Crown Cementation and Pulpal Health

REVIEW

Crown cementation and pulpal health

C. W. Lam & P. R. Wilson

School of Dental Science, University of Melbourne, Melbourne, Australia

Abstract

Lam CW, Wilson PR. Crown cementation and pulpal

health (Review). International Endodontic Journal, 32, 249±256,

1999.

Literature review A direct result of the liquid

continuum within the pulpo-dentine complex is the effect

of restorative dentistry on the health of the dental

pulp. Better understanding of the role of the complex

in relation to restorative dentistry enables strategies to

be devised in preserving pulp vitality. A review of the

literature produced good laboratory evidence to

support the prophylactic sealing of crown preparations

with dentine bonding agents.

Keywords: cementation, crowns, dentine, pressure.

Introduction

The pulp and dentine are located in series to form the

pulpo-dentine complex. The complex represents a

continuum between intratubular dentinal fluid and

pulpal fluid (Pashley 1992). A direct result of this

continuum is the effect of restorative dentistry on the

health of the dental pulp, as evidenced by the pulpal

necrosis rate of 1% year for vital crowned teeth

(Bergenholtz & Nyman 1984, Karlsson 1986). Under-

standing the biomechanics of the complex is crucial not

only in explaining the pulpal necrosis rate, but also in

enabling strategies to be devised in an attempt to reduce

pulpal damage caused by routine restorative dentistry.

This review therefore aims to discuss the dynamics of the

liquid continuum and pulpal pressures in relation to

forces and pressures of cementation. The concept of

dentine sealing to preserve pulpal health is also discussed.

Structure of dentine

Dentine is composed of approximately 50% (v/v)

mineral, 30% (v/v) organic matter, and the remainder

is fluid. As a living tissue, there are four elements that

make up the hydrated composite of mineral and

organic matter: (i) dentinal tubules, surrounded by (ii)

a peritubular zone, embedded in (iii) an intertubular

matrix, and perfused by (iv) dentinal fluid (Marshall

1993).

Dentine is therefore much like a microscopic sponge

filled with tubules in connection with the pulpal micro-

vasculature via both the intratubular dentinal fluid

and pulpal fluid (Pashley 1992). Physiologically, the

liquid continuum is confined in a dynamic state of

equilibrium within the complex. This serves to

replenish the various nutrients required for the living

cells, such as the odontoblasts residing intratubularly.

Following the exposure of the tubules postoperatively,

the equilibrium is disturbed and the dentinal fluid is

not restricted to the tubules. Fluid replacement and

loss can result at the pulpal and at the enamel end of

the tubules. Dentinal fluid dynamics can therefore be

analysed in three parts, namely the pulpal, intratubu-

lar and peripheral ends.

Pulpal end ± the fluid source

At the pulpal end, there is richly vascularized pulpal

tissue. The pulpal microvasculature serves as a source

to replenish the outward flow of fluid through the

exposed tubules. Matthews et al. (1993) stated that,

q 1999 Blackwell Science Ltd International Endodontic Journal, 32, 249±256, 1999

Correspondence: Dr P. R. Wilson, School of Dental Science, University

of Melbourne, 711 Elizabeth Street, Melbourne, VIC 3000, Australia

(fax: 613 93410437; e-mail: [email protected]).

This article is based on a thesis submitted to the School of Dental

Science, the University of Melbourne, in partial fulfilment of the

requirements of the degree of Master of Dental Science.

249

presumably, the water lost from the peripheral

(enamel) ends of tubules is immediately replaced by

movement of water from pulpal blood vessels out into

pulpal interstitial fluid and thence into the dentinal

tubules. Such replacement maintains a net water

content of dentine that probably does not really

change. The notion of `dehydrated' dentine as a result

of overdrying with an air syringe needs to be reconsid-

ered (Matthews et al. 1993), although the loss of

tubule fluid may lead to a delay in refilling the tubule,

and thereby challenge the pulpal tissue. The haemody-

namics governing such fluid movement in the pulpal

microvasculature is discussed below in the section on

pulpal pressures.

