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The healing powers of the dental pulp
THE HEALING
POWERS OF THE DENTAL PULP
Prunlc R. Shro#‘, D.D.S.,’
M
Dunedin,
New Zealand
has been written over the years on the effects of various preparations in the production of calcified bridges over the surfaces of exposed pulps. This literature is extensive (see Hess4 and Nyborg6 for bibliography), and in reviewing it one cannot help but be somewhat discouraged upon observing that we have progressed very litt,le since calcium hydroxide preparations were first advocated by Hermann in 1936. An extraordinary variety of materials has been suggested at different times for encouraging healing of exposed pulp wounds, but when one studies this extensive list of drugs and other materials one cannot help being unfavorably impressed by the fact that not one of these can be rightly placed into the category of materials which Hess4 calls a biologic wound dressing. In a previous paper7 it was pointed out that the ideal of true pulp healing was not beyond attainment and that we seem to be on the right road as long as we do not become blinded by false assumptions. It is generally accepted that the mechanisms of tissue repair are essentially the same as those by which the tissue formed originally in the embryo. It is also true of all wounds that the process of healing involves three phases: (1) inflammation, during which irritants are a factor, (2) repair of the exposed surface, and (3) regeneration of lost tissue. There is no reason why this sequence of events should not also occur with wounds of the dental pulp, but certainly it will not be encouraged by the use of materials which bring about necrosis. It is true, also, tha.t the best method available today involves the USC of calcium hydroxide preparations which are essentially necrotizing in their action. These materials produce a dystrophic calcification which substitutes for the normal repair of the exposed surface but which certainly cannot be regarded as the ideal. It is the purpose of this article to show that the pulp normally possesses the power of healing its exposed surface by the production of a calcified collagenous barrier beneath which regeneration of normal dentine may occur and that these events may occur in quite unfavorable circumstances and in the absence of any form of treatment. A study of these cases shows that this is the normal mechanism of pulp healing. As with any other tissue, however, it does UCH
*Associate Professor of Oral Pathology and Anatomy and Head of Department of Basic Dental Sciences, University of Otago, Dunedin, New Zealand. Present address: Visiting Professor, College of Dentistry, University of Illinois, 808 South Wood St., Chicago, Illinois. 1249
not proceed to completion nnlcss it is assistcld by the removal of irritants and thtt encouragement of norni;~l growth l~i~o~csscs,and it certainly is not assisted 1~) the use of damaging tlrugs. ()\.(‘I’ il IllUtl~)C~~ 01’ ycZlI3, T 1LilTe ObSC~~CXl tllfW2 healing rcsponscs in ni;~n>~diffcrc~nt typc>s of pulp cqosurc, and the t’ollowing cases are a few selcctctl to sho\\~ Ihr t;~pic;rl hcalin, (I lTilCtiOr1 which ma>- occur as
Fig. l.-Attempted healing reaction beneath carious exposure. A, Low-power magniflcation. B, Area marked in A showing three successive calcified bridges, odontoblastic Phliferation at the margins of the third bridge (OBJ and OBZ) and osteoblastic reaction at OB.” (Magniflcations : A, X10 ; B, X98 ; reduced $43.) (Pi,. 1, 0 to 0 on pages 1251 and 1252.) OBSERVATIONS
Fig. 1 shows a carious cavity in the dentine which has extended to the pulp dentine border. Initially, atubular secondary dentine has been formed across the damaged pulp surface in response to the advancing carious lesion. This
Fig. 1. C to F.-C’, Higher magnification of area marked in A’ showing the third bridge forming ating at OBJ. 0, Higher magnification of area marke:l in C showing the formation of the collagenous E, Higher masnlflcation of area OB’ in A. F, Higher magnification of area OB? in A. (Magnifications: x240; F, x1,000; each reduced 6/11.) (Fig. 1, G on page 1252.)
and odontoblasts prolifermatrix of the third bridge. C, X240 : D, X1,000 ; E,
0. 5.. 0 hl. B 0. I’ I)Lrolw, I’)i’i
SHBOFF
may be regarded as a calcified bridge, hut it, is well known that such s~o~~tla I’? ilcntine la~ycrs do not fotm a compldc barrier to adv;lneing (xarics anti that subsequently the pulp is again exposed. In this instance, the scquencc of orcnts has occurred on two further successive occasions, CVK~time with thcl production None of these bridges has been WI~Iof a calcified bridge across the surfarr. pletcd; one would expect this under the ad\-crse condit,ions obtaining, 11 thirtl
Fig.
