacytes.
 Adherence of leukocytes to the endothelium at the site of inflammation may result in
activation of leukocytes.
 The activated leukocytes release proteolytic enzymes and tonic oxygen species with
may cause endothelial injury and increased vascular leak ness
 In affects moslty venules and is a late response.
Example : are seen in sites where leukocytes adhere to the vascular endothelium
Ex : in pulmonar venules and capillaries.
v) Neovascularisation :
 The necoly formed capillaries under the influence of vascular endothelial growth
factor (VEGF) during the process of repair and in tumors are excessively leaky.
 It should be noted that although (there four) mechanism are separable all may play a
role in response to one stimulus.
 For example in various stages of a thermal burn, leakage results from chemically
mediated endothelial contraction as well as direct and leukocytedependent injury- and
from regenerating capillaries when the burns heal.
II. Cellualr Events :
 The cellular phase of inflammation consists of two processes ;
1. Exudation of leukocytes
2. Phagocytosis
 Exudation of leukocytes :
- The esacpe of leukocytes from the lumen of microbasculature to the
interstitial tissue is the most important feature of inflammatory response
- In acute inflammation PMNs comprises the first line of body defense followed
by moncytes and macrophses
- The changes leading to migration of leukacytes are as follows.
1. Margination, rolling and adhesion
2. Fmigration toward a chemotactis stimulus

1) Margination :
 Initially the rate of flow of blood is increased due to vasodilatation.
 But subsequently there is slowing or stasis of blood stream.
 The normal axial flow consists of central stream of cells comprised by leukocytes
and RBCs & peripheral cells comprised by leukocytes and RBCs and peripheral
cell-free layer of plasma close to vessel wall.
 Due to slowing and stasis, the central stream of cells widens and peripheral
plasma zone becomes narrower because of loss of plasma by exudation.
 This phenominon is known as Margination.
  As a result of this, (the neutrophils of the central coloumn come close to the
vessel wall. This is known as pavementing) endothelium can be virtually lined by
leukocytes, an appearance is called pavementing.

Rolling and adhesion:

 Peripherally marginated and pavemented neutrophils slowly roll over the endothelium
(cells, lining the vessel wall (rolling phase).
 This is followed by transiently bond between the leukocytes and endothelial cells,
finally leukocytes coming to rest at where they adhese firmly. (Adhesion phase).
 The following adhesion molecules bring about rolling and adhesion phases: affected
these process by modulating the surface expression.
i) Selections : mediate rolling of PMNs over endothelial surface.
ii) These consists of P-selectin preformed and stored in endothelial cells and
platelets.
iii) E-selectin (synthesized by cytekine-activated endothelial cells).
iv) L-selectin (expressed on the surface of lymphocytes & neutrophils).
ii) Intigrins are transmembrane interodimen’s glycoprotein. On the endothelial cell
surface are activated during the process of loose transient adhesions between
endothelial cells and leukocytes.
 At the same time the receptors for integrins on the neutrophils are also
stimulated.
 This process brings about firm adhesion between leukocyte and endothelium.
iii) Emigration:
 After striking of neutrophils to endothelium, the former move along the
endothelial surface till a suitable site between the endothelial cells is found where
the neutrophils throw out cytoplasmic pseudopods.
 Subsequently, neutrophils lodged between the endothelial cells and basement
membrane, cross the basement membrane by damaging it locally with secreated
collagenases and escape out in to the extravascular space: This is known as
emigration.
  Neutrophils are the dominant cells in acute inflammatory exudate in the first 24
hrs and are short lived (24-48 hrs). monocytes – macrophages appear in the next
24-48 hours and survive much longer.
 The N, M, L, E & B all use the same pathway to migrate from b1. Into tissues.
 Simultaneous to emigration of leukocytes, escape of red cells through the gaps
between the endothelial cells, Diapedesis, takes place.
 Diapedesis is a passive phenomemon RBCS being forced out either by raised
hydrostatic pressure or may escape through the endothelial defects.
 Left after emigration of leukocytes.
 Diapedesis gives haemorrhagie appearance to the inflammatory exudate.

Chemotanis : Emigration to a site of injury along a chemical gradient.

 The chemotactic factor – mediated transmigration of leukocytes after crossing several
barriers (Endothelium, basement membrane, perivascular myofibroblasts and matrix)
to reach the interstitial tissues is called chemotanis.
 The concept of chemotaxis is well illustrated by Boyden’s chamber expt.,
 In this, a millipore filter (3mm pore size) separater the suspension of leukocytes from
the test solution in tissue culture chamber.
 If the test solution contains chemotaetic agent, the leukocytes migrate through the
pores of filter towards the chemotactic agent.

Fig Chemokines:
 The agents acting as potent chemotactic substances for different leukocytes called
chemokines.
 They are as follows:
i) Leukotriene B4 (LT-B4).
ii) Platelet factor 4 (PF4).
iii) Components of complement system (C3, C5 in particular)
iv) Cytokines (Interleukins IL-1, IL-5, IL-6).
v) Soluble bacterial products (such as formylated peptides).
vi) Monocyte chemattractant protein (MCP-1).
 vii) Chemotactic factor for CD4 + T Cells.
viii) Eotaxin chemotactic for eosinophils.