The intratubular course

Dentinal tubules can be regarded as a semi-permeable

biological barrier. Solvent and/or solute movement

across the biological barrier involves two mechanisms

of permeation: (i) convective transport, and (ii)

diffusive transport (Merchant et al. 1977). Anatomi-

cally, the two processes use the same channels for

transport. Mechanistically, there are some differences,

which are discussed below.

Convective transport. This is a mechanism for solute and

solvent transport across dentine; it is also known as

bulk fluid movement or fluid filtration. One of the ear-

liest pieces of evidence for convective transport came

from Fish (1928). The intrapulpal placement of India

ink in vital dog teeth led to the peripheral movement

of ink particles into and along dentinal tubules in a

matter of hours. As the particles moved over long dis-

tances in a short time, bulk fluid movement was sug-

gested.

Fluid filtration is defined by the PoiseuilleHagen

equation:

V � p�4=8x� (1)

where V is the volume flow; �P is the hydrostatic

pressure differences across dentine; � is the viscosity of

the fluid; x is the length of tubules; and r is the tubular

radius (Pashley 1985).

As can be seen from equation (1), the pressure

gradient (�P), either hydrostatic or osmotic, is the

energy source for the bulk fluid movement. In a phy-

siological situation (Fish 1928), the positive hydrostatic

pressure of pulpal tissue provides the gradient. In a

hypertonic external solution, as exaggerated when

eating sugary confectionery, an osmotic gradient is

created. The net result is the same for both types of

gradients: convective transport across dentine.

Centrifugal (outward) fluid filtration occurs under a

positive pulpal pressure gradient. Centripetal

(pulpward) fluid filtration occurs under reversed pulpal

pressure gradients, such as in cementation and

mastication (Pashley 1990).

Since the actual transport is bulk fluid movement

or filtration, the diffusion coefficients of solutes are

therefore not important. Fluid flow is directly propor-

tional to the fourth power of the radius. The

filtration rate is therefore very sensitive to small

changes in tubular radius. The ease of bulk fluid

filtration is quantitated as the hydraulic conductance

(Lp) (Merchant et al. 1977, Pashley 1985, Pashley

1990) or the filtration coefficient (Kf) (Pashley

1990).

Diffusive transport. This is defined by the Fick equation:

J � DA dc/dx (2)

where J is the solute flux; D is the diffusion coefficient;

A is the diffusional surface area; and dc/dx is the

change in concentration (c) over distance (x) (Pashley

1985).

As distinct from convective transport, the concentra-

tion gradient serves as the potential energy source. The

diffusion coefficients of substances are therefore

important. The diffusive permeability is quantitated as

a permeability coefficient or a clearance (Merchant

et al. 1977).

The peripheral end

The enamel end of the exposed tubules represents an

air-dentinal fluid interface. However, the interface is

initially established at the junction of a pool of dentinal

fluid or water coolant lying on top of the wet dentine.

As evaporation occurs, the interface is shifted closer to

the tubule orifice until it reaches the smear layer. This

layer, being very porous to water vapour, may permit

air to penetrate it to set up an interface at the tubular

orifice (Matthews et al. 1993).

Two processes are at work at this interface: (i) the

expression of capillary forces when an air±liquid

interface is established at the orifice of an exposed

tubule (the capillary forces can allow sudden outward

movement of dentinal fluid); (ii) the evaporation of

fluid from dentine, which sustains the outward fluid

movement. This can occur at the very high rate of

1 mL minÿ1 cmÿ2 (Matthews et al. 1993).

International Endodontic Journal, 32, 249±256, 1999 q 1999 Blackwell Science Ltd

Crown cementation and pulpal health Lamb & Wilson

250

Pulpal pressures

Pulpal haemodynamics

The pulpal microvasculature serves as a fluid source to

replenish the outward flow of fluid through the

exposed tubules. Such fluid replenishment, which is ex-

tracellular to the pulpal capillaries and venules, is

regulated by three key mechanisms.

