Endodontics

A review of aging of dental components and a retrospectiveradiographie study of aging of the dental pulp and dentinin normal teethDonald R. Morse* / John V, Esposito"M. Lawrence

/ Robert S, Schoor*** / Frank L. Williams**** /

A review of aging of dental components is followed by a clinieal radiographie study.Patients received radiographs at 5-year intervals with a 10-year minimum followup. Dataobtained were age. gender, tooth, and systemic diseases. Measurements taken were toothlength, coronal length, apieal length, cervical width, midroot width, and apical width.Root eanal shrinkage was calculated vertieally. horizontally, and as a combination (ver-tical and horizontal). Jiesults showed statistieally significantly more shrinkage in men,the elderly, and people with calcification-related diseases. Shrinkage increased with ad-vancing age. With further studies, radiographically determined root canal measurementscould prove useful in anthropology, forensics, and as a biomarker of aging.(Quintessence Int 1991:22:711-720)

Introduction

Teeth, the hardest bodily structures,' are useful in fo-rensics.̂ "̂ Fully formed teeth show aging changes thatmirror those seen systemically. Hence, teeth can beused to give an age range for anthropology and fo-rensics and can act as a biomarker of aging. Teethwere first used as a barometer of age in the ISOOs,̂when age determination was related to factory em-ployment of children and to the supposition that chil-dren under 7 years were not criminally culpable.

Professor and Research Director, Departmenl of Endodün-tology. Temple University, School of Denliitry, 3223 NorthBroad Street, Philadelphia, Pennsylvania 19140.Associate Professor, Department of Endodontology. TempleLIniversity.Ctinicat Professor, Department of Peri odontology. TempletJniversity,Associate Professor, Department of Oral Medicine, TempleUniversity,Associate Professor, Department of Oral Medicine, TempleUniversity,

Aging of the tooth components

Enamel

Age-related changes in enamel are a loss in permea-bility and an increase in brittleness,' The organic sub-stance between enamel prisms apparently becomescalcified, causing brittleness and fractures,^ The nitro-gen content of enamel appear? to increase,' which cor-relates with increased pigment, leading to tooth dark-ening.'" Refractive and light absorptive changes arerelated to enamel and dentinal structural changes,"Tbe aspartic acid in enamel exhibits increasing racem-ization,'^ which could become useful as a biomarkerof aging.- The level of fluoride in enamel also increas-es,'' which could partly be a result of fiuoridation,"The rate of enamel attrition is not an accurate meansof age deteiTOination.'""''

Cement um

With age, cementum increases in width (mainly api-cally). '̂""'" Rhythmic cementum accumulation (an-nulation) has been used for age determination in an-imals, Cementum annulations, counted from photo-

Quintessence internationai Volume 22, Number 9/1991 711

Endodontics

graphs of extracted teelh, have been used as ii methodto estimate hutnan age,-' but the method is inaccuratebecause of the functionai elaboration of cementum.Apical résorption is functional; hence, it is not anaccurate measure for systemic aging.'^"'

Dentin

With aging, the pulpal cavity becomes smaller becauseof continuous deposition of secondary dentin.-- In ad-vanced age, secondary dentin becomes irregular, agradual loss of dentinal tubules occurs, and odon-toblasts undergo degenerative changes, atrophy, anddisappear in most areas of the dental pulp."

Increases occur in peritubular dentin; uitiinately, thedentinal tubules are occiuded by sclerotic (transpar-ent) dentin. Formation of transparent dentin beginson the root apices, and, with age, the dentin graduallyadvances toward the crown."-^ Formation of scleroticdentin has been used with generally encouraging re-suits as a tooth-related measure of systemicggg i,i6,2]-2s ^ significant age-related reduction in den-tinal tubules occurs."*-"*

Age-related dentinal changes have also been ob-served in totally impacted teeth. In impacted teeth, theage-related formation of secondary dentin is firstfonnd in the apical region, from which it proceedscoronally. In functioning erupted teeth, formation ofsecondary dentin begins in the coronal region. An-other change found in aging impacted teeth is a hnearincrease in the width of predentin.'"

Mineralisation apparentiy increases with advancing

Dental pulp

The age-related changes ofthe dental pulp are difficultto separate from physiologic defensive changes andpathologic irritant-induced changes,-'^''' Since impact-ed teeth are functionless, it was believed that theycould yield a realistic estimate of aging changes.Nevertheless, because impacted teeth never erupt, ob-served changes do not reflect normal situations.

