BIOLOGICAL CONSIDERATION IN OPERATIVE DENTISTRYSARANG SURESH HOTCHANDANIDentist @ Bibi Aseefa Dental College, SMBBMU.Larkana, Sindh, Pakistan

2

Contents •Enamel

•Dentine

•Pulp

•Gingiva

3

ENAMEL

4

Enamel Functions

• Provide the shape & hard, outer covering for teeth.

• Protect underlying dentine & pulp.

• Esthetics provided by enamel’s color & form.

5

Enamel • When enamel is exposed to an oral environment of occlusal, chemical and bacterial challenges, its crystalline mineral makeup and rigidity is damaged from acid demineralization, attrition & fracture.

• Repair or replacement of enamel can only be accomplished through dental therapy.

6

Enamel Permeability

• Inorganic hydroxyapatite– 96% by weight – More than 86% by volume

• Small volume of organic matrix

• Water – 4 – 12 % by volume– Water is contained in network of micro pores,

which open into external surface of oral cavity in inter-crystalline spaces of enamel.

– This network provides connection b/w oral cavity & dentinal fluid & pulp interstitial space.

7

Enamel Permeability

• Enamel is semipermeable– That’s why various fluids, pigments, ions, LMW

substances acid demineralization, remineralization, fluoride uptake & vital bleaching is possible in enamel.

• CLINICAL POINT– When teeth become dehydrated from;

• Nocturnal mouth breathing during sleep OR• Rubber dam isolation

– Then enamel appears chalky & lighter in color, it is reversible when enamel become wet again.

– That’s why shade matching should be determined with full spectrum of light before isolation with rubber dam.

8

Effects of Aging on

Permeability of Enamel

• Color (hue) is increased or intensified

• Following things in enamel decreases with aging.– Acid solubility of enamel– Pore volume – Water content – Permeability

9

Clinical Appearanc

e & Defects

• Key diagnostic signs on enamel includes; – color changes, – white spots, – plaque, – crake, – craze lines, – demineralization, – erosion/abrasion, – attrition, – restoration margin integrity.

10

Color • Enamel translucency (clearness) is directly proportional to degree of mineralization.

• COLOR OF ENAMEL DEPENDS UPON;– Thickness of enamel

• 2.5 mm at cusp tips & 2.0 mm at incisal edges• Thickness decreases below deep occlusal

fissures and tapers to become very thin in the cervical area near CEJ

• Young anterior teeth have translucent grey or slightly bluish hue (shade/color) near the incisal edge

• Yellow – orange shade predominates cervical because of thin enamel present from which color of underlying dentine is visible.

– Color of underlying dentine

11

Color • In about 10% of teeth, a gap b/w enamel & cementum in cervical area is present which exposes vital and highly sensitive dentine.

• Natural color of enamel can be altered by;– Anomalies of development & mineralization– Extrinsic stains– Antibiotic therapy– Excessive fluoride– Dental caries

• White spot lesion

12

White Spot Lesion

• It is early caries lesion characterized by subsurface enamel porosity result from demineralization caused by few streptococci mutans within biofilm.

• Clinically appear as milky white opacity after air drying of enamel.

• When this subsurface demineralization reaches DEJ, this white spot opacity become visible not only with air drying but also when it is we with saliva.

13

White Spot Lesion

• Early fissure caries lesions are difficult to be visualized on bitewing radiographs but can be assessed by visually examining discoloration enamel around pits & fissures.

• It takes 4 to 5 years for this white spot lesion demineralization to progress through enamel.

• When the caries involves dentine, the clinical sign which indicate dentine involvement is;– Blue or grey shade of enamel

• Invasive restorative procedures should only be considered when;– Caries is extended to dentine confirmed by above

mentioned clinical sign of discoloration– Enamel is cavited into dentine– Caries is visualized on radiographs

• If these above mentioned conditions are not present preventive measures can be applied.

14

Cavitation• Smooth surface enamel caries lesion

when seen in two dimensions, as in radiographs, it appears triangular with the base of triangle at the enamel surface. While in three-dimension view, smooth surface lesion is cone shaped with base at enamel surface and apex of cone at DEJ.