Characteristics of C. Factors:
 Stimulate the direction of migration.
 Able to combine with the receptor site.
 Water soluble and hence dissusable.
 Exogenous / Endogenous in origin.
 Small proteins or peptides.

Phagocytosis (Cell Eating)

 Phagocytosis is defined as the process of engultment of solid particulate material by
the cells.
 The cells performing this function are called phagocytes.
 There are 2 main types of phagocytic cells:
i) Polymorphonuclear neutrophils (PMNs) which appear early in acute
inflammatory response, also called as microphages.
ii) Circulating monocytes and fixed tissue mononuclear phagocytes called as
macrophages.
 The process of phagocytosis is similar for both polymorphs and macrophages.

Steps involved in Phagocytosis:

1) Recognition and attachment stage (Opsonisation).
2) Engulfment stage.
3) Secretion (Degranulation) stage.
4) Digestion or degradation stage.

Recognition and attachment stage:

 The phagocytie cells are recognised and attracted to bacteria by chemotactic factors
released by bacterial products as well as by tissue proteins.
 In order to establish a bond between bacteria and the cell membrane of phagocytic
cell, the micro-organisms get coated with opsonins, which are naturally – occuring
factors in the serum.
 The main opsonins present in the serum and their corresponding receptors on the
surface of phagocytic cells (PMNs or macrophages) are as follows.
i) IgG opsonin is the fragment of immune globulin G.
 It is the naturally occuring antibody in the serum that coats the bacteria while
MNs posses receptors for the same.
ii) C3b opsonin is the fragment of complement.
 It is generated by activation of complement pathway.
 It is strongly chemotactic for attracting PMNs to bacteria.
iii) Lectins are carbohydrate – binding proteins in the plasma which bind to
bacterial cell wall.

2. Engulfment stage:
 The opsonised particle bound to the surface of phagocyte is ready to be
engulfed.
 This is accomplished by formation of cytoplasmic pseudopods around the
particle (due to activation of actin filaments beneath cell wall) enveloping it in
a phagocytic vacuole.
 Eventually, the plasma membrane enclosing the phagocytic vacuole breaks
from the cell surface so that membrane lined phagocytic vaucole lies free in
the cell cytoplasm.
 The lysosomes of the cell fuse with phagocytic vacuole and form
phagolysosome or phagosome.

3. Degranulation stage:
 The preformed granule-stored products of PMNs are discharged or
secreted in to the phagosome and the extracellular environment.
 The specific or secondary granules of PMNs are discharged while the
azurophilic granules are fused with phagosomes.
 4. Killing or Degradation Stage:
 The micro-organisms after being killed by antibacterial substances are
degraded by hydrolytic enzymes, thus completing the role of phagocytes
as scavenger cells.

The antimicrobial agents act by either of the following mechanisms:

i) Oxygen – dependent bactericidal mechanism
ii) Oxygen – independent bactericidal mechanisms &
iii) Nitric oxide mechanism.

Oxygen – dependent bactericidal mechanism:

 An important mechanism of microbicidal killing is by the production of reactive
oxygen metabolites (O2, H2O2, OH, HOCl, HOI, HOBr).
 [A phage of increased oxygen consumption (respiratory burst) by activated
phagocytic leukocytes requires the essential presence of NADPH oxidase.]
 NADPH –oxidase present in the cell membrane of phagosome reduces oxygen to
super oxide ion (O2).

ZO2 ZO2

NADPH (Superoxide anion )

Onidase

NADPH NADP+H+
 Superonide subsequently converted in to H2O2 which has bactericidal properties.

ZO2 + 2H+ H2O2 ( Hydrogen peroxide)

 This type of bactericidal activity is carried out either via enzyme myeloperoxidase
(MPO) present in the granules of neutrophils and monocytes, or independent of
enzyme MPO.
a) MPO-dependent killing (H2O2 –MPO-halide system).
 In this mechanism, the enzyme MPO cuts on H 2O2 in the presence of halides
(chloridem iodide or bromide) to form hypochalous acid (HOCl, HOI, HOBr) which
and more potent antibacterial agent than H2O2
H2O2 MPO HOCl + H2O

Cl, Br, I (Hypochlorous acid)

b)

5.


iv)
iv)

2)
v)

C.

-

 Clinical Implications

The root canal is the seat of infection. The micro-organisms in the root canal are

rarely m and do not move from the root canal to the periradicular tissue.

However they can multiply sufficiently to gra out of the root canal or the

metabolic procky of then micro-organisms or toxic products tissue necrosis may diffused

to the perioradicular tissues.

On reaching the periradicular area, these noxious products produce bone

resorption & granulation tissue in place of normal perioradicular tissues.

The periradicular pathologic tissues contain PMNs, Lymphocytes, plasma cells,

macrophay and mast cells. Along inmunoglobulin IgG, IgA, IgM, IgE and complement.

The may cause anaphylactic, cytotoxic, antigen antibody complex and delayed

hypersensitive reactions.

Recent reports indicate that some endodontic flare-ups are mediated by IgE

reactions & the bone resorption is mediated by a lympha called osteoclytic-activating

factor.