Diagnosis requires tissue examination. The follow-ing age changes have been reported: compromised cir-culation and innervation; fat droplet deposition;odontobiastic vacuolization; reticular atrophy; pulpalfibrosis; hyahne degeneration; fat replacement; pulpal"cysts'"; mucoid degeneration; and calcifications. '̂• '̂

Conipromi.sed circulation and innervation. Apicaldeposition of secondary dentin and cementum in-

creases, narrowing the originally wide-open root apex.Because the pulp's blood, lymphatic, and nerve sup-plies come through the apical foramen, these suppliescan be compromised as the apex narrows. In extremeold age, the deposition of dentin and cementum eanbe so complete that the blood, lymphatic, and nervesupplies to the pulp are almost shut off. Blood vesselsto the aged pulp undergo arteriosclcrotic changes thatresult in a diminished blood supply to the pulpal cells.The arterial intima thickens and the adventitia calci-fies."'' Lymphatics also show age-related degenerativechanges. Nerves entering the aged pulp show miner-alization of the sheath and nerve, and the number ofpulpal axons usually decreases."

Fill droplet deposition is cither a definitive change'*or an artifact.̂ ^ Fatty deposits have been described inodontoblasts, nuclei of pulpal cells, walls of pulpaltissue capillaries,"* and lysosomal enzymes (CristofaloV: Personal communication, 1990).

Odontoblastic vacuolization is either an artifact* orthe next sign of pulpal aging.'' The odontobiastic cellsare pushed apart and separated from the dentinal wallby the apparent pressure of an intercellular accumu-lation of fissue fluid."

Reticular atrophy is either an artifact*'"' or the nextstage in pulpal aging.'* The tissue has a netlike ap-pearance that is apparently related to an abundanceof mtercellular fluid and a reduction in the numberof pulpal cells.

Pulpal fibrosis. Next, a mariced cellular reductionand an apparent coilagenous fiber increase occur. Theremaining odontoblasts become smaller and moreflattened. With the reduced size of the pulp (as theresult of secondary dentinal formation) and decreasednumber of cells, the remaining pulpal space is filledmore with fibers. With the great reduction in numberof fihrobiasts, more coilagenous fibers cannot be pro-duced."" Fibroblasts from young pulp contain numer-ous fine intracytoplasmie fibrils and organelles.Fibroblasts from old pulp have few intracytoplasmiefibrils and organelles."*- Some fibers in older pulp areremnants from previous production, and there is anincreased polymerizafion and aggregafion of previ-ously existing smaller units of collagen.*''' This couldbe related to a reduction in reducible collagen cross-links and an increase in nonreducing cross-links.'^''"Collagen synthesis decreases as the pulp ages.''* Oftheten genetically distinct types of collagen,'" the dentalpulp contains types I and III.'" With age, type I (themain type) decreases, and type III (associated withreticulin) increases.

712 Quintessence International Volume 22, Number 9/1991

Endodontics

Blood capillaries, lymphatics, and nerves decreasein number. These are all encased in connective tissuesheaths. As the vessels and nerves decrease in number,their connective tissue sheaths remain and becomepart of the remaining fibrous pulp. There is also anincrease in type III collagen-containing reticular fibers(found mainly around blood vessels),•'̂ ••" Acid muco-polysaccharides first increase (wbile the collagenforms) and then decrease,''* In time, all that remainsis fibrous tissue with no viable fibroblasts (senile fi-brosis, pulposis, atrophie pulp).

Hyaline degeneration is usually an intermediatestage in the formation of pulpal calcification. Often,minor circulatory disturbances can result in hyalini-zation of areas of pulpal tissue (a change in the mi-croscopic appearance of the intercellular fibers),^' Hy-alinization is usually a sequela to long-standing fi-brous degenerafion. In time, hyahne and shrinkagespaces become fat-filled (fat replacement stage'),'*

Fat replacement. In wax sections, fat appears as cir-cular spaces in the tissues because the fat dissolves inChe preparation of the specimen. This is either anartifact"- '̂ a replacement phenomenon,'* or a degen-era ti o n.''̂ ''̂ Calcification often occurs in these fattydeposits and can lead to denticles and diffuse calci-fications,"

Pulpal "cysts" are either an artifact-^ or spaces filledwith fluid and surrounded by fibrous connective tis-sue,'"'̂ They can result from isolated pulpal atrophyalong with tissue shrinkage.'*

Mucoid degeneration. Mucoid hes in tbe interstitialspaces between cells and reticulum. With aging, mu-coid increases and acid polysaccharides decrease,*''̂

Calcifications are divided into denticles and diffusecalcifications.* '̂" Diffuse calcifications invariably in-crease with age, while denticle increase is inconsist-ent.«'"