1, G.-Higher
magnification
of area
OBZ in A.
(Mapniflcation,
X1,000
: reduced
(i/11.)
bridge is just in the process of forming. Even under these un Fn~orable eonditions, however, odontoblasts map bc sun spreading across bcncath this third bridge on both sides of the lesion (OB’ and OP) while in other regions osteoblast-like cells (OR”) have diffcrentiwtcd, a form of mctaplasi;l which is not uncommon in the healing of specialized tissues but, again, not, sonicthing which is to bc cncouragc~d. Fig. 2 shows a response which has occurred when a grossly c~xposed pull) has become hypcrplastic. In this instance the h,vperplast,ic tissue has bccomc Again. epithelized a.nd the inflammatory changes have subsided considcmbly. a calcified bridge has bcrn formed almost completely across one root canal and is commencing to form across the other. Just how close this bridge is to coniplct.ion can be seen when serial sections are examined. In many ot’ thesr 111~ bridge appears complete (Fig. 2, C) , and only in a few sections does t,hc opening still persist. The fact that this is a vital reaction on the part of the pulp tissue is shown in Fig. 2, D, where the variation in odontohlnstic response is shown, the variation depending upon varying degrees of intensity of the irritant agent. Where thn irritant is weaker, they arc, able t,o preser1.c theit processes and thus tubular dcntine is formed, although in an irregular fashion and at an increased rat,c; \\herc the irritant is st,rongcr, an atubula I’ drnt,incz barrier which is analogous to and continuous with the calcified bridge is formed.
HEALING
POWERS
OF DENTAL
PULP
1253
Fig. 2.-Attempted healing reaction across the exposure region of a hyperplastic pulpitis. A, Epithelized pulp poly~us. B, Higher magnification of area marked in A showing formation of a calcified bridge almost completely across one root canal. A similar appearance can be observed across the other canal in other sections of the same series, neither bridge being complete. C, Another section from the same series showing the same canal in which the bridge appears compIete. Only a few sections showed the opening persisting. D, Higher magniflcation of area marked in (: showing the variation in the type of tissue produced in response to different degrees of stimulation. Below, tubular dentine continues to form at an increased rate while, above and closer to the irritant, atubular dentine forms and this is continuous with the calcified bridge as seen in C. At the same time the odontoblasts change their morphology. (Magnifications : A, x10; B, X120; C, X120; D, X300; each reduced 6/11.)
d
Volume 12 Number
IO
HEALING
POWERS
OF DENTAL
PULP
1255
Fig. 3 also shows a hyperplastic pulp, but in this instance there is no Even in epithelial covering and the hyperplastic tissue is grossly inflamed. these extremely unfavorable circumstances, small segments of calcified tissue may be seen forming across the exposure region through which a large vessel passes to the hyperemic hyperplastic polypus (Fig. 3, B) . Across two-thirds of the roof of the pulp chamber a thin remnant of dentine extends (Fig. 3, C), and although this dentine is partly carious, it has been covered, both above and below by t,he same type of calcified scar tissue (Fig. 3, D). The fact that the area adjacent to the polypus has developed the same type of calcified covering as that next to the palp tends to support the view that the formation of such t,issue is a function of the fibroblastic elements of the pulp bissuc and that such a function is not, necessarily the sole prerogative of the more specialized odontoblast cells. DISCUSSION