These findings point to the important role that imnunologic reactions play in the

physiology & pathology of the periradicular tissue

The reaction of the periradicacular tissues to nanious products of tissue necrosis,

bouteriol products & autigentic agents from the root canal has been described by Fish.

He conducted the experiment in the jaws of guinea pigs by drilling openings in

the bone & pasking in wool fibers saturated & a broth culture of micro-organisms.

Four well defined zones of reaction were found.

 1) Zone of infection

2) Zone of contamination

3) Zone of invitation

4) Zone of stimulation

Zone of infection:

This zone is characterized by PMNs.

The infection was present in the center of the lesion & micro-organisms were

found only in that area.

Zone of contamination:-

This zone is characterized by round cell infiltration.

Infl response in pulp is different from any other C.T.

Pulp is totally surrounded by hard tissue.

With hb efficient collateral circulation (limited space to expand during inflation

reaction)

Elevation in interstitial tissue pressure.

Vaso outive nemropeptides like substance P &

Culcitonin gene – related peptides.

Causes of infl’ of pulp physical, chemical produce changes

Boutenial, (iatrogenic, Traumatic, Idiopathic in pulp)

Mediators:

- Leulcotaxins

- Eicosanoids

- Cytokines

- Platelet activating factors.

Chromic infl’in pulp is low grade long standing response to canal irritants.

Mild to moderate noxious stimuli to to the pulp may produce sclerosis of D.T, formation

of reparative dentine or verertible infl’.

Irreversible infl changes caused by severe injury can lead to necrosis of pulp.

Conclusion:

Understanding the mechanism of the inflammation and role of inflammatory cells

in body defense & very important helps to dev, a new therapent agents for wide diversity

of serious disease a infl. process.

INFL

(Inflammatory process) is a body defense reaction which is a nature gift to the living

beings, understanding the mechanism of inflammation is very important helps to develop

a new therapeutic agets (fa wide diversity of diseases).

Infln of pulp is called as pulpitis initially the infl Reversible pulpitis.

Reversible is a mild-to moderate inflammatory condition of the pulp caused by nonious

stimuli in the pulp is lafoable of returning to the uninflammed state follows the removal

of the stimuli.

Characterized by sharp pain lasting for a memory.

It is more often brought by cohd than hot being

Histopathologicaly.

- Reparative dentin, disruption of DT, dilated blood vessels, extravassition of

edema flu & presence of emmunologically competent chronic inflammatory

cells. By pallicut proceed.

Irriressible Pulpitis:-

I.P. is a persistent infl cond of the pulps symptomatic or asymptotic caused by nanious

stimulus.

Post capillary venucles become congested & affects circulation in the pulp, causing

pathologic changes. Such as necrosis, these necrotic areas attract PMN., ( by chumotaln

& vesl . phagoaptosis by PMN occur.

Exudation: The escape of fluid, proteins and blood cells from the vascular system into

the interstitial tissue or body cavities is known as exudation.

An exudate: Is an inflammatory extravascular fluid that has a high protein concentration,

cellular Deloris & a specific gravity above 1.020.

Transudate: Is a fluid e Low protein content (most of e is albumin) & a specific gravity

of less than 1.012. It is essentially an ultrafiltrate of blood plasma.

Edema: Denotes an excess of fluid in the interstitial or serious cavities. It can be either

an exudate or a Transudate.

Pus: A purulent exudate, is an inflammatory exudate rich in leulcocytes mostly

neutrophits, the debris of dead cells and microbes. Arterioles, capillanics, veiumics.

PMNs are destroyed by release of proteolytic enzepment Dead PMN & debric of

forms pul rate it imosreplas monocytes

Micro –S.

 Aveas of abscess

 Zone of neorotic tissue e micro-orgenine

 Chr. Inf cells lymphocytes, plasma cells & macrophages.

 If the abscess drains into oral cavity reduces intrapulpal pressme.

Questions:

1) Difference between the pulpal inflammation compared to other C.T.

CGRP  (PDL)

Neuropeptide.
 DEVELOPMENTAL ANAMOLIS OF TEETH

CONTENTS:

 Introduction

 Classification

 Disturbances in size of teeth.

 Disturbances in shape of teeth

 Disturbances in number of teeth

 Disturbances in structure of teeth

 Disturbances of growth (eruption) of teeth

 Conclusion

 Reference.
Developmental disturbances in size of teeth.

I. Microdontia

II. Macrodontia.

Microdontia

This term is used to describe teeth which are smaller than normal

Types of Microdontia.

1) True generalized Microdontia

2) Relative generalized Microdontia

3) Microdontia involving a single tooth.

True generalized Microdontia

 All the teeth are smaller than normal.

 This condition is exceedingly rare.

 Teeth are well formed, merely small.

Relative generalized Microdontia:-

 Normal or slightly smaller than normal teeth & there is an illusion of true

Microdontia.

 A person may inherif the jaw size from one parent and tooth size from the other

parent, the role of hereditary factors in producing such a condition is obvious.

Microdontia involving only a single tooth

 It is a common condition

 It affects most often the maxillary lateral incisor & the third nular.

 These 2 teeth are among those most often congenitally missing.

 The maxillary and mandibular second premolars seldom exhibit Microdontia.

 Supernumerary teeth, however, are frequently small in size.