• The shape of pit and fissure enamel caries is complex, because it occurs simultaneously at confluence of two or more cuspal lobes.– In two dimension, fissure caries has also

triangular shape with base towards & parallel to DEJ and apex in pit or fissure.

15

Cavitation• Unless, preventive

measures or remineralization reverse the process of demineralization, the dentine is compromised and can no longer support the enamel which result in development of cavity.– Untreated cavity will lead

to;• Compromise crown & strength

of tooth.• Jeopardize the vitality of pulp

due to active proliferation of bacteria.

16

Enamel Wear

• Enamel is as hard as steel.– Knoop hardness number of enamel is 343– Knoop hardness number of dentine is 68

• Wear of enamel occur because of following reasons;– Attrition– Frictional contact against opposing enamel or

restorative material – Bruxism – Erosion – Malocclusion – Age – Other parafunctional habits– Hard diet– Compromised occlusal function

• In preparing tooth for restoration, outline form should have designed in such a way that the margins of restorative material avoid critical high stress areas of occlusal contacts.

17

Enamel Wear

• Normal physiologic wear rate for enamel is 15 – 29 micrometer per year.

• Tooth wear causes loss of vertical dimension of tooth structure.– This can be counteracted by

active tooth eruption & apical cementogenesis.

18

Enamel Faults & Fissures

• Faults as named below are defects of enamel surface which contribute to the accumulation and retention of plaque.– Perikymata (parallel ridges

formed by cyclic deposition of enamel)

– Pitting defects (formed by termination of enamel rods)

– Hypoplastic areas– Linear defects or craze line

19

Enamel Faults & Fissures

• Fissure is formed by incomplete fusion of lobes of cuspal enamel in the tooth.– Fissures provide the protected niche for

acidogenic bacteria and the nutrients they require for caries development.

• Caries lesions are 5 times more to occur on occlusal fissures than on the facial or lingual fissures.– Caries lesions are 2.5 times more to

occur on facial or lingual fissures than on proximal surfaces.

• Resin fissure sealant is effective preventive method for this caries.

20

Enamel Cracks

• A cracked tooth that is symptomatic or involves dentine requires following treatment;– Crown – Splinting

21

Rod & Interrod Crystal

Structure

• The carbonated component in the hydroxyapatite crystal;– Produce destabilizing effect on the

crystal – Most susceptible to demineralization

and the first to be solubilized.

• in the presence of fluoride, enamel crystals are replaced with Fluorapatite or fluorohydroxyapatite which is relatively insoluble.

22

Rod & Interrod Crystal

Structure

• Ameloblasts cytoplasmic extension named tomes’ process;– Secret enamel protein matrix – Initiate the mineralization – Orient the enamel crystal

• After orientation of enamel crystals two structural units of enamel are formed;– Cylindrical enamel rods – Inter rod enamel

• The matrix protein enamelin and water forms the envelop of crystal.

23

Rod & Interrod Crystal

Structure

• Enamel rods and inter rod enamel differs only in orientation of crystals.– Inter rod crystals are perpendicular to

enamel rod crystals.– Crystals in the enamel rods are parallel

to long axis of rods, while rods are perpendicular to enamel surface.• Enamel rods are separated by rods sheaths

which is composed of organic material.

• Hydroxyapatite crystal is hexagonal in shape with cross sectional dimension of;– 30 x 60 nanometer

24

Hunter – Schreger

bands These are alternative light and dark bands in the enamel seen under magnification in cut or fractured sections of tooth structure.This occurs because of variation of light reflection from the bands of the enamel crystals that are oriented in different directions.

25

Enamel & Acid

Etching

• Initially, acid etchant removes about 10 micros – meter of surface enamel which does not contain any rod structure.

• After removal of this, rods & inter – rods of enamel are exposed.– Dissolution of this rod & inter – rod

creates macro – porosity.

• The acid etched enamel surface has high surface energy so that resin flows into and polymerize within the resin tags into pores up to depth of 20 micrometers.

26

How Micro porosity is Created in

Enamel Etching???