Rationale for current study

Horses' teeth can be used as an indicator of their age,because horses usually have the same life-long diet.This leads to distinctive, attrition-induced, age-relatedwear facets on mandibular incisors. In contrast, hu-mans do not cat the same type of diet and do notshow wear patterns solely on mandibular anteriorteeth. Humans also suffer from dental caries, abra-sion, erosion, and attrition. Hence, a human's age can-not be deduced by wear facets. Some investigators donot believe that teeth can be used to determine a hu-man's age,*' However, the condition of dental struc-

tures can be a biomarker for generalized aging if thefollowing criteria are met; (I) the individual had notundergone prolonged corticosteroid therapy or had asystemic disease such as progeria, den tin o genesis im-perfecta, or vitamin D-resistant rickets (ail show rootcanal closure as a manifestation""^*); (2) involvedteeth are in functional occlusion without local diseasesor treatments, which can accelerate dental componentaging; (3) evaluation is by the use of periodic periap-ical radiographs, which result in a more subjectiveevaluation than does histologie examination, but his-tologie evaluation does not permit foilowup: in ad-dition, periapical radiographs are noninvasive; havebeen taken by dentists on a regular basis for manyyears; are the only type of radiograph that is regularlytaken over a period of years (in contrast to chest, back,or sinus radiographs, which are taken on an as-neededbasis); and can show manifestations of aging of thecementum. dentin, and dental pulp (calcification andpulpal fibrosis, increased sclerotic dentin and second-ary dentin, and hypercementosis) that are visible andmeasurable (eg. decrease in the width and length ofthe root canal); and (4) a correlation could be foundbetween degrees of pulpal fibrosis and calcification(as determined by root canal length and width relativeto the overall length and width of the tooth) and anindividual's age.

To do this, a substantial number of normal teethmust first be examined and correlated with both anindividual's age and state of health. If a significantcorrelation is found between dental component agingand systemic aging, by examination oían individual'snortnal functioning teeth, it could be determinedwhether physiologic age matches chronologic age.

Method and materials

From the alphabetically arranged dental office files ofone investigator (RSS), who had been in practice atthe same location for 20 years and had kept followups,including periodic periapical radiographs, on a largenumber of patients, the office manager selected therecords of the first 104 patients that met the followingcriteria: (I) had undergone no corticosteroid therapyor root canai closure systemic disease; (2) had beenpatients for at least 10 years; and f3) had complete-mouth periapical radiographs taken by tbe long conetechnique'' at 5-year intervals (minimum of 10 years)using same angle and exposure and developed andfixed within same time limits.

Only relatively straight, single root canal, disease-

Quintessence International Volume 22, Number 9/1991 713

Endodontics

Table I Mean tooth length (mm)

Group

MenWomen

50 and older49 and younger

60 and older39 and younger

Calcification-relateddiseases

No ealcification-related diseases

No. of subjects

4262

5153

1018

25

79

Tooth length

24.523.7*

24.024.5*

24.924.8*

24.6

24.1*

23-39

60-8055-5950-5445^940-̂ 14

50

4027373535

24.324.424.223.624.3

No statistically significant difference.Statislicatly significant difference frotn olher age groups

free teeth, of approximately the same length (maxillaryincisors and canines and mandibular incisors, canines,and premolars) were to be used. The patients involvedin this study had periodontal treatments, but on theselected teeth, they only had routine cleanings. In adental office with adult patients, it is virtually impos-sible to find patients that have never had a routinecleaning. Periodic, routine cleanings apparently causeminimal pulpal and dentinal changes. With some ofthe involved teeth, over time, horizontal bone loss oc-curred. However, no evidence of calculus or traumawas found. Therefore, the horizontal bone loss wasconsidered to be an aging change and not related toperiodontal disease.

One tooth per patient that fulfilled the above criteria

plus the following two criteria was randomly selectedby the ofHce manager: measured radiographie toothlength was about the same size at all time intervals(to ensure that no tooth shortening was a result ofattrition, caries, trauma, or change in anguiation); andthe radiographie density and contrast was relativelyconstant for all time periods (did not fade, yellow,smudge, or become distorted with age).

The following data were then entered for each pa-tient: age (range and mean from first visit to last);gender; tooth selected; and history of systemic disease(if any).