 One of the common forms of localized Microdontia is that which affects the maxillary

lateral incisor, a condition called as ‘Peg lateral’.

 The sides converge or taper together incisally, forming a peg-shaped or cone-shaped

crown.

 The root on such a tooth is frequently shorter than usual.

 Radiological feature:- Normal but frequently it is malformed.

 Syndromes – Pituitary dwarfism

- Odonto onychial dysplasia

- Hemifacial microsomia

- Downs syndrome

- Ectodermal dysplasia.

Macrodontia
 Macrodontia refers to teeth that are larger than normal.

Types:

1) True generalized Macrodontia

2) Relative generalized Macrodontia

3) Microdontia involving a single tooth.

True generalized Macrodontia:

 The condition in e all teeth are larger than normal, has been associated e pituitary

gigantism. But is extremely rare.

Relative generalized Macrodontia:

 Is somewhat more common & a result of the presence of normal or slightly larger

than normal teeth in small jaws.

 Usually crowding is seen.

Syndrome - Hemifacial hypertrophy

- Otodental syndrome.

Macrodontia of single teeth:

 It is relatively uncommon, but is occasionally seen.

 It is of unknown etiology.

 The tooth may appear normal in every respect except for its size.
 True Macrodontia of a single tooth should not be confused e fusion of teeth in e, early

in odontogenesis, the union of two or more teeth results in a single large tooth.

Developmental Disturbances in shape of teeth:

 Gemination

 Fusion

 Concrescence

 Talon cusp

 Dens in Dente

 Dens evaginatus

 Taurodontism

 Supernumerary roots.

Gemination:

 Geminated teeth are anomalies e arise from an attempt at division of a single tooth

germ by an invagination, with resultant incomplete formation of two teeth.

 The structure is usually one two completely or incompletely separated crowns that

have a single root and root canal.

 It is seen in deciduous as well as permanent dentition.

 It is not always possible to differentiate between gemination and fusion between

normal tooth & a supernumerary tooth.

Fusion:

 Fused teeth arise through union of two normally separated tooth germs.

 Fusion may be either complete or incomplete.

 It has been thought that some physical force or pressure produces contact of the

developing teeth & their subsequent fusion.

 If this contact occurs early, at least before qualification begins, the two teeth may be

completely united to form a single large tooth.

 If the contact at teeth occurs later, when a portion of the tooth crown has completed

its formation, there may be union of the roots only.

 The tooth may have separate or fused root canals.

 The condition is common in both deciduous as wells as permanent dentition.

 Fusion may also occur between a normal tooth and a supernumerary tooth such as the

mesiodens or the distomolar.

 It levels to a reduced number of teeth in the dental arch.

Concrescence:

 Concrescence of teeth is actually a form of fusion occurs after root formation has

been completed.

 Teeth are united by cementum only.

 It is thought to arise as a result of frammatic injury or crowding of teeth resorption of

the interdental bone so that the two roots are in approximate contact and become

fused by the deposition of cementum between them.

 If may occur before or after the teeth have erupted and although it usually involves

only two teeth.

 It can be diagnosed by radiographic exam

 Failure to recognize it will result in extraction of two adjacent tooth.

 If the union is during tooth dey it is called as true concrescence. If may be due to lock

of space or dislocation of tooth germ.

 If the union & after completion of root formation the condition is called acquired.

Dilaceration:

 Dilaceration refers to an angulation, or a sharp bend or curve, in the root or crown of

a formed tooth.

 It may be due to trauma during tooth formation

 The curve or bend may occur anywhere along the length of the tooth, sometimes at

the cervical portion, at midway, at the open of the root.

 It can complicate tooth extraction.

 There may be chances of instrument breakage in the root.

Talon’s Cusp:
 It is an anomalous structure resembling an eagles talon, projects lingually from the

cingulum areas of a maxillary or mandibular permanent incisor.

 This cusp blends smoothly with the tooth except that there is a deep developmental

groove where the cusp blends the sloping lingual tooth surface.

 It is composed of normal enamel and dentin and contains a horn of pulp tissue.

 They have recommended prophylactically restoring the groove to prevent caries.

 If there is occlusal interference, it should be removed but exposure of the pulp horn,

necessiating endodontic therapy (requires endo therapy).

 It is relatively uncommon but it appears to be more prevalent in persons the

Rubinstein - Taybi syndrome (Dev. retardation, broad thumbs & great toes,

characteristic facial features).

Dens in Dente:

[Dens invaginatus, dilated composite odontome].

 It is a dev variation is thought to arise as a result of an invagination in the surface of

tooth crown before calcification has occurred.

 It may be due to

- Localized external pressure

- Focal growth retardation

- Focal growth stimulation in certain areas of tooth bud.

 The permanent man lateral incisors are the teeth most frequently involved
 The maxillary central incisors are sometimes involved.

 (If appears as an accentuation in the dev of the lingual pit).

 It is characterized by the presence of an invaginated lingual pit that extends for

rarying distance into the tooth.

 The term dense in dente originally applied to a severe invagination that gave the

appearance of a tooth within a tooth,

 Is actually a misnomer, but it has continued in usage.

 In the mild form, there is a deep invagination in the lingual pit area, may not be

evident clinically. Radiographically, it is recognized as a pear shaped invagination of

enamel & dentin I narrow contriction at the opening on ten surface of the tooth &

closely approximating the pulp in its depth.