• As you know crystals in the enamel rod run parallel to length of enamel rods & enamel rods always run perpendicular to tooth surface– So, the rods which are present in

that wall which is perpendicular to tooth surface will expose the sides of rods & their crystals during acid etching & while those rods which are present in that wall which is parallel to surface will expose the transverse section or face of crystals and create micro – porosities in the core of these rods.

27

How Micro porosity is Created in

Enamel Etching???

• In these micro – porosities micro tags are formed.– It is these mini tags which are

formed within individual crystal core contribute the bond strength in enamel – resin bond.• There are about 30,000 – 40,000

enamel rods per millimeter of enamel and etching increases the surface area 10 – 20 folds

• That’s why beveling is done in composite restoration to expose the face of rods and increase the bonding.

28

Enamel Strength & Resilience

• Enamel demineralization is much slower than dentine because, apatite crystals in enamel are 10 times larger than dentine crystals.

• Enamel rods are in spiral shaped at cusp tips.– If the enamel were uniformly

crystalline, it would shatter with occlusal function.

29

DENTINE

30

Dentine Functions

• Provide color & elastic foundation for enamel.

• Form bulk of the tooth.• Provide strength & durability to

crown of tooth.• Protective barrier & chamber for

the vital pulp tissues.• Does not have any vasculature or

innervation.• Respond to external thermal,

chemical or mechanical stimuli

31

Dentino Enamel Junction

(DEJ)

• It is a transitional area demarcating the junction of enamel & dentine.

• The width/ thickness of DEJ range from 2 – 15 micrometers.– Width of DEJ is different in

different locations of teeth.

32

Dentino Enamel Junction

(DEJ)

• DEJ is scalloped with wave – like crests pointing outward toward enamel.– This scalloping provides the strength

b/w enamel & dentine.– Scalloping is larger in posterior teeth.

• The part of dentine which is present in DEJ is soft & is mantle layer of dentine.– This layer of dentine is called as SOFT

ZONE.– This soft zone provides cushioning soft layer

b/w enamel & dentine.

33

Dentine Support

• Maximum bite force is 738 N (166lb)

• Resistance to tooth fracture is compromised with increasing depth and/or width of cavity.

• Endodontically treated tooth retain only 1/3 of the fracture resistance of normal intact tooth.

• In MOD coronal stiffness decrease more than 60% of normal tooth.

• So, try to conserve the tooth structure during preparation.

34

Morphology of

Dentine

• Dentine is composed of small, thin apatite flakes of crystals embedded in a collagen matrix.– Thickness of apatite crystals near

DEJ is 3.5 mm while, near pulp they are approx. 2 mm in thickness.

– usually, these crystals are randomly oriented but they are parallel to each other at cusps.

• Matrix formation & mineralization is controlled by odontoblasts.

35

Morphology of

Dentine

• Thickness of dentine from pulp chamber to DEJ is about 3.0 to 3.5 mm.

• Diameter of dentinal tubule– 2.5 micrometers near pulp– 0.8 micrometers near DEJ

• Tubules comprise 10% of dentinal volume.

36

Morphology of

Dentine

• Dentinal tubules follow “S – shaped” curve in axial areas of teeth while;– Dentinal tubules are straight in

the occlusal areas & root areas.

• Odontoblastic process extends within dentinal tubule to about 1/3rd of dentinal thickness.

37

Morphology of

Dentine

• Dentine is;– 45% - 50% inorganic apatite – 30% organic matrix– 25% water– Pale yellow in color– Harder than bone

• Dentine is of two types;– Inter-tubular dentine

• Forms bulk of dentine– Peritubular dentine

• Present only in lining of tubule walls

38

Dentine Permeabilit

y

• When external covering of teeth; enamel & cementum is removed due to following mentioned reasons, the exposed dentinal tubules become conduits b/w the pulp and external oral environment.– Cavity preparation – Root planning– Caries– Trauma– Abrasion – Erosion

• Exposure of dentinal tubules is compensated by smear layer.– Removal of smear layer leads to;

• Increased permeability of dentinal tubules.• Outward flow of dentinal fluid.