An investigator (JVE) unaware of the demographicdata used a magnifying lens, a milhmeter ruler, and adental viewing box to obtain the following radi-ographie measurements:("/y tooth length (Table ]);(2) coronal length (distance from incisai edge to topof pulpal chamber); (3¡ apical length (distance fromroot apex to apical end of root canal); (4) root canallength (tooth length minus coronal length minus ap-ical length); (5) cervical width (width of root canalat the cervix); (6) midroot width (width of root canalat the halfway point); and (7) apical width (width ofroot canal at the apex). From these measurements,calculations were made of root canal shrinkage (ra-diographie evidence of calcification and fibrosis); ina vertical direction (coronal plus apical shrinkage); ahorizontal direction (combined cervical, midroot, andapical shrinkage); and as a combined factor (com-bined vertical and horizontal shrinkage) (Fig 1).

Because the gender distribution was fairly close,men (n = 42) were compared to women (n = 62).When the mean ages of all patients were obtained, itwas found that there was an almost equal distributionof patients aged 50 and older and 49 and yotmgerHence, comparisons were made between patients witha mean age of 50 and older (n == 51) and 49 andyounger (n = 53). It was also found that there was acomparable distribution of patients with a mean ageof 60 and older (n = 10) and those with a mean ageof 39 and younger (n = 18); comparisons were madebetween those two groups. Because it was hypothe-sized that an increase in soft tissue calcification thatis more prevalent in advanced age (eg, arthritis)^*could also be found in aged dental pulps, patients withpossible calcification-re la ted diseases were comparedto those without calcification-related diseases. Pa-tients with arthritis, gout, kidney stones, gallstones,atherosclerosis, and hypertension were classified ashaving a ealcification-related disease (n = 25). Allothers were placed in a second group (n = 79),

714 Quintessence International Volume 22, Number 9/1991

Endodontics

Fig 1 Representation ot the radi-ographie measurements and cal-culations of a hypothetical mandi-bular central incisor in the samepatient at 23 and 45 years of age.

CoronilLengths5.0 mm

CervicalWidlh^1.5 mm I \

RoolCanal

Tool hLength (23 mm).CoronalLength (5 mm)-ApicalLength (O mm)=IS mm

ApicalLcngth-0.0 mm

Rool canal widlh-cervicalwidth (1.5 mm) + mid-rootwidth (1.0 mm) + apicalwidth (0.S inm|=3,0 mm

Root canal Iength=l8 mm at age 23

CorunalLen|;lh=9.0 mm

RoutCanalLength:Tool hLenglh (23 mm)-CoronalLength (9 mm)-ApicalLength (3 mml=11 mm

ApicalLength-3.0 mm

Root canal widths^cervicalwidth (O.g mm) 4̂ mid-roolwidth (0.5 mm) t apicalwidth (0.0 mm)=l.3 mm

Root canal length=1I mm at age 4S

Vertical root canal shrinkaKe-0.3Z mm/yr (18.0 mm-12.0 mm/22 yr)Coronal root canal shrinkage=O.I8 mm/vr (9.0 mm-S.O mm/22 yr)Apical root canal shrinkage-0.14 mm/yr (3.0 mm-0,0 mm/22 yr)

Horizontal root canal shrinkage-0.07 mm/.vr (3,0 mm-1.3 mm/22 yr)Cervical root canal shrinkaee-0,03 mm/jr (I.S mm-0.8 mm/22 jr)Mid-root root canal shrinkage^O.OZ mm/yr (l.t) mm-0.5 mm/22 yrlApical root canal shrinkage-0.02 mm/yr (0.5 mmO.O mm/22 vr)

Combined root canal shrinkagc=0.39 mm/yrVertical root cnnal shrinkage=0.32 mm/yrHori/ortal root canal shrinkage=0.07 mm/yr

Root canal measurements of the previously selectedteeth at various ages were compared.* We also meas-ured an additional 120 single-rooted, disease-free teethfrom individuals of various ages. After the measure-ments were examined, it was found that there wereinsufficient numbers of patients at any one age to give

' It was originallj' believed that increased denticle formation andincreased cementum deposition could be evaluated from periap-ical radiographs. However after the radiographs were esamined,it was found that /I) it was not possible to observe a sufficientnumber of patients with radiographicaliy visible denticles, andeven in those patients in whom they could be observed, changesover time were variable; And(2) increases in cemetltum depositionwith age, if they occurred, were too small to be visible on periap-ical radiographs.

Statistically significant results. Therefore, it was fellthat, it would be necessary to determine if a patternof root canal measurements (eg, length and width)could be found for different age ranges. Hence, thepatients were placed in six age groups (Table ] ). Foreach group, measurements taken per tooth were toothlength, root canal length, root canal width at the cer-vix, root canal width at midroot, and root canal widthat the apex.