 Food debris may become packed in this area resultant caries and infection of the pulp,

 The more severe forms of ‘dens in dente’ may exhibit an invagination that extends

nearly to the open of the root and these present radiographic picture, reflecting a

severe disturbance in the normal anatomic and morphologic structure of the teeth.

 The mild forms are more common than severe forms.

 To prevent caries, pulp infection and premature loss of the tooth, the condition must

be recognized early and the tooth prophylactically restored.

 The defect can be recognized Radiographically even before the teeth erupt.

Dens Evaginatus:
[Occlusal tuberculated premolar, leong’s premolar, evaginated odontome, occlusal

enamel pearl].

 It is a dev. condition that appears clinically as an accessory cusp or a globule of

enamel on the occlusal surface between the buceal and lingual cusps of premolars,

unilaterally or bilaterally,

 Although it has been reported to occur rarely on molars, cuspids & incisors.

 It has been thought to dev only in persons of Mongoloid ancestry, chinese, japaness,

filipinos, Eskimos & American Indians.

 The pathogenesis of the lesion is thought to be the proliferation and evagination of an

area of the inner enamel epithelium and subjacent odontogenic mesenchyme into the

dental organ during early tooth dev.

 The clinical significance of the condition is similar to that of the talon cusp, This

extra cusp may contribute to incomplete eruption, displacement of teeth & or pulp

exposure subsequent infection following occlusal was or fracture.

 It is also called as LEONG PREMOLAR.

Taurodontism:

 Taurodontism was originated by Sir Arthur Keith in 1913 to describe a peculiar dental

anomaly in the body of the tooth is enlarged at the expenses of the roots.

 The term means ‘bull like’ teeth and its usage is derived from the similarity of these

teeth to those of ungulate or cudchewing animal.

Classification of Taurodont teeth [show]

1) Hypotaurodont form

2) Mesotaurodont form

3) Hypertaurodont form  Extreme form

Causes of taurodontism [Mangion]

1) A specialized or retrograde character

2) A primitive pattern

3) A mendelian recessive trait

4) An atavistic feature

5) A mutation resulting from odontoblastic deficiency during dentinogenesis of the

roots.

 Hammer & his associates believe that the taurodont is caused by failure of Hertwing’s

epithelial sheath to invaginate at the proper horizontal level.

Clinical Features:

 It affects either the deciduous or permanent dentition, although permanent tooth

involvement is more common.

 Teeth involved are molars, sometimes only a single tooth, at other times it affects

several molars in the same quadrant.

 The condition may be unilateral or bilateral

 The teeth themselves have no remarkable or unusual morphologic clinical

characteristics.
Radiographic Features:

 The unusual nature of this condition is best visualized on the radiograph.

 Envolved teeth frequently tend to be rectangular in shape rather than taper toward the

roots

 The pulp chamber is extremely large a much greater apico-occlusal height than

normal.

 The pulp lacks the usual constriction at the cervical of the tooth & the roots are

exceedingly short.

 The bifurcation or trifurcution may be only a few millimeters above the apices of the

roots. (this condition is seen in)

 It occurs in amelogenesis imperfect, klinefelter syndrome, downs syndrome,

ectodermal dysphasia.

 It need no treatment but a problem during RCT.

 It has longitudinally entarged pulp chamber crown is normal in shape & size but body

is elongated and the roots are short.

Supernumerary Roots:

 It is a common condition & may involve any tooth.

 Teeth that are normally single rooted, particularly the mandibular bicuspide and

cuspids, often have two roots.

 Both maxillary and mandibular molars, particularly 3rd molars. Also may exhibit one

or more supernumerary roots.

 This phenomenon is of considerable significance in exodontia, for one of these toots

may be broken off during extrcution and, if unrecognized and allowed to remain in

the alveolus, may be the source of future infection.

 They are common in maxilla (90%) than mandible

 Located in between the maxillary central mesodents maxillary fourth molar & para

molar.

 In mandible it is between premolar.

 It may resemble the normal teeth or if may be conical in shape it may be on the

buccal aspect or palatal side.

Developmental Disturbances in number of teeth.

Anodontia:

 True anodontia: congenital absence of teeth. May be of two types, total and partial

 Total anodontia in

- All teeth are missing

- May involve both deciduous and permanent dentition

- This is a rare condition; when it occurs, it is frequently associated a more

generalized disturbance, ex- Hereditary ectodermal dysplasis.

Pseudo anodontia:-

 Is applied to multiple unerupted teeth

 [Hypodontia or oligodontia]

 Involves one or more teeth and is a rather common condition.

 There is a tendency for certain teeth to be missing more frequently than others.

 Frequency of missing 3rd molars is more common.

 Other teeth that are more commonly missing are maxillary lateral incisors and

maxillary or mandibular second premolars, often bilaterally

 Congenitally missing deciduous teeth are uncommon but when occurs, usually

involves the maxillary lateral incisor.

 Mandibular lateral incisors and mand cuspids may also be missing

 The etiology of missing tooth is unknown.

Ex – Hereditary ectodermal dysphasia may be associated partial anodontia.

