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Journal of Clinical Periodontology 1978: 5: 213-225

Key words; Tooih mobiliiy — trauma from occlusion — periodontitis.Accepted for publication; September 5, 1977.

The effect of progressive toothmobility on destructive periodontitis

in the dog

STUKE NYMAN, JAN LINDHE AND INGVAR ERICSSON

Department of Periodontology, Faculty of Odontology, University of Gothenburg,Gothenburg, Sweden

Abstract. The aim of the present study was to assess the influence of traumatic forcescausing a gradually increasing tooth mobility on an ongoing destructive periodontitis.

The experiments were performed in five dogs fed a diet which permitted dental plaqueaccumulation. Periodontal breakdown was induced around the mandibular third and fourthpremolars (4P, sP and P3, Pa) by the placement of plaque retention ligatures around theneck of the teeth. After 330 days, when approximally 50 % of the supporting tissues hadbeen lost, mucoperiosteal flaps were raised around the four premolars and notches pre-pared in the buccal root surfaces at the marginal termination of the alveolar bone. Thenotches served as landmarks for measurements to be made in histologicai sections. Theflaps were resutured and new plaque retention ligatures placed around the roots of alifour teeth.

One week later (Day 0), P3 and P4 (test teeth) were subjected to jiggling forces in abucco-lingual direction with the use of an elevator. The jiggling procedure which had aduration of 30 seconds, was repeated on Days 4, 8, 12 and 16, and was guided in such away that the tooth mobility gradually increased during the experimental period. The ani-mals were sacrificed on Day 26, and sections of 4P, .iP and Pa, F4 were prepared for lightmicroscopic examination.

The results of the study demonstrated that jiggling forces, resulting in a progressive in-crease of tooth mobility, mediated an enhanced rate of destruction of the supporting ap-paratus in dogs with an ongoing process of periodontal tissue breakdown.

The significance of trauma from occlusion with one or a varying number of teeth"as an etiologic or contributing factor in pe- (Stones 1938). Findings from autopsy mate-riodontal disease has been controversial ever rial (for review see Svanberg 1974a) havesince Karolyi in 1901 postulated an inter- also led to the conclusion that occlusal trau-actlon between occlusal stress and "alveolar ma is "an integral part of the disease peri-pyorrhea". Early reports from animal ex- odontitis rather than an unrelated diseaseperiments by Box (1935) and Stones (1938) entity. As such, trauma from occlusion is anseemed to indicate that "traumatic occlusion etiologic factor in the formation of infra-is an etiological factor in the production of bony pockets and angular or crater-likethat variety of periodontal disease in which osseous defects" (Glickman 1967). The lackthere is vertical pocket formation associated of proper controls, however, in the studies

214 NYMAN, LINDHE AND ERICSSON

referred to, makes it rather difficult to eval-uate the significance of the coticlusionsmade.

Experiments carried out in different lab-oratory animals (e.g. monkeys, dogs, rats)have clearly demonstrated that occlusalforces are incapable of inducing inflamma-tion in an initially non-inflamed gingiva orincrease the extent or severity of a plaque-induced overt gingivitis (for review seeSvanberg 1974a). Indeed, findings by Waer-haug (1955), Ramfjord & Kohler (1959),and Svanberg (1974b) have conclusivelydemonstrated that forces produced by mas-tication do not interfere with the supra-alveolar tissues. Hence, today it is a unani-mously accepted fact that trauma from oc-clusion can neither produce tissue alter-ations characteristic of chronic gingivitis,nor shift a chronic gingivitis into a destruc-tive periodontitis.

Evidence from clinical trials and animalexperiments have shown that microorga-nisms wliich form dento-gingival plaquesare capable of producing gingivitis (for re-view see Page & Schroeder 1976). Findingshave also been reported which show thatlong-standing gingivitis in the presence ofsubgingivally located plaque eventually de-velops into a progressive and destructive pe-riodontitis (Lindhe et al. 1975). This meansthat at least one form of periodontal diseaseis of bacterial origin. The question ariseswhether or not forces produced by the mas-ticatory muscles can interfere with the rateof progression of plaque-induced periodont-itis.