39

Dentine Permeabilit

y

• Outward flow of dentinal fluid occurs in response to following effects which are caused by injury to dentine during above mentioned process.– Pulpal vasodilation– Increased pulpal blood flow– Increased interstitial fluid pressure

• In vitro studies shown that outward flow of dentinal fluid decreases the inward permeability of toxic substances by 50% - 60%.– Also, during outward flow, dentinal fluid also

contains albumin & other immunoglobulins which provide immune response to bacteria and prevent their inward flow to pulp.

40

Dentine Permeabilit

y

• Prevention of inward permeability can also be achieved by;– Blockage of dentinal tubules.

• Another method of preventing inward diffusion of exogenous products in exposed pulp is presence of greater amount of remaining dentine thickness (RDT)– Remaining dentine thickness

represents small dentinal tubule diameter and greater tubules length.

41

Dentinal Tubule

Diameter & Dentine

Permeability

• Small constricted diameter prevents the movement of exogenous products

• Functional diameter of dentinal tubule is much smaller than the anatomic diameter. And bacteria are unable to pass through this functional diameter of tubule.

• Anatomic diameter; overall lumen of dentinal tubule.

• Functional diameter; dentinal tubule is filled with cellular, collagenous and mineral particles, so empty space which is left after these materials is functional diameter of tubule.

42

Dentinal Tubule

Diameter & Dentine

Permeability

• The coronal occlusal dentine (pulpal floor of cavity) is less permeable than dentine around pulp horn or axial surface.

• In restored teeth diffusion of toxic material through dentinal tubules can occur via a process of micro leakage.– Micro leakage occurs due to;

• Polymerization shrinkage• Condensation gaps around restorative

material.• Differences in thermal expansions.

43

Dentinal Tubule

Diameter & Dentine

Permeability

• This micro leakage can lead to;– Marginal staining– Sensitivity – Chronic pulpitis

• Without treatment loss of tooth structure can occur.– If the stimuli are moderate and slow then

defensive reactions of dentine occur as mentioned below.• Hyper mineralization or sclerosis of

dentinal tubules.• Formation of tertiary dentine

44

Dentinal Substrates

• Variation in the form & composition of dentine occurs throughout the life of tooth. Which result from;– Natural developmental or aging

process– External factors;

• Caries, injury, wear etc.

• Reason for studying this dentinal tissue variation;– To evaluate the long – term success of

dental procedures or therapies.

45

Dentinal Substrates Physiologic Dentine

• Outer Dentine• Inner Dentine

Carious Dentine

Altered Dentine• Sclerotic Dentine• Hyper mineralized Dentine

46

Primary & Secondary Physiologic

Dentine

• Dentine which is formed from before physiologic apexification of maturation of tooth is called as primary dentine.– Mantle dentine; it is primary dentine near

DEJ.• It is 150 micrometers thick• 4% less mineralized than circumpulpal dentine.• Unlike circumpulpal dentine, collagen fibers in

this dentine are arranged perpendicular to DEJ– Circumpulpal dentine; primary bulk

dentine except mantle dentine, which surround the pulp chamber and canal.• It is formed at a rate of 4 – 8 micrometers per

day and after apex closure, its formation declines and secondary dentine begin to form.

47

Primary & Secondary Physiologic

Dentine

• Secondary dentine is laid gradually and asymmetrically and leads to;– Decrease in dimension of pulp chamber &

canal.• Occluso – gingival decrease in dimension is

more frequent.

• With reduction in size of pulp chamber & root, the risk of pulp exposure is decreased with aging.

• That’s why always evaluate radiographically size of pulpal tissue in relation to size or location of caries in order to assess the need for indirect or direct pulp exposure.

48

Outer Dentine

• It is the dentine which is present in the periphery near DEJ.

• Dentinal tubules in this are far apart and have narrow lumen due to continued & excessive deposition of peri – tubular & inter – tubular dentine.

• Number of tubules in outer dentine is approx. 20,000 tubules/mm2.

– Diameter of lumen in outer dentine about 0.8 micrometers.