In all these instances the first two stages of the healing process occur (inflammation followed by repair of the damaged surface), repair in this instance taking the form of a calcified scar tissue. This is undoubtedly due to the fact that the pulp is normally a. calcifiablc tissue, its peripheral regions constantly undergoing a change to calcified dentine. Regeneration does not occur easily in the higher animals in any organ, and in such specialized tissues repair is confined to the production of scar tissue. One would not normally expect to find regeneration under the unfavorable conditions pertaining in these cases, but the fact that there is even a vestige of such a response shows that,, with the right form of assistance, there is little doubt that new dcntine could be encouraged to form, although full regeneration of lost tissue can never be expected to occur. There is no reason why the pulp, once healed by scar tissue, should not again develop its capacity for the continued formation of dentine, a modified Such a process again takes place in three phases2 : (1) form of regeneration. formation of a mass of undifferentiated cells by loss of different,iation in the tissues near the site of injury and by migration of other cells to t.he site, (2) redifferentiation of thtsc into their more specialized forms, and (3) reorganization of the tissues by differential growth. That these processes can occur in the pulp has been demonstrated many times before and again in this article; odontoblasts differentiate, and tubular dentine forms bencath calcified scar tissue. The important principle, however, is not the fact that this process can occur but the understanding of the manner in which it takes place. If me understand this, then we may be able to develop ways of encouraging and facilitating such regenerative power. Moreover, if we accept the fact that repair takes place in the same way as tissues were first formed, then we cannot expect to understand pulp healing Attention was until we underst,and the way in which dcntine forms normally. drawn to this fact in a previous article7 and, although there are gaps in our
SHHOFE
1256
I3,V
\-iYtlle
01: th(‘il’
pOsitiOr1,
it
W(Jl.I~d
Smll
hi&l)-
IJrOh:l~)l(’
th:Jt
the
vs-
Ollt I)> scntial pr-elimiriarics I’or tlrc formation of dcntinc ill’? 1101’111il1 ly cai~ritd tht> activity of tlr(> odorrIohl;lsti(~ WI Is and that v:tr?atiorrs in t’;ttc it’ formation ilrrd the structur’r of the tissues art’ rncdiatcd 1)~ their functional arltl oth(ll. stimulation. If’ thwe stimuli are cstremc, then atuhular dentinc results and this is Yeally calcified SVill' tissue or il calcified bridge. It is highly pl’olXLblC that if we could rwrrow irritating factors and apply a rcall~- biologic wvourrd dressing, then tllc p~~wss of pulp healing would simply cwntinuc along its nornial lines. l’ht~ clinical pl’ObhlS associakd with healing Of pulp xvounds itJY! thJWfold: (1) amoral of existing irritants, mainly bacterial: (2) thr provision of il seal which \vill yrWi(Y~t the healing \vollrld fJVJJl the OYill ell\iKJrl1ll~~1lt ; ;llltl (3) the incorporation, c6tllcr in or lwrcath such :I swl, oi’ a rectally biologic TvOl7nd
dJ*essing
Which
\Vill
c’llcOl7r~lgc
tll(,
?lorrJln~
ilJltl
1lZltUlXl
gJ’OI\-th
iIrl(I
heill-
ing processes. Calcium hydr-oxide dots only two of these thrw things hut falls far short of the ideal in the third, for rather thJ1 ilet ilS il biologic dressing it destroy mor*c tissue. I Act us not, hc th~luded hy the partial clinical succ’~w ilchievcd with c2l~cillfJl h)dYOsidC hut let 17s pPOchecd f77J’thCr 011 I’iltiOJl~l~ lirlc:; in the encouragcmont of tr7lv pnlp healing.
1. Brlanger, I,. I’. : (‘anad. J. Biochrm. & Pllysiol. 32: 161, 1954. 2. Cameron, G. R.: Pathology of the Cell, London, 19+-.> Oliwr & Howl, I‘td. T~urzell)eharlcilul~g, Frnnkfurt, 1936, TV. ‘Krxmcr & (‘o., quotc~~l 3. Hcrmann, IS. : l3iologischc hv HeSS.~ 4. Hess, \C.: Intr~niat. I). J. 1: 10, 1950. 5. Irving, J. T.: J. Dent. A. South Africa 13: 295, 1958. 6. Xyhorg, H.: Odontol. Tidskr. 66: 296, 1958. ;.
Hh~ff,
F. R. :
OKAL
HURG., OKAL
MED.
& ORAL
PATH.