In 1958 Wentz et al. studied the effect of"jiggling forces" (i.e. forces applied alter-nately in a buccal and lingual direction) onthe periodontai tissues of teeth with normalgingiva or overt gingivitis. They reportedthat this type of trauma resulted in resorp-tion of bone and connective tissue and ledto an increasing widening of the periodontalligament. After 3-6 months of the experi-

ment, the ligament around the jiggled teethwas more than three times as wide as in anon-traumatized tooth. However, Wentz etal. (1958) stated that at one point the dam-aging effect of the jiggling trauma becamenullified by the extreme width of the perio-dontal space and no further resorption oc-curred. The tooth had become extremelyhypermobile but the periodontal ligament,the alveolar bone and the cementum hadbecome adapted to altered functional de-mands. In this study, trauma from occlusionresulted in the formation of angular osseousdefects but not in loss of periodontal tissuesupport to the teeth. The authors concludedthat "the question may still remain, how-ever, of what consequence would a perio-dontal inflammation have in the presence ofthe damaged tissues caused by continuedocclusal trauma".

This problem has recently been studied inthe dog by Lindhe & Svanberg (1974) andin the monkey by Meitner (1975). The re-sults obtained in these two studies are, how-ever, somewhat conflicting. Lindhe & Svan-berg (1974) observed an increased rate ofpocketing in teeth subjected to the combinedeffect of marginal periodontitis and jigglingtrauma as compared to teeth with periodon-titis alone. Meitner (1975), on the otherhandj found such an aggravating effect bytraumatic forces in oniy one of four toothsurfaces studied and conciuded that "itseems unlikely, therefore, that there is a co-destructive factor effect on the loss of con-nective tissue attachment". Differences in-herent in the experimental design of thetwo studies referred to may explain the dis-crepancy between the results obtained. Thus,Lindhe & Svanberg worked with dogs,whereas Meitner used squirrel monkeys. Inthe dog experiments, cap-splints elicitedtraumatic forces on the experimental teetheach time the animals occluded and disoc-cluded. These forces produced tooth hyper-mobility and repeated measurements using

PROGRESSIVE TOOTH MOBILll'Y AND PERIODONTITIS 215

the Periodontometer (Muhlemann 1954) re-vealed that the amplitude of the tooth move-ment gradually increased during the entireexperimental period. This means that theperiodontal tissues around the experimentalteeth were unable to adapt to the alteredfunctional demands during the observationperiod (Lindhe & Nyman 1977). In themonkey experiments, the traumatizing forcewas produced by inserting an orthodonticelastic between the first and second bicuspidand between the third bicuspid and the firstmolar alternately, the direction of the forcebeing changed only once every second day.This "repetitive mechanical injury" resultedin an increased tooth mobility, the amplitudeof which was limited by the approximal con-tacts established by the neighbouring teeth.Hence, iu the monkey model experiment,the periodontal tissues evidently were al-lowed to adapt to the jiggling forces.

The studies referred to above demon-strate that in different situations traumafrom oeclusion may or may not act as a co-destructive factor in the presence of an on-going destructive periodontitis. It is impor-tant therefore to further assess under whatcircumstances traumatic forces may aggra-vate progressive periodontitis.

In the present study an attempt was madeto assess if traumatic forces causing a pro-gressive tooth mobility influence the rate ofdestructive periodontitis.

Material and Methods

Five mongrel dogs, about 8 months of ageand weighing 13-15 kg, were used. The ani-mals had been itioculated against distemperand canine hepatitis (Dohyvac D. H.®,Philips-Duphar, Amsterdam, The Nether-lands) hefore 3 months of age.

Preexperimental ProcedureDuring a period of 4 weeks preceding theexperiment, the teeth of the dogs were

Fig. 1. Radiographic appearance of the lowerright premolar region of dog No. 4 at the startof the study (Day — 337).Rontgenbild der Situation in der Region desuiUeren rechten Prdmolaren beim Hund Nr. 4zu Anfang der Studie (Tag —337).Aspect radiographique de la region des premo-laires droites chez le chien No 4 au debut deI'etude (Jour—337).

cleaned with toothbrush and dentifricethree times a week. At the end of this pre-paratory period, healthy gingivae had beenestablished in all animals. No pathologicallydeepened pockets could be detected andradiographs obtained at the start of thestudy revealed that tbe supporting alveolarbone had normal height (Fig. 1).