Analyses of variance with repeated measures wereemployed for all comparisons. For the four compari-sons involving gender, age, and calcification-relateddiseases, the repeated measures were vertical shrinkage(combined coronal and apical), coronal shrinkage, ap-ical shrinkage, mesiodistal shrinkage, and combined

Quintessence International Voltjme 22, Number 9/1991 715

Endodontics

Table 2 Mean pulp canal shrinkage*

Verticalshrinkage

(mm/yr)

Coronalsbrinkage

Apicalshrinkage

Mesiodistalshrinkage

Combinationshrinkage

No, Mean SD Mean SD Mean SD Mean SD Mean SD

MenWomen

Mean

4262

0,3J50,249

0,276

0.1430,165

0,154

0,1630.132

0.144

0,0930.094

0.094

0.1520,117

0,131

0-1200.117

0,119

0.0620,055

0.058

0-0290.037

0,033

0.3780.304

0.334

0.1530.184

0.169

Calcification and fibrosis.

Table 3 Two-factor analyses of variance with repeated measures for ptilp canal shrinkage

Source

Sex (A)Subjects with groupsRepeated measures (B)ABB X subjects with groups

df

1102

44

408

Sum of squares

2269,71250739.85552967.473

741.88828693,439

Mean square

2269.712497-450

13241.868185-47270,327

F

4,563

188.2902.637

P

.0351

,0001,0336

Table 4 AB incidence

Repeatedmeasures

Level 1(men)Level 2(women)Total

No-MeanNo,

MeanNo,

Mean

Vertical

4231,5246224.887

10427,567

Coronal

4216,3106213.161

10414, 433

Apical

4215,2146211,726

10413,135

Mesiodistal

426,238

625.827

1045,827

Combined

4237.7626230.435

10433.294

Total

21021,410

31017-152

52018,871

shrinkage (combined vertical and mesiodistal). For thefifth set of comparisons (various ages), the repeatedmeasures were root canal length, rool canal width atthe cervix, root canal width at midroot, and root canalwidth at the apex.

For computer use, the data were analyzed as inte-gers; this is refiected in the summary of analyses ofvariance presented. However, the summary of meanvalues is shown in the original thousandths of a mil-limeter- All analyses were performed by an investigator(MLF) who was bhnd to the demographic aspects ofthe study.

Results

The mean values and analyses of variance for cotn-parison of men and women are presented in Tables 2to 4, Because of the extensive data, only summariesare presented; detailed tabular restilts are availablefrom the senior author-

Statistical significance was found with respect togender, repeated measures, and interaction betweengender and repeated measures (Table 3), For purposesof examining each repeated measure separately, post-hoc analyses were performed with the Scbeffé F test-

716 Quintessence Internationai Volume 22. Number 9/1991

Endodontics

Differences in vertical shrinkage were found to bestatistically significant (F = 4.53; P = .0357). Themean value for men (0.315) was greater than that forwomen (0.249) (Tables 2 and 4). Differences in coronalshrinkage, apical shrinkage, and mesiodistal shrinkagewere not statistically significant. Differences betweengender (men = 0.378; women = 0.304) in combinedshrinkage were statistically significant (F = 4.53;P - .0357).

Statistical significance was found with respect toage, repeated measures, and interaction between ageand repeated measures. Differences in vertical shrink-age, coronal shrinkage, apical shrinkage, mesiodistalshrinkage, and combined shrinkage were statisticallysignificant; mean values for individuals age 50 andolder were greater than for individuals age 49 andyounger, and mean values for those 60 and older weregreater than values for those 39 and younger.

Statistical significance was also found with respectto disease, repeated measures, and interaction betweendisease and repeated measures. For vertical shrinkage,coronal shrinkage, apical shrinkage, and combinedshrinkage, statistical significance was found; meanvalues for individuals with calcification-related dis-eases were greater than values for individuals withoutthose diseases. Differences in mesiodistal shrinkagewere not statistically significant.

Statistical significance was found with respect toage, repeated measures, and interaction between ageand repeated measures for individuals aged 23 to 39compared to all other age groups. For root canallength and cervical width, statisticaily significant dif-ferences were found for individuals aged 23 to 39 com-pared to all other age groups. Mean values for indi-viduals aged 23 to 39 were greater than those for in-dividuals aged 60 to 80, 55 to 59, 50 to 54, 45 to 49,and 40 to 44, Root eanal midroot width was statisti-caily significantly greater for individuals aged 23 to

39 than for all other age groups except the group aged40 to 44. Root canal apical width was stafisticallysignificantly greater for individuals aged 23 to 39 thanfor all other age groups except the group aged 55 to59. Representative patients are shown in Figs 2 to 4.