5:
51, 1952.
POWERS OF THE DENTAL PULP
Prunlc R. Shro#‘, D.D.S.,’
M
Dunedin,
New Zealand
has been written over the years on the effects of various preparations in the production of calcified bridges over the surfaces of exposed pulps. This literature is extensive (see Hess4 and Nyborg6 for bibliography), and in reviewing it one cannot help but be somewhat discouraged upon observing that we have progressed very litt,le since calcium hydroxide preparations were first advocated by Hermann in 1936. An extraordinary variety of materials has been suggested at different times for encouraging healing of exposed pulp wounds, but when one studies this extensive list of drugs and other materials one cannot help being unfavorably impressed by the fact that not one of these can be rightly placed into the category of materials which Hess4 calls a biologic wound dressing. In a previous paper7 it was pointed out that the ideal of true pulp healing was not beyond attainment and that we seem to be on the right road as long as we do not become blinded by false assumptions. It is generally accepted that the mechanisms of tissue repair are essentially the same as those by which the tissue formed originally in the embryo. It is also true of all wounds that the process of healing involves three phases: (1) inflammation, during which irritants are a factor, (2) repair of the exposed surface, and (3) regeneration of lost tissue. There is no reason why this sequence of events should not also occur with wounds of the dental pulp, but certainly it will not be encouraged by the use of materials which bring about necrosis. It is true, also, tha.t the best method available today involves the USC of calcium hydroxide preparations which are essentially necrotizing in their action. These materials produce a dystrophic calcification which substitutes for the normal repair of the exposed surface but which certainly cannot be regarded as the ideal. It is the purpose of this article to show that the pulp normally possesses the power of healing its exposed surface by the production of a calcified collagenous barrier beneath which regeneration of normal dentine may occur and that these events may occur in quite unfavorable circumstances and in the absence of any form of treatment. A study of these cases shows that this is the normal mechanism of pulp healing. As with any other tissue, however, it does UCH
*Associate Professor of Oral Pathology and Anatomy and Head of Department of Basic Dental Sciences, University of Otago, Dunedin, New Zealand. Present address: Visiting Professor, College of Dentistry, University of Illinois, 808 South Wood St., Chicago, Illinois. 1249
not proceed to completion nnlcss it is assistcld by the removal of irritants and thtt encouragement of norni;~l growth l~i~o~csscs,and it certainly is not assisted 1~) the use of damaging tlrugs. ()\.(‘I’ il IllUtl~)C~~ 01’ ycZlI3, T 1LilTe ObSC~~CXl tllfW2 healing rcsponscs in ni;~n>~diffcrc~nt typc>s of pulp cqosurc, and the t’ollowing cases are a few selcctctl to sho\\~ Ihr t;~pic;rl hcalin, (I lTilCtiOr1 which ma>- occur as
Fig. l.-Attempted healing reaction beneath carious exposure. A, Low-power magniflcation. B, Area marked in A showing three successive calcified bridges, odontoblastic Phliferation at the margins of the third bridge (OBJ and OBZ) and osteoblastic reaction at OB.” (Magniflcations : A, X10 ; B, X98 ; reduced $43.) (Pi,. 1, 0 to 0 on pages 1251 and 1252.) OBSERVATIONS
Fig. 1 shows a carious cavity in the dentine which has extended to the pulp dentine border. Initially, atubular secondary dentine has been formed across the damaged pulp surface in response to the advancing carious lesion. This
Fig. 1. C to F.-C’, Higher magnification of area marked in A’ showing the third bridge forming ating at OBJ. 0, Higher magnification of area marke:l in C showing the formation of the collagenous E, Higher masnlflcation of area OB’ in A. F, Higher magnification of area OB? in A. (Magnifications: x240; F, x1,000; each reduced 6/11.) (Fig. 1, G on page 1252.)
and odontoblasts prolifermatrix of the third bridge. C, X240 : D, X1,000 ; E,
0. 5.. 0 hl. B 0. I’ I)Lrolw, I’)i’i
SHBOFF
may be regarded as a calcified bridge, hut it, is well known that such s~o~~tla I’? ilcntine la~ycrs do not fotm a compldc barrier to adv;lneing (xarics anti that subsequently the pulp is again exposed. In this instance, the scquencc of orcnts has occurred on two further successive occasions, CVK~time with thcl production None of these bridges has been WI~Iof a calcified bridge across the surfarr. pletcd; one would expect this under the ad\-crse condit,ions obtaining, 11 thirtl
Fig.