Two opposing sets of Starling forces (1896). The forces

promoting extravascular filtration are the capillary hy-

drostatic pressure (Pc) and the interstitial tissue osmo-

tic pressure (pi). Both interstitial fluid pressure (IFP)

and plasma osmotic pressure (pp) oppose the move-

ment of fluid out of the capillary. The net effect of these

forces along an average capillary at transmicrovascular

fluid exchange equilibrium is represented by equa-

tion (3) (Van Hassel 1971):

Pcÿ pp � IFPÿ pi (3)

Hydrostatic buffering. Physiologically, Pc is highest at

the arteriolar end of the capillaries and lowest at the

venular end. Under some conditions, slightly more fluid

is filtered than is reabsorbed on the venous side. This

net fluid filtration can cause an increased interstitial

fluid volume (IFV) (Pashley 1992). Unlike other tissues

with high compliance, the encasement of the pulp in

rigid dentine walls creates a low compliance environ-

ment. Thus, even small variations in the IFV can result

in relatively large changes in interstitial fluid pressure

(IFP). The increased IFP will in itself act as a negative

feedback mechanism and counteract further filtration.

Thus, the inability of the pulp to expand (low compli-

ance) enables the hydrostatic buffering via a compen-

satory rise in IFP. Hydrostatic buffering serves as a

rapid and efficient oedema-preventing mechanism

(Heyeraas 1989).

Pulpal lymphatics. The maintenance of a low colloid os-

motic pressure in interstitial fluid is also required to

prevent an increasing IFP. In high compliance tissues,

this is achieved by increasing net filtration for dilution

or osmotic buffering. However, such negative feedback

is not effective because of a relatively constant volume

in a low compliance system like the pulp. Hence, it

was proposed that increased IFP initiates increased

lymphatic flow and drainage of proteins (Heyeraas

1989). The lymphatic removal of excess interstitial

fluid and plasma proteins permits continuous net capil-

lary filtration without increasing the pulpal volume

and tissue pressure (Pashley 1992). However, the exis-

tence of pulpal lymphatics is controversial. This is be-

cause of the difficulties in distinguishing lymphatic

capillaries from blood capillaries and venules (Bernick

1977, Heyeraas 1989, Pashley 1992).

Interstitial fluid pressure (IFP)

As shown in equation (4) below, IFP is a direct

function of Pc (Heyeraas 1989). Therefore,

measurement of Pi (IFP) serves as an effective means of

monitoring pulpal microcirculatory status (Van Hassel

1971, Ciucchi et al. 1995):

IFP � Pcÿ�p (4)

The early measuring techniques for IFP were invasive,

requiring direct exposure of pulpal tissue, e.g. the

closed cannulation technique (Wynn et al. 1963,

Beveridge & Brown 1965, Van Hassel 1971, Stenvik

et al. 1972), the tonometric technique (Christiansen

et al. 1977) and the micropuncture technique (Tonder

& Kvinnsland 1983).

Direct pulpal exposure alters the local compliance (a

measure of the change in tissue volume per unit

change in pressure) of the pulpal tissue. In addition,

some studies (Brown et al. 1969) have measured the

baseline compliance of the system investigated, whilst

others (Heyeraas 1985, 1989) have not done so. To

further complicate matters, there are other interrelated

factors, such as the inflammatory reactions associated

with pulpal tissue damage and the uncertainty of

vascular influence (Wynn et al. 1963, Beveridge &

Brown 1965, Stenvik et al. 1972, Christiansen et al.

1977).

As a result, a range of IFP values (0±50 mmHg)

are available for humans, dogs, cats and monkeys,

depending on the different measuring techniques

used. It remains questionable whether the recorded

pulpal pressures represent normal physiological

values, after the tissue damage associated with the

invasive techniques is considered (Tonder &

Kvinnsland 1983).