 The teeth present may be deformed or misshapen frequently cone shaped

 Downs syndrome

 Chelio - gnatho palatoschisis, Hypodontia cleft

 Thalidomide embryopathy, Riegers syndromes.

Supernumerary Teeth:-

 A supernumerary tooth may closely resemble the teeth of the group to which it

belogs, i.e. mdars. Premolars, or anterior teeth or it may bear little resemblance in size

or shape to the teeth which it is associated.

 The theory, well supported in the literature, is the hyperactivity theory, which

suggests that supernumerles are formed as a result of local, independent, conditioned

hyperactivity of the dental lamina.

 The etiology of supernumerary teeth is not completely understood.

 Occurrence may be single or multiple, unilateral or bilateral, erupted or impacted &

in one or both jaws.

 The conditions commonly associated include

- Cleft Lip and palate

- Cleidocranial dysplasia, crowzan, sturge weber

- Gardner syndrome, Downs syndrome

- Males are affected approximately twice as frequently as females in the

permanent dentition.
Classification:

According to morphology

1) conical

2) Tuber culate

3) Supplemental

4) Odontome

Comical:

 It is small peg-shaped conical tooth

 Most commonly found in permanent dentition & usually presents as a mesidens.

 If may occasionally be found high and inverted into the palate or in a horizontal

position.

 If can result in rotation or displacement of the permanent incisor, but rarely delays

eruption.

Tuberculate:

 The tuberculate type of supernumerary possesses more than one cusp or tubercle.

 It is frequently described as barrel-shaped & may be invaginated.

 Root formation is delayed compared to that of the permanent incisors.

 T.S. are often paired and are commonly located on the palatal aspect of the central

incisors.
 They rarely erupt and are frequently associated delayed eruption of the incisors.

Supplemental:

 The supplemental S refers to duplication of teeth in the normal series and is found at

the end of a tooth series.

 The most common S.S. tooth is the permanent maxillary lateral incisor but S

premolars & molars also occur.

Odontome:

 The term ‘odontoma’ refers to any tumor of odontogenic origin.

 However this category is not universally accepted.

 The odontoma represents a hamartomatous malformation rather than a neoplasm.

 The lesion is composed of more than one type of tissue and consequently has been

called a composite odontoma.

 Two separate types have been described, the diffuse man of dental tissue is totally

disorganized is known as complex composite odontoma.

Predeciduous Dentition.

[Premature eruption, natal teeth, Neonatal teeth]

 Infants occasionally are bore e structures e appear to be erupted teeth, usually in the

mandibular incisor area.

 These structures must be distinguished from true deciduous teeth, or the so called

natal teeth e may have erupted by the time of birth.

 Predeciduous teeth have been described as hornified epithelial structures without

roots, occurring on the gingiva over the crest of the ridge e may be easily removed.

Dev. Disturbances in structure of teeth:

Amelogenesis Imperfecta:

[Hereditary enamel dysplaria, Hereditary brown enamel, Hereditary brown opalescent

teeth]

It is a structural defect of tooth enamel.

 It may be differentiated into three main groups.

1) Hypoplastic

2) Hypocalcified depending on clinical presentation of the defects

3) Hypomature & stage of enamel formation that is primarily affected.

 Witkop classification [1989]

Type I Hypoplastic

A Hypoplastic, pitted autosomal dominant

B Hypoplastic, Local autosomal dominant

C Hypoplastic, Local autosomal recessive

D Hypoplastic, Smooth autosomal dominant

E Hypoplastic, Smooth X-linked dominant

F Hypoplastic, Rough autosomal dominant

 G Enamel agenesis, autosomal recessive

Type II Hypomaturation

A Hypomaturation, pigmented autosomal recessive

B Hypomaturation, X- linked recessive

C Snow-capped teeth, autosomal dominant

Type III Hypocalcified

A Autosomal dominant

B Autosomal recessive

Type IV Hypomaturation – Hypoplastic taurodontism.

A. Hypomaturation – Hypoplastic e taurodontism atuosomal dominant

B. Hypoplastic – Hypomaturation e taurodontism autosomal dominant.

Radiographic features:-

 The overal shape of the tooth may or may not be normal, depending upon the amount

of enamel present on the tooth.

 The enamel may appear totally abscent on the radiograph, or when present, may

appear as a very thin layer chiefly over the tips of the cusps and on the interproximal

surfaces.

Histologic Features:-
 There is a disturbance in the differentiation or viability of ameloblasts in the

Hypoplastic type & this is reflected in defects in matrix formation up to and including

total absence on matrix.

 In hypocalcification types there are defects of nutrix structure & of mineral

deposition

 In the Hypomaturation types there are alterations in enamel rod and rod sheath

structures.

Treatment:

There is no except for improvement of cosmetic appearance.

ENAMEL HYPOPLASIA

Enamel hypoplasia may be defined as an incomplete or defective formation of the organic

enamel matrix of teeth.

Two basic types of enamel hypoplasia exist:

1) A hereditary type, described previously under amelogenesis imperfecta, and

2) A type caused by environmental factors.

 In the hereditary type, both the deciduous and permanent dentitions usually are

involved and generally only the enamel is affected.

 In contrast, when the defect is caused by environmental factors, either dentition may

be envolved and sometimes only a single tooth. Both enamel and dentin are usually

affected, at least to some degree.