Discussion

Teeth were examined only from patients who had noevidence of local disease and trauma or systemic dis-ease that could cause or accelerate root canal closure.Therefore, the radiographie findings of significantlyincreased root canal closure in men compared to wom-

en and with advancing age apparently is the result ofgenetic and physiologic, age-induced calcification andfibrotic changes that accelerate in men and older in-dividuals. The finding that the dental pulp of womenshowed fewer aging changes is apparently related tothe general finding that women live longer than men."However, since statistical significance was only foundfor the vertical shrinkage eomponent of the combinedroot canal shrinkage, gender does not appear to be asimportant as age in the determination of root canaland secondary dentinal calcification and fihrosis. Age-related changes in dental pulp were further corrobo-rated by the even higher rate of root canal closurefound at age 60 and older compared to that found atage 39 and younger.

This hypothesis is further supported by the findingsobtained when vertieal root canal shrinkage was sep-arated into its two component parts: coronal root can-al shrinkage and apieal root eanal shrinkage. Coronalroot canal shrinkage (from the biting surface towardthe top of the pulpal chamber) (see Fig 1) is mostlikely a response to normal biting and chewing, whichare generally stronger in younger individuals becauseofthe better development ofthe muscles of masfica-fion and the stronger biting force. In advanced age,these muscles usually beeome weaker, and with theloss of teeth, biting forces generally are weaker. Apiealroot canal shrinkage (from the root end toward theapical end ofthe root canal) is most likely a responseto physiologic aging. Therefore, if only normal chew-ing and eating were responsible for root canal closure,it would be expected that root canal closure would beat a maximum when chewing forces are optimal (prob-ably in the 23- to 39-year-old group).

However, the findings showed that root canal clo-sure increased as patients aged, and it was at a max-imum in advanced age (the 60- to 80-year-old group).The findings showed that it was the apical componentof root canal shrinkage that accelerated in older in-dividuals. In the older age group, the mean apicalshrinkage was significantly higher than the mean co-ronal shrinkage. In younger people, apieal shrinkagewas almost identical to coronal shrinkage. Thus, itappears that root canal closure in the elderly is mainlyphysiologic.

Age-related pulp calcificafion and fibrosis could bepartially related to a disease-induced increase in softtissue calcification, as indicated by the finding thatpatients with calcification-related diseases showed ahigher rate of root canal closure than did patientswithout these diseases.

Quintessence International Volume 22, t^umber 9/1991 717

Endodontios

Fig 2a Age Fig 2b Age 62.

Fig 3a Age 54, Fig 3b Age 64.

Fig 4a Age 50, Fig 4b Age 64,

Figs 2a and 2b Periapical radi-ographs of a mandibular right eet̂tral incisor in a female patient, (ar-rows) Root canals.

Figs 3a and 3b Periapical radi-ographs of a mandibular right lat-eral incisor in a female patient, (ar-rows) Root canais.

Figs 4a and 4b Periapical radi-ographs of a mandibular left cen-trai incisor in a male patient, (ar-rows) Root canals.

718 Quintessence International Volume 22, Number 9/1991

Endodontics

The present finding of a statistically significant re-duction in the length and width of root canals withadvancing age appears to show that increased rooteanal calcification and tlbrosis and sclerotic and sec-ondary dentinal formation, as evidenced by radi-ographie measurements, are physiologic processes re-lated to increased calcification and fibrosis of soft tis-sues.̂ ^ Because the current sample was too small toprovide a valid estimate of the mean length and widthof a root canal of a normal tooth at a specific age. itis necessary to do a cross-sectionai study of periapicalradiographs of patients' teeth at various ages (pres-ently under study). Should valid and reliable meas-urements of root canals at specific ages be found, thenthese findings could prove helpful in age identificationfor forensics and anthropology

If ftitnre studies show that lifestyle can affect rootcanal closure, then radiographie root canal measure-ments of normal teeth cotild prove helpful as abiomarker of aging.̂ ^

Références

t. Mjör lA: Human coronal denline: structure and reactions. OralSurg Oral Med Oral Palhol 1958;33:810-823.