More recently, the work of Vongsavan & Matthews

(1992) is considered important, because they

developed a technique which did not directly enter the

pulp chamber, and therefore avoided the pulpal

response to injury. They indirectly estimated IFP, for

intact pulps in cats, by measuring outward dentinal

fluid movement as a function of exogenous hydrostatic

pressure. The intact dentine preserved the normal low

pulpal compliance (Pashley 1992).


Lamb & Wilson Crown cementation and pulpal health

251

Crown cementation

A wide range of cementation forces have been used in

many studies, ranging from a minimum of 22.5 N

(Wang et al. 1992) to a maximum of 700 N (Moore

et al. 1985). With such an extensive range of forces

documented, it is not certain what constitutes a

relevant force clinically. There seems to be some

consensus for 100 N to be used in laboratory studies

(Grajower et al. 1985, 1989, Gerzina & Hume 1990,

Al-Fawaz et al. 1993,). The 100 N load is similar to

that found clinically by Grieve (1969). An average

force of 90 N was obtained over a period of 1 min

during which a crown was cemented using a model

bite pad. The range of forces measured was between

15 and 230 N. On the other hand, it has been shown

more recently that the typical force used for crown

cementation was initially 60 N for the first few

seconds, followed by a constant force of 20±30 N

(Black & Amoore 1993).

Forces used in cementation can generate intracoro-

nal hydraulic pressure. This cementation pressure has

been successfully measured in vitro using brass and

stainless steel dies (Hoard et al. 1978, Kay 1984) and

extracted human teeth (Wylie & Wilson 1994, Wilson

& Wong 1997). The pressure has been postulated to be

sufficient to precipitate pulpal necrosis (Kay 1984).

Jorgensen (1960) noted that as pressure was exerted

on dental cement, filtration of cement constituents into

a solid and a less viscous (most reactive) liquid phase

occurs.

During cementation, the cut dentinal tubules

provide a pulpward route for the less viscous cement

constituents that are potentially toxic. Components

such as hydrogen ions, 2-hydroxyethylmethacrylate

(HEMA) and 2,2-bis {4-(2-hydroxy-3-methacryloyloxy-

propoxy)-phenyl} propane (BIS-GMA) have been

rapidly detected in the pulp chambers of extracted

human teeth within minutes following cementation

(Gerzina & Hume 1990, Al-Fawaz et al. 1993). The

clinical situation is more complex, in that there would

be an opposing outflow of fluid from the pulp, although

it has been shown that the use of local anaesthetic

with adrenaline vasoconstrictor reduces pulpal

pressure to very low values (Kim 1984). It is plausible

that the pulpward movement of potentially toxic con-

stituents would also be facilitated by a pulpward mass

transport via the tubules, driven by the cementation

pressure pulse.

The centrifugal pulpal fluid movement through fluid

spaces as a result of evaporative forces can set up

disruptive forces. Such forces can cause tissue damage

as the fluid streams across small tissue spaces

(Matthews et al. 1993). Similarly, it is plausible to

speculate the reverse. The pulpward pressure pulse

could cause centripetal movement of pulpal fluid. The

shear forces associated with the pressurized fluid

movement through pulpal tissue spaces could also

result in permanent tissue damage.

White et al. (1992) and White & Kipnis (1993)

recommended the application of heavy seating forces

in order to compensate for the increased film thickness

of the resin cements and achieve a good seating

discrepancy. This is, however, not supported by other

workers. Jorgensen (1960) concluded that the film

thickness decreased when the force on the crown is

increased to 5 kg but that the effect of greater forces is

relatively insignificant. Furthermore, Eames et al.

(1978) showed that a rebound effect occurs following

the release of cementation force. The crown contracts

and rebounds occlusally.