– This lumen constitutes about 4% surface area in outer dentine.

49

Dentine

Dentin near the DEJ (outer) and near the pulp (inner) are compared to show relative differences in intertubular and peritubular dentin and in lumen spacing and volume.

50

Outer Dentine

• Dentinal tubule also has got interconnecting branches in outer dentine.

• So, the reason for learning this is that; cavity preparation or caries lesions which are confined to outer dentine do not directly damage the odontoblastic process because odontoblastic process extends no farther than the inner 3rd of adult dentine.

• Cavity preparation or lesions in outer dentine with remaining dentine thickness of about 2 mm or more provides sufficient physiologic barrier to protect the pulp.– However, there is an exception in case of crown

preparation. • Although crown preparation if occurring in near outer dentine

can damage the pulp due to heat generated without cooling.

51

Inner Dentine

• It is dentine near pulp

• Thickness of Predentine; 20 micrometers.– It consists of newly secreted organic

matrix which is waiting to be mineralized.

• Number of tubules in inner dentine are approx. 58,000/mm2. And contain odontoblastic process.

• So try to carefully prepare tooth to avoid damage to odontoblastic process

52

Inner Dentine

• Tubule diameter are about 2.5 – 3.0 micrometers.– Peritubular dentine is very small or absent in inner

dentine.– Tubules are very close in inner dentine as shown in

above pic.– Area occupied by inter – tubular dentine is about 12% – Tubule lumen constitute about 80% of surface area in

inner dentine.

• Inner dentine is about 22x times more permeable & cause wetness after tooth preparation than outer dentine.

• Fluid in tubule is extension of fluid from pulp and has pressure of about 5 – 20 mmHg.– So deeper the cavity more the wetness. ;)

53

Carious Dentine

• Progressive destructive changes in non – intervened caries process;– Subsurface demineralization – Dentinal demineralization– Cavitation – Infection of demineralized

dentine– Dentine matrix dissolution – Pulp necrosis

54

Carious Dentine

• Initial response of dentine in an incipient, non – Cavitated enamel;– Very initially, Hyper mineralization of peritubular

dentine which are subjacent to those enamel rods which have been dissolved due to acid. • Increased permeability of these rods stimulate this

response from dentine.– Demineralization of dentine result when acid

reach at DEJ.• Demineralization in dentine is more rapid because

of;– Tubular network

• High surface to volume ratio of hydroxyapatite crystals embedded into collagen.

55

Carious Dentine

• Clinically affected dentine is distinguished from normal dentine by;

• Decreased hardness • Yellow – brown discoloration

– Discoloration is due to acid effect on organic matrix or exogenous staining.

• However, at this stage dentine lesion is sterile because of intact enamel.– This type of lesion can be arrested

with plaque control or other non – invasive preventive therapy.

56

Carious Dentine

• When the enamel surface become Cavitated, a pathologic cycle of tooth destruction, infection and tubular invasion of dentine structure occurs.– Demineralization of peritubular walls and

intertubular crystals occurs.– Proteolytic destruction of collagen of dentine.

• Infected dentine is soft, readily excavated, wet & generally light yellow to orange color.– Below this infected dentine, lies affected

dentine which contain intact dentine matrix and is invaded by a very few microorganisms.

57

Carious Dentine

• Bacterial fill and demineralize the lumens of tubules peripherally, but dissolved minerals repercipitate at deeper levels stimulate the sclerosis of dentine below caries.

• Reparative dentine with irregular tubules forms a final obstruction against caries bacteria and their metabolites.

• After cavitation and dentinal infection, restorative treatment is necessary to remove the infected dentine and restore the integrity of coronal surface.

58

Carious Dentine

Bacterial fill and demineralize the lumens of tubules peripherally, but dissolved minerals repercipitate at deeper levels stimulate the sclerosis of dentine below caries.

Reparative dentine with irregular tubules forms a final obstruction against caries bacteria and their metabolites.

After cavitation and dentinal infection, restorative treatment is necessary to remove the infected dentine and restore the integrity of coronal surface.