1, G.-Higher
magnification
of area
OBZ in A.
(Mapniflcation,
X1,000
: reduced
(i/11.)
bridge is just in the process of forming. Even under these un Fn~orable eonditions, however, odontoblasts map bc sun spreading across bcncath this third bridge on both sides of the lesion (OB’ and OP) while in other regions osteoblast-like cells (OR”) have diffcrentiwtcd, a form of mctaplasi;l which is not uncommon in the healing of specialized tissues but, again, not, sonicthing which is to bc cncouragc~d. Fig. 2 shows a response which has occurred when a grossly c~xposed pull) has become hypcrplastic. In this instance the h,vperplast,ic tissue has bccomc Again. epithelized a.nd the inflammatory changes have subsided considcmbly. a calcified bridge has bcrn formed almost completely across one root canal and is commencing to form across the other. Just how close this bridge is to coniplct.ion can be seen when serial sections are examined. In many ot’ thesr 111~ bridge appears complete (Fig. 2, C) , and only in a few sections does t,hc opening still persist. The fact that this is a vital reaction on the part of the pulp tissue is shown in Fig. 2, D, where the variation in odontohlnstic response is shown, the variation depending upon varying degrees of intensity of the irritant agent. Where thn irritant is weaker, they arc, able t,o preser1.c theit processes and thus tubular dcntine is formed, although in an irregular fashion and at an increased rat,c; \\herc the irritant is st,rongcr, an atubula I’ drnt,incz barrier which is analogous to and continuous with the calcified bridge is formed.
HEALING
POWERS
OF DENTAL
PULP
1253
Fig. 2.-Attempted healing reaction across the exposure region of a hyperplastic pulpitis. A, Epithelized pulp poly~us. B, Higher magnification of area marked in A showing formation of a calcified bridge almost completely across one root canal. A similar appearance can be observed across the other canal in other sections of the same series, neither bridge being complete. C, Another section from the same series showing the same canal in which the bridge appears compIete. Only a few sections showed the opening persisting. D, Higher magniflcation of area marked in (: showing the variation in the type of tissue produced in response to different degrees of stimulation. Below, tubular dentine continues to form at an increased rate while, above and closer to the irritant, atubular dentine forms and this is continuous with the calcified bridge as seen in C. At the same time the odontoblasts change their morphology. (Magnifications : A, x10; B, X120; C, X120; D, X300; each reduced 6/11.)
d
Volume 12 Number
IO
HEALING
POWERS
OF DENTAL
PULP
1255
Fig. 3 also shows a hyperplastic pulp, but in this instance there is no Even in epithelial covering and the hyperplastic tissue is grossly inflamed. these extremely unfavorable circumstances, small segments of calcified tissue may be seen forming across the exposure region through which a large vessel passes to the hyperemic hyperplastic polypus (Fig. 3, B) . Across two-thirds of the roof of the pulp chamber a thin remnant of dentine extends (Fig. 3, C), and although this dentine is partly carious, it has been covered, both above and below by t,he same type of calcified scar tissue (Fig. 3, D). The fact that the area adjacent to the polypus has developed the same type of calcified covering as that next to the palp tends to support the view that the formation of such t,issue is a function of the fibroblastic elements of the pulp bissuc and that such a function is not, necessarily the sole prerogative of the more specialized odontoblast cells. DISCUSSION