Of greater significance is the finding that force and

pulpward pressure are directly related, with `simple

proportionality' (Kay 1984). Wong & Wilson (1997)

have confirmed this relationship in a further study.

The postulation on pulpal necrosis (Kay 1984)

together with pulpal detection of the pressure in vitro

(Wylie & Wilson 1994, Wong & Wilson 1997) and the

consolidation of the linear relationship between force

and pressure (Kay 1984, Wong & Wilson 1997) add

strength to the protocol of low force cementation

proposed by Wilson et al. (1990) and Wilson (1996).

The protocol uses a combination of a low force

together with internal crown relief (space for cement

on the axial and occlusal surface) for cement space to

achieve clinically acceptable seating (Wilson 1996,

Wong & Wilson 1997). The space allows easier

expression of cement trapped occlusally and reduces

the filtration effect of particle size (Wilson 1992). The

space also enables easier movement of the crown on

the tooth, resulting in faster seating by eight times

compared with unspaced crowns. This would be

significant clinically for complete seating before cement

setting (Wilson et al. 1990).

An alternative to cement space is perforation

venting, where a hole is placed in the crown well

away from the margin to allow outflow of cement

(Bassett 1966, Cooper et al. 1971, Kay 1984, Wilson

et al. 1990). It limits the stacking or accumulation of

cement particles and relieves any residual intracoronal

pressure (Hoard et al. 1978). In the absence of

appropriate internal crown relief, it is equally plausible



252

that the dentinal tubules act as internal vent holes for

pulpward, instead of occlusal, cement escape. This

form of biological internal relief for cement could occur

at a biological cost. Pulpal damage may result from cy-

totoxicity of the ingressed cement components (Hume

1990) and cellular disruption by the pulpally

transmitted pressure (Kay 1984). Although of small

extra magnitude, the combination of cement space and

venting is additive in improving seating for an already

well seated crown (Van Nortwick & Gettleman 1981).

Grajower et al. (1985) found that repeated trial

seating improved seating because of deepening of pre-

existing furrows in axial walls by internal contacts of

the crown. It has been argued that the highly acidic

(pH 2.14) unset aqueous part of zinc phosphate

cement exerts a self-etching effect on the dentine. High

contacts were said to be preferentially dissolved and

allowed better seating (White & Kipnis 1993). It is also

plausible that such self-etching also removes the smear

layer and increases the possibility of pressure transmis-

sion to the pulp chamber.

Dentine surface treatment

Dentine acts as a buffer zone to obnoxious stimuli

external to the pulp. The hydroxyapatite in dentine

can buffer the H+ ions of strong acids (Hume 1990,

Gerzina & Hume 1994). The hydroxyapatite in whole

dentine is more effective in H+ ion buffering because of

the additional effects of calcium phosphate, protein

and/or other macromolecular components. Hydroxide

(OH) ions are also buffered, but less so than for H+

ions, by displacing the less electronegative phosphate

ions from hydroxyapatite (Wang & Hume 1988).

Other factors also offer protection. Remaining dentine

thickness (RDT) of 1 mm or more has been shown to be

effective in counteracting the toxicity of both zinc

phosphate and glass ionomer cements (Palmeijer et al.

1991). The positive interstitial pulpal pressure against

the walls of the pulp chamber also offers some resistance

to pulpward ingress of toxins. However, it has been

shown that the IFP reduces, but does not prevent, the

pulpward ingress of toxins (Gerzina & Hume 1995). The

clearance of toxin into pulpal blood vessels also

determines the concentration and therefore toxicity to

pulpal tissue (Jacob & Yen 1991).

Strategies of dentine surface treatment

There are two aims to dentine surface treatment post-

operatively: to modify or remove smear layer in order

to improve the quality and quantity of dentine

substrate for optimizing adhesive bond strength; and to

occlude the dentinal tubules exposed following

operative procedures. Restoratively, the smear layer is

an unsatisfactory intermediary layer between tooth

and restoration. Various strategies have been devised

to either modify or remove it, in an attempt to achieve

optimal adhesive bond strength (Van Meerbeek et al.