59

Altered Dentine

• Alteration in dentine morphology occurs due to;– Aging process – Localized defensive and repair responses to injury

from caries, trauma etc.

• Hard tissue defensive and repair responses, which restrict the tubular diffusion of noxious agents.– Dentinal tubule hyper mineralization– Sclerosis– Tertiary dentine formation

• Pulpal defensive and repair responses;– Activation of odontoblastic and sub odontoblastic

cells.– Proliferation of vascular & neural tissues– Initiation of immune response & inflammation.

60

Sclerotic Dentine

• It is characterized by blockage of the tubules with whitelockit crystals and by a denatured collagen network.

• Usually form in Non-carious lesions of tooth;– Abrasion– Attrition – Erosion– Occlusal stress

• Exposed dentine in non-carious lesion appear;– Deep yellow in color– Transparent glossy surface– Sensitive to touch

• Sclerosis occur in those tubules which are exposed due to non – carious lesions.

61

Hyper Mineralized Dentine

• Secondary dentine produced throughout life of teeth cause increase in thickness of peritubular walls subsequently narrowing of dentinal tubules, resulting decreased permeability.

• Secondary dentine in physiologic condition deposits very slowly, but the process accelerated during injury to tooth.

62

Hyper Mineralized Dentine

• During acidic environment, minerals are released into acid which gets supersaturated with mineral crystals, if the buffering of acid occur then these minerals repercipitate in tubules and mineralize it and block the diffusion of noxious products.

• The combination of peritubular wall thickness and intra – tubular crystals creates a zone of hyper mineralized dentine beneath carious dentine or exposed dentine.

• Sclerosis and hyper mineralization of dentine depends on;– Rate of caries lesion– Age

63

Tertiary Dentine

• It is newly formed dentine which is formed at pulpal dentine interface and provide the pulpal seal against noxious diffusion through dentinal tubules.

• There are two types of tertiary dentine;– Reactionary tertiary dentine– Reparative tertiary dentine

64

Reactionary Tertiary

Dentine

• It is formed in low grade damage to enamel.– Incipient caries– Non Cavitated lesion

• Formed from already present odontoblasts.

• It may tubular or atubular – It is tubular in mild slow progressing caries lesion

and also resemble with natural secondary dentine.

• In this dentine, tubules are continuous with natural already present secondary dentine.

65

Reparative Tertiary Dentine

• It is formed from newly formed odontoblast like cells generated from stem cell of pulp.

• The formation of these new odontoblast like cells take about 20 – 40 days.

• The tubules in the reparative dentine is less regular (atubular) and not continuous with those of overlying already present secondary dentine.

• Matrix formed during reparative dentine formation is called as interface dentine.

66

Tertiary Dentine

• Both of these reparative or reactionary dentine can form below the same caries lesion.

• However, this type of defense system depends on;– Increased vascularity

– Immune response

– Inflammation

• Now question arises, from where signals for these responses arrives.– Any trauma to dentine pulp complex from caries or

restorative treatment leads to release of growth factors & molecular signals which are embedded in the dentine or pulp and in result these factors stimulate the stem cells to produce these defense responses.

– Example of factors;• Bone morphogenetic factor• Transforming growth factor beta• Etc.

67

Dentine Sensitivity

• Dentine does not have blood or nerve supply.– Only in about 20% tubules in which

nerve fiber from pulp are penetrating not more than few microns.

• The odontoblastic process also does not extend beyond the inner dentine.

• Cell membranes, cell bodies, & process of odontoblastic cells are also nonconductive.

68

Dentine Sensitivity

• There is no any synaptic connection b/w odontoblast cells and terminal branches of pulp nerves.

• When anesthesia is applied on dentine still pain occurs. Or when odontoblastic layer is disrupted, pain still occurs.

69

Mechanism of Dentine Sensitivity

• Theory is given based on capillary flow dynamic of fluid filled dentinal tubules.

• According to this theory, outward flow dentinal fluid caused by various stimuli displaces the odontoblasts which touch the terminal branches of nerves in the pulp and this touching generates action potential in these nerves.