2. Jotianson G: Age déterminations from tiQman teeth. OdoniolRe\- 1971;22. Suppl.

3. Noble HW: The estimation of age from the dentituin. .1 ForenSei Soc 1974;14:215-22I.

4. Sognnaes RF; Forensic stomatology. Part 2. A* Eng! J Med1977:296: t49-t5i.

5. Altini M: Age determination from the teeth: a review. J DemAssoc South Afr t983;38:275-279.

6. Rothwell BR, Haglund W, Morton TH Jr: Dental identificationin serial homicides: the Green River murders. / Am Dem Assoc

7. Stack MV, Feamhead RW: Toolh Enamel. Bristol, England,John Wright and Sons Ltd. 1965.

8. Ketterl W: Age-induced changes in the teeth and their attach-ment apparatus. In! Dem J t983;3î:262-27t.

9. Bhtissery BR: Modifications of the dental pulp during devet-cpment and aging, in Finn SB (ed): Biology of the Denial PulpOrgan. Birmingham, Ala, University of Alabama Press, 1968,pp 145-1 fi8.

to. Brudevold F: Age changes in dentat enamel. Orske Tannlage-farenings Tidende 1957:67:451^58.

11. Dahlberg AA: Clinical aging patterns in teeth of different pop-ulation groups, in Symposium: Aging: Some Sacial and Biolog-ical AspeeLs. Chicago, American Association of Advanced Sci-ence, t959. pp 357-366.

12. Helfman PM. Bdda JL: Aspartic acid racemization in toothenamel from living humans. Proc Nad Aead Sei USA1975;72:289t-2894.

13. Grahnén H, Myrberg N, Oilmen P: Fluoride and dental age.Acta Odonwt Scand

14. Morse DR' Clinical Emimkmlologv. Springfield, III, Charles CThomas Pubi. 1974.

15. Gustafson G: Age delerminations on teeth. J Am Dent Assoi1950;4t:45-54.

t6. Will S: Teslsd accuracy of LI decedent's age by teeth. J fndiamiDem Assoc 1985;64:15-17.

17. Setlzer S: Endodon!olog\. ed 2. Philadelphia. Lea & Fetiiger,I98S.

18. Nitzan D, Michaeli Y, Weinreb M, el LII: The effect of aging ontooth morphology: a sludy on impacted teeth. Oral Surg OralMed Oral Patliol I986;61:54-60.

19. Stein TT, Corcoran JF: Anatomy of Ihe root ape\ and its his-tologie changes with age. Oral Surg Oral Med Oral Pathol1990;60:238-242.

2Ü. Zander HA, Hurzeler B: Continuous cementum apposition./ Dem Res l9i8:37:i035-t044.

2t. Stolt GG, Sis RF. Levy BM: Cemenlal annulation as an agecriterion in forensic demistry. J Den! Re.i 19IÍ2;61:ÍÍ14-817.

22. Settzer S: Classification of pulpal pathosis. Oral Surg Oral MedOrat Pathol 1972;34:269-287.

23. Nalbandian J, Gonzales F. Sognnaes F: Sclerotic age changesin root dentin of htiman teeth as observed by optical, electronand x-ray microscopy. J Dent Res 1960;39:598-607.

24. Naltiandian J: Age changes in human teelh. / Dent Res1959,38:681-682.

25. Mites AEW: Dentition in Ihe estimation of age. J Dem Res1963;42:255-263.

26. Johnson CC: Transparent dentine in age estimation. Oral SurgOral Med Oral Pathol t968;25:834-838.

27. Bang G, Ramm E: Delermination of age in humans from rootdentin transparency. Ada Otiomol Scanil t970;28:3-35.

28. Schwarz HR. Blick U, Liebhardt E: Age determination ofteeth.Beiir Geridul Med 197S;36:369-Î72.

29. Whittaker DK, Kneale MJ: The dentine-predentine interface inhuman teeth. Br Dem J 1979:146:43^6.

30. Carrigan PJ, Morse DR. Fürst ML, et al: A scanning electronmicroscopic evaluation of human denlinat tubules according toage and tocation. / Endod 1984; 10:359-363.

31. Dalilz GD: The hardness of dentine related lo age. Aust Den!J l962;7:463-464.

32 Brinkman B, Hartmann C: Determmatiiin ol" thí mineral con-tent and the Iransparency of the root dentine of human teeth.Forensic Sei Int 1980:15:93-101.

33. Seltzer S, Bender tB: The Denial Pulp, cd 3, Philadelphia, JBLippincolt, 1984.

34. Morse DR: Stress and bruxisni. J Human Slre.^^ t982;8:43-54.

35. Ferguson DB: An overview of physiologicat changes in the agingmouth, in Ferguson DB (ed): The Aging Mouth. New York,Karger, 1987, pp 1-5.

36. Morse DR: A review of age-related changes of the dental pulpcomplexand their relationship to systemic aging. Parts 1-4. OralSurg Oral Med Oral Pathol (in press].

37. Fiied K: Changes in innervation of dentine and pulp with age,in Ferguson DB (ed): The Aging Mouth. New York, üarger,1987, pp 63-84.