Experimental ProcedureExperimental periodontitis and jiggling trau-ma. The design of the experiment is pre-sented in Fig. 2. During the entire studywhich lasted 363 days, all oral hygiene mea-sures were abandoned and the dogs fed adiet (Hamp et al. 1972) permitting grossplaque accumulation. In order to enhancethe rate of breakdown of the periodontaltissues around the lower third and fourthpremolars (̂ P, 3P and Pg, P^), cotton flossligatures (Sjuntorps Fiskegam 8/12) wereplaced around the neck of the teeth on Day


TRAUMAEXP.PEFIIODONIITIS NOTCH

X-RAY I I t t IBIOPSY

X-RAY

DAYS -•-337

c-7

NOTCH BiDPsr

X-RAY

Fig. 2. Outline of the experiment. Periodontal breakdown was induced on Day —337 by placingligatures around 4P, 3P and P3, P4. Notches were prepared in tbe buccal root surfaces of the teethat the marginal level of the alveolar bone crest on Day — 7 . The test teeth were subjected tojiggling trauma on Days 0, -i- 4, -h S, -\- 12, H-16. The experiments were terminated on Day -(-26.Planung der Studie. Die Auflosung der parodontalen Gewebe wurde am Tage —557 durch Le-gen von Ligaturen um die Zahne iP, sP und P3, Pi herum, induziert. Am Tage —7 wurden inder Hohe der maginalen Begrenzung des alveolaren Knochens in die bukkalen Wurzeloberfla-chen der Testzdhne Kerben prdpariert. Die Testzahne wurden dann an der Tagen 0, + 4, -\~ 8,+ 12, + 16 hin- und herkippenden (jiggling) traumatisierenden Kraften ausgesetzt. Das Experi-ment wurde am Tage + 26 abgeschlossen.Plan de I'experience. Une destruction parodontale a ete determinee au Jour —337 en ptagant desligatures autour de iP, sP et Ps, Pi. Des rainures ont ete preparees au Jour —7 sur les faces ves-tibulaires des racines de ees dents au niveau de la limite marginale de I'os alveolaire. Ees dentsexperimentales (test ~ T) ont ete soumises a un traumatisme de type "va-et-vient" (jiggling) auxJours 0, -\- 4, -\- 8, -{- J2, -{- 16. Ees experiences se ,sont terminees au Jour -\- 26.X-ray ~ radiographie. Notch — rainure. C (Control) ~ temoin.

-337. This method of inducing experimentalperiodontitis was described by Kennedy &Poison (1973) and has been modified foruse in dogs by Ericsson et al. (1975). After3 weeks with the ligatures in situ, the de-struction of the supporting tissues hadreached the bifurcation area of 4P4 and gP .̂New cotton floss ligatures were insertedthrough the bifurcations and ligated aroundeach root separately. This resulted in a fur-ther rapid breakdown of the supporting ap-paratus but also in a marked recession ofthe gingival tissues. Once every third weekthe ligatures were exchanged and replacedto a subgingival position.

On Day -137, the pulp tissues of the lowerthird and fourth premolars were extirpatedand the root canals filled with guttapercha.On Day -7, raucoperiosteal flaps were raisedaround the premolars on both sides of themandible. Notches were prepared in thebuccal root surfaces of the premolars at thelevel of the marginal bone crest. The not-

ches served as landmarks for measurementsto be made in histological sections. Theflaps were resutured and new cotton flossligatures were placed around each of theroots of the four teeth.