70

Treatment of Dentine Sensitivity

• So, this sensitivity can be removed by blocking the dentinal tubules so that fluid movement does not occur. This blockage can be accomplished by;– Oxalates, strontium chloride which

are present in tooth pastes.– Other materials which reduce

dentine sensitivity;• Potassium nitrate• Resin glutaraldehyde• Fluoride varnish

– Resin bonding agents

71

DENTAL PULP

72

Dental Pulp

• It is viscous C.T of collagen fibers & organic ground substance supporting the vital cellular, vascular & nerve structure of tooth.

• Composed of;– 75% water– 25% organic material

• No collateral vessels and space for expansion during inflammation.

• Blood is supplied only through apical foramina

73

Functions of Dental

Pulp

• Formative (dentinogenesis)– Primary, secondary & tertiary dentine

• Nutritive – Vascular supply and ground substance for maintenance

of cells of organic matrix.

• Sensory – Nociception/ pain sensation

• Protective – Inflammation, antigenic, neurogenic & dentinogenic

response to injury.– Homeostasis & clearance of noxious substances

through vascular & lymphatic system.

74

Morphology of Dental Pulp

Pulpal histology. Odontoblast cell layer contain immunocompetent dendritic cells,

cell-free zone contains both nerve and capillary plexuses,

cell-rich zone contains fibroblasts and undifferentiated cells, and pulp core.

75

Dental Pulp

core of the pulp is ground substance, which contain pulpal cells, blood vessels & nerves of pulp.In the pulp, collagen fibers are not organized but they are dispersed here & there.

Proportion of collagen increases with age.

76

Pulpal Cells (odontoblast

s)

• Present on outer periphery of pulp.

• They produce & adapt the dentine matrix.– Provide active transport of calcium ions.

• They synthesize collagenous, non-collagenous protein & various growth factors and signaling molecules.

• When they are active; they become large and columnar. While during inactive stage, they become small & flattened.

• These odontoblasts are interconnected by tight or gapped junction.

77

Pulpal Cells (Fibroblasts)

• Most numerous pulpal cells.– Produce, maintain and remodel

pulp matrix and collagen.– Present mostly in cell rich zone.

• Immunocompetent cells– They include macrophages,

lymphocytes & dendritic cells.– Function as host defense

78

Vascular System of

Pulp

• The presence of lymphatic system in the normal pulp is controversial;– Some say that lymphatic vessels are not present in

healthy pulp but they develop during pulpal inflammation.

– While, some say that interstitial fluid of pulp is drained via non endothelialized interstitial channels and exit the tooth through apical foramina.

• The equilibrium b/w diffusion & clearance of products may be temporarily ceased by use of long acting anesthetic agents containing vasoconstrictors. – However, no permanent changes in the pulp occur

due to ischemia because low respiratory requirements of pulp.

79

Vascular System of

Pulp

• During inflammation, blood flow & capillary permeability is increased.– This capillary permeability leads to

edema & increase in the interstitial fluid pressure.

– However, this edema & increased interstitial fluid pressure is confined to inflamed area only because of presence of following features in pulp;• Numerous arterioles • Reverse flow loops of vessels• Arteriole – Venules anastomosis/shunts

80

Vascular System of

Pulp

• This pulpal inflammation, (increased fluid pressures) causes outward flow of dentin tubular fluid.

• The pulpal inflammation also induce hyperalgesia (increased sensitivity due to lowering of threshold of pulpal nerves)

81

Pulpal Innervation

• Pain does not affect the vitality of pulp but it is the inflammation which affect the vitality of pulp.– You can say pulp is non-vital on the basis of

presence of pain in tooth.

• Primary innervation of pulp is from Sensory (afferent) axons whose cells bodies lie in trigeminal ganglion.

• Sympathetic (efferent) axons with nuclei in cervical sympathetic ganglion are also present.– Produce vasoconstriction on activation

82

Pulpal Innervation

• Most sensory interdental nerves are A delta or unmyelinated C fibers.

• About 13% nerves in the premolar are myelinated A nerves.– A delta conduction velocity 13.0 m/second.