 A number of different factors, may give rise to this condition, they are,
1) Nutritional deficiency

(Vit A, C and D)

2) Exanthematous diseases

Eg. Measles, chicken pox, scarlet fever,

3) Congenital syphilis

4) Hypocalcemia.

5) Birth injury, prematurity, Rh hemolytic disease

6) Local infection or trauma.

7) Ingestion of chemicals (chiefly fluoride); and

8) Idiopathic causes

 In mild environmental hypoplasia, there may be only a few small grooves, pits, or

tissures on the enamel surface.

 If the condition is more severe, the enamel may exhibit rows of deep pits arranged

horizontally across the surface of the tooth.

 In the most severe cases, a considerable portion of enamel may be absent, suggesting

a prolonged disturbance in the function of the ameloblasts.

 Hypoplasia results only if the enjury occurs during the time the teeth are developing,

or more specifically, during the formative stage of enamel development.

 Once the enamel has calcified, no such defect can be produced.

 Thus knowing the chronologic development of the deciduous and permanent teeth, it

is possible to determine from the location of the defect on the teeth the approximate

time at which the enjury occurred.

Hypoplasia Due to Nutritional Deficiency and Exanthematous Feverss:

 Rickets during the time of tooth formation is the deficencies of Vit A & C also cause

E.H.

 The most common cause of E.H.

 Some studies have indicated that the enanthematous diseases, including measles,

chickenpox and scarlet fever are etiologic factors.

 In general, it might be stated that any serious nutritional deficiency or systemic

disease is potentially capable of producing enamel hypoplasia.

 It is characterized by pitting of the surface.

Clinical Studies:

 Most cases of enamle H. involve those teeth that form which in the first year after

birth, although teeth that form somewhat later may be affected.

 The most frequently involved are the central& lateral incisors, cuspids and first

molars.

 There has been considerable controversy as to whether there is any relation between

enamel and dental caries experience.

Enamel Hypoplasta due to congenital syphilis:

 It is most frequently not of the pitting variety almost pathognomonic appearances.

 It involves the maxillary and mandibular permanent incisors and the first molars.

 The anterior teeth affected are (sometimes) called ‘Hutchinosons teeth’, while the

molars have been referred to as mulberry molars (Moons molars, Fournier’s molars).

 Characteristically, the upper central incisor is ‘Screw-Driver’ shaped, the mesial and

distal surfaces of the crown tapering and converging toward the incisal edge of the

tooth rather than toward the cervical margin.

 In addition, the incisal edge is usually notched.

 The mandibular central and lateral incisors may be similarly involved, although the

manillary lateral incisor may be normal.

 The cause of the tapening and notching of the maxillary incisor has been explained on

the bases of the absences of the central tubercle or calcification center.

 The crowns of the first molars in congenital syphilis are irregular and the enamel of

the occlusal surface and occlusal third of the tooth appears to be arranged in an

agglomevate mass of globules rather than in well-formed cusps.

 The crown is narrower on the occlusal surfaces than at the cervical margin.

Enamel hypoplasia due to hypocalcemia:

 Tetany, induced by a decreased level of calcium in the blood.

 It may result from several conditions, the most common being Vitamin D deficiency

and parathyroid deficiency (Parathyroprivic tetany).

 In tetany the serum calcium level may fall as low as 6-8mg per 100 ml and at this

level E.H is frequently produced in teeth.

 This type of enamel it is usually of the pitting variety and thus does not differ from

that resulting from a nutritional disturbance or exanthe ematous disease.

Hypoplasia due to birth enjuries:

 The monatal line or ring, described by Schour in 1936 and present in deciduous teeth

and first permanent molars.

 A disturabance indicative of the trauma or change of environment at the time of birth.

 In traumatic births the formation of enamel may even ease at this time.

 Miller & forrester reported that E.H is move common in prematurely born children

than in normal term infants.

Enamel hypoplasia due to local infection/trauma:

 It is a type of Hypoplasia occasionally seen.

 Is unusual in that only a single tooth is involved.

 Most commonly one of the permanent maxillary incisors or a maxillary or mandibular

premolar.

 There may be any degree of hypoplasia ranging from a mild, brownish discoloration

of the enamel to a severe pitting and irregularity of the tooth crown.

 These single teeth are frequently referred to as Turner’s teeth, and the condition is

called Turner’s hypoplasia.

 If a deciduous tooth becomes carious during the period when the crown of the

succeeding permanent tooth is being formed, a bacterial infection involving the

periapical tissue of this deciduous tooth may disturb the ameloblastic layer of the

permanent tooth and result in a hypoplastic crown.

 The severity of this hypoplasia will depend upon the severity of the infection, the

degree of tissue involvement, and the stage of permanent tooth formation during with

the infection occurred.

 A similar type of H may fallow trauma to a deciduous tooth, particularly when the

deciduous tooth has been driven into the alveolus and has disturbed the permanent

tooth bud. If this permanent tooth crown is still being formed the resulting injury

may be manifested as a yellowish or brownish stain or pigmentation of the

hypoplastic pitting defect or deformity.

 The disturbance may be either matrix formation or in calcification, depending upon

the stage of tooth formation at the time of injury.