One week following surgery, i.e. on Day 0(Fig. 2), the sutures were removed and thetest teeth (Pg and P )̂ were subjected to jig-gling forces in a bucco-lingual direction.The forces were intermittently applied tothe teeth for 30 sec using an elevator. Theelevator was inserted from the buccal aspectof the jaw into the interproximal spaces be-tween Pg and P3 and between P^ and M .̂Jiggling was carried out utilizing P^ and Mjas support for the elevator. The force wasapplied to the crown of the teeth in a pre-determined way. The elevator was never al-lowed to reach contact with tbe gingivalmargin. The jiggling procedure was repeatedin the same manner on Days -1-4, -i- 8,-^ 12 and -}- 16. The force utilized to jigglethe teeth was adjusted so that tooth mobility

PROGRESSIVE TOOTH MOBILITY AND PERIODONTITIS 217

in a bucco-lingual direction (assessed hy thePeridontometer, T = 500; Muhlemann1954) following jiggling was around 150mtn/100 on Days 0, + 4 and -i- 8 and 200mm/100 on Days + 12 and -K 16. The ani-mals were sacrified on Day -|- 26.

Tooth mobility. The mobility of test teeth(P3 and P4) and eontrol teeth (̂ P and gP)was assessed prior to jiggling on Days 0,-F 4, + 8, -h 12 and -f 16 and, in addition,on the day of sacrifice. The measurementswere carried out with the use of the Perio-dontometer (T - 500).

1 APEX

Radiographs. Radiographs of the test andeontrol tooth regions were obtained on Days-337, -7 and -f 26 (Fig. 2). A device wasutilized which ensured reproducible X-rayprojeetions (Eggen 1969).Histometric assessments. Foiiowing sacri-fice, the mandibles were removed and di-vided along the midline. Specimens contain-ing the test and control teeth were dissectedand fixed in 10 % formalin. The specimenswere then sectioned en bloc (eaeh block

Fig. 3. Schematic drawing illustrating the vari-ous linear distances and areas which were mea-sured in the histologica! sections.CEJ = cemento-enamei junctionPL = the apical border of the microbial

plaqueA = the apical border of the notchJE = the most apica! cells of the junctiona!

epitheliumICT ~ the apical border of the inflammatory

ce!I infiltrateBC = the marginal alveolar bone crestPLA — periodonta! ligament areaSchematisierte Skizze der versehiedenen linea-ren Abstdnde und Flachen, die in den histolo-gisclien Schnitten vermessen wurden.CEJ = Schmelz-ZementgrenzePL = apikale Grenze der mikrobiellen

PlaqueA = apikale Grenze der KerbeJE — die am weitesten apikal liegenden Zel-

len des EpithelansatzesICT = die apikale Grenze des entzUndlichen

ZellinfiltralesBC = die marginale Grenze des alveoldren

KnochensPLA = die desmodontale RegionRepresentation schematique illustrant les diffe-rentes distances lineaires et les surfaces qui ontete mesurees sur les coupes histologiques.CEJ = jonction cement-emailPL = limite apicaie de la plaque microbienneA •= limite apicaie de la rainureJE = cellules les plus apicales de I'attache-

ment epithelialICT = iimite apicaie de I'infiltration de cel-

lules inflammatoiresBC = Crete marginale de I'os alveolaireFLA = superficie du desmodonte

21.8; NYMAN, LINDHE AND ERICSSON

containing one root), decalcified in 10 %trifluoroacetic acid, dehydrated and embed-ded in paraffin. Bucco-lingual sections ofall roots were prepared with the microtomeset at 5 /xm. The sections were stained withhematoxylin-eosin. From each root, fivesections, 20 /xm apart and representing thecentral portion of the root, were used formicroscopic analysis.

In the histological sections the followinglinear distances at the buccal surfaces oftest and control teeth were assessed in themicroscope (60 X) (Fig. 3):1. a) Cemento-enamel junction (CEJ) - the

apical horder of the notch (A)b) CEJ — the apex of the root

Loss of alveolar bone was expressed

CEJ-Aas the quotient X 100

CEJ-Apex2. the apical border of the notch (A) - the

Fig. 4. Clinical appearance of the test toothregion of dog No. 4 after 330 days (Day — 7)of experimentally induced periodontal break-down.KUnisehes Bild der Testzahnregion des HundesNr. 4 nach 330 Tagen (Tag — 7) experimentellinduzierter Auflosung parodontaler Gewebe.