– Have low sensitization threshold (they are easily stimulated on very low stimuli)

– Pain of A delta; sharp & intense thunderbolt.

• About 78% of axons in premolar are small unmyelinated C fibers.– Conduction velocity of C fibers; 0.5 – 1.o m/second.

– They have high threshold and are activated by a level of stimuli capable of creating tissue destruction just like high temperature or pulpitis.

83

Pulpal Innervation

• C fibers are not affected by tissue hypoxia– So, pain may persist in anesthetized,

infected or even non-vital tooth.– That’s why pain in non-vital,

infected or anesthetized tooth is due to stimulation of C fibers.

• Sensation from C fibers; diffuse burning or throbbing pain & difficult to locate.

84

Restorative Dentistry &

Pulpal Health

• With all restorative procedure, try to maintain thick residual dentine thickness (RDT) to decrease the chances of pulpal irritation or injury.

• Water coolant and intermittent rotary instrument contact with tooth structure during crown preparation is essential to avoid histopathologic damage of pulp.

• Materials utilized in treatment and restoration of dental tissue can have direct effect on pulp tissues;– With reduced RDT, the permeability of dentine increases,

and resulting more freely movement of materials from the restorative materials.

– Some materials can damage the pulp due to high temperatures from their exothermic reactions.• Methacrylate based crowns• Tooth bleaching

85

Age Changes of

Tooth

• Reduced blood supply• Small pulp chamber• Decreased number of pulpal cells

– Lower ratio of pulp cells to collagen fibers• Loss and degeneration of myelinated

nerves,• Decreased neuropeptides• Loss of water from ground substance• Increased intra pulpal mineralization

(denticles)• Decreased sensitivity due to;

– Sclerosis – Tertiary dentine formation.

86

GINGIVA

87

Gingiva • Both the width and thickness of gingival tissue should be evaluated before placement of restorations that will extend subgingivally. In compromised areas muco-gingival therapy should be considered.

88

Biological Width

• Dento – gingival junction; It is combination of two gingival tissue (junctional epithelium & it’s Connective Tissue)• Stabilize & seal the gingiva around the tooth.

• Biologic Width; it is vertical dimension (width) of Dento – gingival unit.

• Dento – gingival complex; biologic width plus the sulcus depth.

• Clinical attachment level; the distance from CEJ to the tip of probe when the probe is in the sulcus.

89

Biological Width

• Biologic width and dento-gingival complex. Note that the gingival crown Cavosurface margin is ideally no more than ½ mm into the sulcus. The tip of the periodontal probe has been pushed through the DEJ (junctional epithelium and connective tissue attachment) to the osseous crest (bone sounding).

• Violation of biologic width will lead to;– Chronic inflammation– Loss of attachment – Bone resorption – Gingival recession

90

Biological Width

• Restorations should not be placed more than 0.5 mm below the gingival margin.

• Margins of restoration in sub gingival areas should be parallel to cemento enamel junction in all surfaces.

• If the vertical dimension of gingival complex is less than 3.0 mm, this can be treated by;• Muco gingival flap

• Osseous resection (crown lengthening)

91

Defective Restoratio

n & Periodontal

Health

• Poor quality of restoration impairs the periodontal health.– Marginal opening (marginal

discrepancy)– Marginal roughness– Overhanging.– Over contoured axial surface– Traumatic occlusion– Defective inter proximal

contacts

92

Defective Restoratio

n & Periodontal

Health

• Ideally, marginal discrepancy for cast metal restoration should be less than 10 micrometers. While, marginal discrepancy for ceramic restoration should be less than 50 micrometers.– Marginal discrepancy can be increased by;

• Thick cement • Faulty tooth preparation

– Effects of increased marginal discrepancy;• Increased gingival problems • Bone loss • Biofilm retention • Rough interface

93

Defective Restoratio

n & Periodontal

Health

• Effects of overhanging restoration;– Bone loss– Attachment loss – Increased pocket depth– Increased gingival inflammation

• The large the size of overhang, more the destruction of periodontium.

94

THE ENDSummit’s Fundamentals of Operative Dentistry

A Contemporary Approach (4th Edition)