E. H. Due to Fluoride:

Mottled Enamel:

 M.E. is a type of enamel hypoplasia that was first described by G.V. black &

Frederick S. Mckay in 1916.

 They suggested that it was a result of some substance in the water supply, later it was

shown that fluorine was the causative agent.

Etiology:

 Ingestion of fluoride – Containing drinking water during the time of tooth formation

may result in mottled enamel.

 The severity of mottling increases with an increasing amount of fluoride in the water.

 Mottling because progressively evident above the level of 0.9 – 1.0 part per million.

Pathogenesis :

 This type of Hypoplasia is due to a disturbance of the ameloblasts during the

formative stage of tooth development.

 The exact nature of the injury is not known, but since there is histologic evidence of

cell damage.

 It is likely that the enamel matrix, is defective or deficient.

 With higher levels of fluoride there is interference with the calcification process of

the matrix.

Clinical features:

 Depending upon the level of fluoride in the water supply, there is a wide range of

severity in the appearance of mottled teeth, varying from

1) Questionable changes characterized by occasional white flecking or spotting of

the enamel.

2) Mild changes manifested by white opaque areas involving more of the tooth

surface.
 3) Moderate and severe changes showing pitting a corroded appearance of the teeth

and brownish staining of the surface.

4) Those teeth with are moderately or severely affected may show a tendency for

wear and even of the enamel.

5) It is difficult to retain the restoration in such teeth.

Geographic Distribution:

 M.E. has been reported in many parts of the world, including Europe, Africa & Asia

as well as the united states. West & East of Mississippi River (Texas Pinhandle).

Treatment:

 For cosmetic reasons, it has become the practice to bleach the affected teeth with an

agent such as hydrogen peroxide.

 This is frequently effective, but the produce must be carried out periodically, since the

teeth continue to stain.

Hypoplasia Due to Ediopathic Factors:

 Clinical studies have shown that, even with careful histories, the majority of cases are

of unknown origin.

 Since the ameloblast is a sensitive type of cell and easily damaged, it is likely that in

those cases in which the etiology cannot be determined, the causative agent may have

beeeeen some elluess or systemic disturbance so mild that it made no impression on

the patient.

Dentinogenesis Imperfecta:
 This is an autosomal dominant condition.

 Affects both deciduous and permanent teeth

 Affected teeth are gray to yellowish – brown and have broad crowns with constriction

of the cervical area resulting in a ‘tulip’ shape.

 Radiographically, the teeth appear solid, lacking pulp chambers and root canals.

 Enamel is easily broken leading ot exposure of dentin that undergoes accelerated

attrition.

 The gene maps to chromosome H. It encodes a protein called dentin

sialophosphoprotein (DSPP).

 This protein constitutes about 50% of the noncollagenous component of dentin

matrix.

 It is not known how the mutant protein causes near obliteration of the pulp.

Shields:

Classification : ( Revised)

1) Dentinogenesis Imperfecta 1 :

Dentinogenesis Imperfecta without osteogenesis imperfecta (opalescent dentin). This

corresponds to dentinogenesis imperfecta type II of shields classification.

2) Dentinogenesis Imperfecta 2 :

Brandy wine type dentinogeneses imperfecta : This corresponds to DI type III of

sheild’s classification.
 It is characterized by too little rather than too much dentin resulting in ‘shell teeth’.

Dentinogenesis Imperfecta 1 :

[Opalescent dentin, DI without osteogenesis imperfecta, opalescent teeth without O.I

shields type II capdepont teeth.]

 Dentinogenesis Imperfecta 1 is caused by mutation in the DSPP gene encoding

dentin phosphoprotein and dentin sialoprotein.

 Dentinogenesis Imperfecta is an entity clearly distinct from O.I with opalesent teeth

and affects only the teeth.

 There is no increased frequency of bone with in this disorder.

 The teeth are blue-gray or amber brown and opalescent.

 On dental radiographs, the teeth have bulbous crown, roots that are narrower than

normal, and pulp chamber and root canals that are smaller than normal or completely

obliterated.

 The enamel may split readily from the denting when subjected to occlusal stress.

 A deficiency of dentin sialophospho protein had been suggested as a causative factor

in Dentinogenesis Imperfecta.

 Affected members in three generations showed discoloration and sever attrition of

their teeth, with obliterate pulp chambers.

Dentinogenesis Imperfecta 2

(Shields type III, Brandy wine type Dentinogenesis Imperfecta)

 This disorder was found in the brandy wine triracial isolate in southern Muryland.

 The crowns of deciduous and permanent teeth wear rapidly after eruption and

multiple pulp exposures may occur.

 The dentin is amber and smooth.

 Radiographs of the deciduous dentition shows very large pulp chambers and root

canals, at least during first few years although they may become reduced in size with

age.

 The permanent teeth have pulpal spaces that are either smaller than normal or

completely obliterated.

 Patients with the Brandy wine type, do not have stigmata of osteogenesis imperfecta.

 Recent studies are consistent with the hypothesis that DGI-1 and DGI-2 are allelic or

the result of mutations.

 DGR-2 can differ from DGE1 by the pressure of multiple pulp exposures.

 Normal nonmineralized pulp chambers, and canals and a general appearance of ‘Shell

teeth’.