Aspect clinique de la region des dents expiri-mentales du chien No 4 apres 330 jours (e'est-a-dire au Jour — 7) de destruction parodontaleprovoquee experimentalement.

most apical cells of the junctional epi-thelium (JE)

3. A - the marginal level of the alveolarbone crest (BC)

4. A - the apical border of the inflamma-tory cell infiltrate (ICT)

5. the apical border of the microbial plaque(PL) - !CT.

In addition, the size of the marginal 2 mmof the buccal periodontal ligament area(PLA) was determined by the use of a plani-meter (9527-12 Ingut® Polar CompensatingPlanimeter, Ingut Ltd. Sweden). The plani-metric measurements were carried out onmagnified (X 50) drawings of the micro-scopic specimen. This method was describedin detail by Svanberg & Lindhe (1973). Fi-nally, the number of osteoclasts lining thesurface of the alveolar bone within PLAwas determined.

Statistical analysis. Student's paired t-testand analysis of variance were used to assessdifferences between test and control teethregarding histometric as wel! as tooth mo-bility data.

Results

During the 330 days of experimental perio-dontal breakdown, the supporting tissues ofboth test and control teeth markedly deteri-orated. On Day -7, the gingivae around Pg,Pj as well as ^P, ^P displayed obvious signsof inflammation in conjunction with markedgingival recession and open bifurcationareas (Fig. 4). The radiographs obtained onDay -7 revealed that around 50 % of thealveolar bone of the lower premolars waslost (Fig. 5A, B).

At the time of sacrifice (Day -f- 26), theradiographs of the test teeth disclosed pro-nounced further loss of supporting bone(Fig. 6A). In the controls the further break-down of the alveolar bone was less pro-nounced (Fig. 6B).


Fi>. 5. Radiographs from the test (A) and con-trol (B) tooth regions of dog No. 4 on Day — 7.Rontgenbilder der Test- (A) und KontroUregio-nen (B) des Hundes Nr. 4 am Tage -— 7,Radiographies des regions des dents experimen-tales (A) et temoin (B) du chien No 4 au Jour— 7.

Tooth Mobility (Fig. 7)On Day 0, the average mobility of the testand control teeth was similar (test 21 mm/100 ± 5 (S.E.), control 19 mm/100 + 4).During the 16 days of repetitive mechanicalinjury, the test teeth displayed a graduallyincreasing mobility, whereas the mobilityvalues of the controls did not markedlyvary. The mobility measurements carriedout immediately prior to jiggling on Days-h 4, + 8, -I- 12, + 16 and on the day ofsacrifice. Day -f- 26, gave the following

Fig. 6. Radiographs obtained of test (A) andcontrol (B) tooth regions of dog No. 4 at thetime of sacrifice (Day -f 26). Note the enhancedfurther loss of alveolar bone around the testteeth (Pa and P4).Rontgenbilder der Test- (A) und der Kontroll-zahnregionen (B) des Hundes Nr. 4 zur Zeitdes Opferns (Tag + 26). Beachten Sie den wei-ter fortsehreitenden erhohten Verlust des alve-oldren Knochens der Testzdhne (F3 und P4).Radiographies des regions des dents experimen-tales (A) et temoin (B) du chien No 4 au mo-ment du sacrifice (Jour -\- 26). Noter I'augmen-lation de la resorption de I'os alveolaire encours autour des dents experimentales (Ps et

average values: 89 mm/100 ± 11 (S.E.),74 ± 5, 149 ± 34, 194 + 12 and 232 mm/100 + 15. This gradual increase of thetooth mobility was statistically significant(P < 0.001).

NYMAN, LINDHE AND ERICSSON

MM

280

240-

200

160

120

80'

40'

TOOTH MOBILITY500

OTESTD CONTROL1 SE

1 ll-26

•DAYS

Fig. 7. Diagrammatic presentation of the aver-age mobility values obtained of test and controlteeth on Days 0, + 4, + 8, + 12, + 16, + 26(mean ± standard error).Das Diagramm veransehaulicht die durch-schnittlichen Mobilitatswerte der Test- undKontroltzdhne an den Tagen 0, + 4, -h 8, -i-16,+ 26 (Mittelwert ± Standardirrtum).Diagramme presentant les valeurs moyennes dela mobiiite des dents experimentales et temoins(T et C) aux Jours 0, + 4, + 8, + 12, + 16,+ 26 (moyenne + erreur-type).