In all these instances the first two stages of the healing process occur (inflammation followed by repair of the damaged surface), repair in this instance taking the form of a calcified scar tissue. This is undoubtedly due to the fact that the pulp is normally a. calcifiablc tissue, its peripheral regions constantly undergoing a change to calcified dentine. Regeneration does not occur easily in the higher animals in any organ, and in such specialized tissues repair is confined to the production of scar tissue. One would not normally expect to find regeneration under the unfavorable conditions pertaining in these cases, but the fact that there is even a vestige of such a response shows that,, with the right form of assistance, there is little doubt that new dcntine could be encouraged to form, although full regeneration of lost tissue can never be expected to occur. There is no reason why the pulp, once healed by scar tissue, should not again develop its capacity for the continued formation of dentine, a modified Such a process again takes place in three phases2 : (1) form of regeneration. formation of a mass of undifferentiated cells by loss of different,iation in the tissues near the site of injury and by migration of other cells to t.he site, (2) redifferentiation of thtsc into their more specialized forms, and (3) reorganization of the tissues by differential growth. That these processes can occur in the pulp has been demonstrated many times before and again in this article; odontoblasts differentiate, and tubular dentine forms bencath calcified scar tissue. The important principle, however, is not the fact that this process can occur but the understanding of the manner in which it takes place. If me understand this, then we may be able to develop ways of encouraging and facilitating such regenerative power. Moreover, if we accept the fact that repair takes place in the same way as tissues were first formed, then we cannot expect to understand pulp healing Attention was until we underst,and the way in which dcntine forms normally. drawn to this fact in a previous article7 and, although there are gaps in our
SHHOFE
1256
I3,V
\-iYtlle
01: th(‘il’
pOsitiOr1,
it
W(Jl.I~d
Smll
hi&l)-
IJrOh:l~)l(’
th:Jt
the
vs-
Ollt I)> scntial pr-elimiriarics I’or tlrc formation of dcntinc ill’? 1101’111il1 ly cai~ritd tht> activity of tlr(> odorrIohl;lsti(~ WI Is and that v:tr?atiorrs in t’;ttc it’ formation ilrrd the structur’r of the tissues art’ rncdiatcd 1)~ their functional arltl oth(ll. stimulation. If’ thwe stimuli are cstremc, then atuhular dentinc results and this is Yeally calcified SVill' tissue or il calcified bridge. It is highly pl’olXLblC that if we could rwrrow irritating factors and apply a rcall~- biologic wvourrd dressing, then tllc p~~wss of pulp healing would simply cwntinuc along its nornial lines. l’ht~ clinical pl’ObhlS associakd with healing Of pulp xvounds itJY! thJWfold: (1) amoral of existing irritants, mainly bacterial: (2) thr provision of il seal which \vill yrWi(Y~t the healing \vollrld fJVJJl the OYill ell\iKJrl1ll~~1lt ; ;llltl (3) the incorporation, c6tllcr in or lwrcath such :I swl, oi’ a rectally biologic TvOl7nd
dJ*essing
Which
\Vill
c’llcOl7r~lgc
tll(,
?lorrJln~
ilJltl
1lZltUlXl
gJ’OI\-th
iIrl(I
heill-
ing processes. Calcium hydr-oxide dots only two of these thrw things hut falls far short of the ideal in the third, for rather thJ1 ilet ilS il biologic dressing it destroy mor*c tissue. I Act us not, hc th~luded hy the partial clinical succ’~w ilchievcd with c2l~cillfJl h)dYOsidC hut let 17s pPOchecd f77J’thCr 011 I’iltiOJl~l~ lirlc:; in the encouragcmont of tr7lv pnlp healing.
1. Brlanger, I,. I’. : (‘anad. J. Biochrm. & Pllysiol. 32: 161, 1954. 2. Cameron, G. R.: Pathology of the Cell, London, 19+-.> Oliwr & Howl, I‘td. T~urzell)eharlcilul~g, Frnnkfurt, 1936, TV. ‘Krxmcr & (‘o., quotc~~l 3. Hcrmann, IS. : l3iologischc hv HeSS.~ 4. Hess, \C.: Intr~niat. I). J. 1: 10, 1950. 5. Irving, J. T.: J. Dent. A. South Africa 13: 295, 1958. 6. Xyhorg, H.: Odontol. Tidskr. 66: 296, 1958. ;.
Hh~ff,
F. R. :
OKAL
HURG., OKAL
MED.
& ORAL
PATH.
5:
51, 1952.