38. Boyle PE: Kroiifeld's Hisiopalhology of the Teeth and Their Sur-rounding Structures, ed 4. Philadelphia. Lea & Febiger, 1955.

39. Bhaskar SN: Synopsis of Oral Pmhology. ed 6. St Louis, CVMosby Co. 1961.

40. Kramer IRH: Pulp changes of non-bacterial origin. Im Dent J1959;9:435-450.

Quintessence Internationa! Volume 22, Number 9/1991 719

Endodontics

41. Nielsen CJ: Coltagen changes in the dental pulp, in FergusonDB (ed); The Aging Moiilh. New York, Karger, 1987, pp 111-125.

42. Childress R, Sayegh F: Effects of age on pulp ultrastructures,J Dent Re.i 1979;5R;246.

43. Quigley MB; Functional and geriatric changes of the humanpulp. Oral Siirg Oral Med Oral Futliol I97k32:795-8O6,

44. Shik:U;.i H, Utsumi N, Fujimoto D; Collagen in aging bone ofthe jaw. in Ferguson DB (ed): The Agini; Mouth. New York,Karger, 1987. pp 85-95,

45. Nielsen CJ. Bentley J, Marshall V\ Agc-rclaled changes iu re-ducible cross-links of humati detital pulp collagen Arch OralBiol 1983;2S;75<)-764,

46. Bhussery BR, Emmel V; Changes in the nitrogen content of theenamel with age, J Dent fief iy55:34;672.

47. Bernick S, Nedelman C; Effect of aging on the human pulp.

48. Stewart JM: The possible significance uf lipids in calcification,in Finn SB (ed); Biologv of the Dental Pulp Organ. Birmingham,AUi, University of Alabama Press, 1968, pp 249-263.

49. Bunting RW, Hill TJ; A Textbook of Oral Pathologv. ed 2.Philadelphia, Lea & Febiger, 1940.

50. Bernick S; Age changes to the dental pulp, in Ferguson DB ¡ed];77ic Aging Mouth. New York, Karger, 1987, pp 7-30.

51. Somerman M¡, Hoffeld JT, Baum BJ; Basic biology and phji!-iology of oral tissues: overview and age-associated changes, inTryon AF (ed): Oral Heatth and Aging: An Interdisdplinary Ap-pnimh to Geriatrie Dentistry. Littleton, Mass, PSG Publ Co,l9Bf>.

52. Gold SI; Root canal calcification associated with predtiisonetherapy: a case report. / Am Dent Asîot 19R9; 119:523-525.

53. Album MA, Hope JW: Progeria; report of case. Oral Surg Ora!MedOrai Patltol 195S;ll;985-989.

54. Witkop CJ; Symposium on Cenetie.i Related to Dental Heailh.New York, McGraw-Hill Book Co. 1962.

55. Goaz PN, White SC; Oral Radiography. Principles and later,pretation. St Louis, CV Mosby Co, 1982.

56. Morse DR; Aging; causes and control. Int J Psychosim19883512^2

57. Morse DR, Fürst ML. Women Under Stress. New York, VanNostiand Reinhold, 1982.

58. Mein KC; Permars Oral Embryology and Microscopic Anatomy.ed 7. Philadelphia, Lea & Febiger, 1982. D

Books on

Ceramics

Esthetic Approach to MetalCeramic Restorations for theMandibular Anterior RegionK. Müterthíes

Ciomplelely describes all stages of fabricating a

tnandibular anterior bridge. Every step is clearly

shown in more than 140 full-color illustrations,

whicb are accompanied by practical advice from

the author.

Contents include: Natural-Look ing Crowns and Bridges;Framework Fabrication, Ceramic Buildup; Definitive Shaping;and more.

94 pp/149 color illus/$48/Code; 2206

Replication of Anterior Teethin the Four Seasons of LifeK. Miiterthies

A guide to creating full-coverage crowns that include

age-specific characterizations. An atlas format of

over 260 color photographs depicts the step-by-step

technical procedures for fabricating one tooth for

each "season" of life.

Conlenls: Four Seasons: The Life of Man—includes The Springtooth; The Summer tooth; The Autumn tooth; The Winter tooth:Four individual teeth as examples; Tooth form; Surface structureand characterization; Suntime ceramics. The Atlas—includesPreparalion of the framework; A Spring tooth: A Summer tooth;An Autumn tooth; A Winter tooth; Staining.

92 pp/3ei illus/$62/C(ide: 2362

To order Quintessence Books, use the order card bound in this issue.

720 Quintessence International Volume 22. Number 9/1991