1992). It has also been condemned as a depot of

bacteria and toxins when produced under septic

conditions (BraÈnnstroÈm & Nyborg 1973, Bergenholtz

et al. 1982).

The strategies devised in dealing with the smear

layer are (i) modification to produce a resin-

impregnated smear layer, (ii) partial removal to

preserve the smear plugs and create only a limited

resin-impregnated dentine layer, and (iii) complete

removal and decalcification of the dentine top layer to

produce a resin-impregnated hybrid layer (Van

Meerbeek et al. 1992).

Biologically, the smear layer can be viewed as a

useful barrier to external stimuli that are noxious to

the pulp. It is responsible for as much as 86% of the

total resistance to fluid flow across dentine into the

pulp (Pashley et al. 1978) and exerts a steric resistance

to bacterial ingress (Pashley et al. 1981).

However, the protection is only short-term, as the

smear layer is very labile to acid degradation. Its acid

lability is due to its fine particle size, which gives a

high surface area/mass ratio. The smear layer can

therefore be dissolved by saliva or dentinal fluid, or

organic acids produced by bacterial metabolism

(Bergenholtz et al. 1982).

Different topical agents have been devised in an

attempt to occlude the tubules more permanently. As

such, they are used essentially in the management of

dentine hypersensitivity. They can be broadly classified

into three groups (i) fluoride-containing products, e.g.

sodium fluoride, (ii) oxalates such as potassium

oxalate, and (iii) resin and adhesives (Collaert &

Fischer 1991).

Dentine sealing in fixed prosthodontics

The concept of sealing dentinal tubules has also been

applied to postoperative sensitivity associated with

teeth prepared for crowns. BraÈnnstroÈm (1996)

recommended the use of Tubulicid cleansing agent

(Dental Therapeutics AB, Nacka, Sweden) followed by

Tubulitec Lining System (Dental Therapeutics AB,

Nacka, Sweden). The cleansing agent contains 1%



253

sodium fluoride, which precipitates calcium fluoride to

reduce dentine permeability. Another precipitation

technique uses oxalates (Pashley et al. 1978, Pashley &

Galloway 1985). However, the oxalate crystals may

interfere with subsequent attempts to bond cements

(Richardson et al. 1990) or adhesive resins (Pashley

et al. 1993) to the treated surfaces.

More recently, dentine bonding agents have been

recommended in prophylactically sealing the dentinal

tubules of crown-prepared teeth. The aim is to reduce

postoperative problems associated with crown-prepared

teeth (Clinical Research Associates 1993).

Various studies on dentine sealing of teeth prepared for

crown have been conducted in extracted human teeth

using silver nitrate penetration, fluid filtration rates and

liquid chromatography (Pashley et al. 1992, White et al.

1992, Al-Fawaz et al. 1993), and in monkeys using his-

topathological studies (Suzuki et al. 1994). Although

evidence of efficacy remains largely anecdotal at this

stage, there seems to be a good deal of evidence to

support such a concept, at least in early laboratory

(Pashley et al. 1992, White et al. 1992, Al-Fawaz et al.

1993) and animal studies (Suzuki et al. 1994).

Conclusions

A direct result of the liquid continuum within the

pulpo-dentine complex is the potential for restorative

dentistry to affect the health of the dental pulp.

Flow of fluid in dentinal tubules has been demon-

strated, both in vitro and in vivo, and may be a

mechanism for pulpal damage. This review of the

literature has produced laboratory evidence that

dentine bonding agents can reduce fluid flow

through tubules, both prior to direct restorations

and during cementation.

It is proposed that sealing of dentine before crown

cementation would be a useful clinical procedure

that may be beneficial and which is unlikely to be

harmful.

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Crown Cementation and Pulpal Health