Histometric assessments (Tables 1 and 2)The measurements made in the histologicaisections showed that the method utilizedto induce periodontitis between Day —• 337and Day — 7 resulted in a breakdown of the

/CEJ-Aperiodontal tissues j - -%; Table 1

\ CEJ-Apexthe degree of which was similar around testand control teeth. Thus, in the test toothregions the average breakdown amounted to42.7 % (S.E. 1.1) of the root length. Thecorresponding figure for the controls was44.6% (S.E. 1.2). This difference was notstatistically significant.

The histometric assessments revealed thatthe test teeth as compared to the controlshad lost more connective tissue attachment(A-JE, Table 1) during the period betweenDay — 7 and Day + 26. Thus, the averageattachment loss in the test regions amounted

to 621 ^ra (+ 84) compared to 146 fxm(± 32) in the controls. Out of 10 experi-mental teeth, eight displayed an attachmentloss which was larger than that of the eon-tralateral control tooth. In no case couldinfrabony pockets he detected. The averagedistance between the notch and the bonecrest (A-BC, Table 1) in the test and controlteeth was 1399 /im (+ 165) atid 883 ^m(± 116) respectively (p < 0.05). Further-more, the average apical extension of theinflammatory cell infiltrate (A-ICT, Table1) was in the test tooth regions almost twicethat noticed in the controls (1252 .̂m +239; 632 fim ± 102). The distance betweenthe most apically located portion of the bac-terial plaque and the apical border of ICT(PL-ICT) was similar in the test and con-trol teeth (Table 1).

The planimetric measurements (Table 2)showed that the size of the periodontal liga-ment area (PLA) of the test teeth was sig-nificantly {P < 0.001) larger than that ofthe controls. The number of osteoclasts lin-ing the bone surface adjacent to PLA wason the average 6.9 in the test regions and0.6 in the control regions (P < 0.001).

Discussion

The present experiments demonstrated thatrepetitive mechanical injury resulting in aprogressive increase of tooth mobility, pro-duced an enhanced rate of destruction ofthe supporting apparatus in dogs with anongoing process of periodontal tissue break-down.

This observation should be evaluated incontext with the results presented by Svan-herg & Lindhe (1973) and Lindhe & Svan-berg (1974). They studied the effect of jig-gling forces on premolars of dogs witheither normal periodontium or with an on-going experimentally induced periodontitis.In dags with normal periodontium, jigglingforces induced one phase of increasing tooth


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Table 2. Results from histometric assessments.1) the size (in units) of the marginal 2 mm ofthe periodontal ligament area (PLA) and 2) thenumber of osteoclasts lining the alveolar bonewithin PLA. T ~ test tooth. C = control tooth.X = mean. S.E. — standard error of the mean.N.S. •= not significantDie Resultate histometrischer Werte. 1) DieFldche (in Einheiten ausgedriickt) der am wei-testen marginal gelegenen 2 mm der desmodon-taien Region (PLA) und 2) die Anzahl der denalveolaren Knochen dieser Region (PEA) be-kleidenden Osteoklasten. T = Testzahn. C =Kontrollzahn. X = Mittelwert. S.E. = Standard-irrtum des Mittelwertes. N.S. — nicht signifi-kantResultats des evaluations histometriques: 1) di-mensions (en unites) de la superficie des 2 mmmarginaux du desmodonte (PLA) et 2) nombred'osteoclastes bordant I'os alveolaire dans I'in-tervalle PEA. T = dent experimentale. C =dent temoin. X = moyenne. S.E. = erreur-typede la moyenne. N.S. = non significatif

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mobility which had a duration af around 60days, and was foUawed by a phase duringwhich the tooth mobility was increased butno longer increasing. During this latterphase, the periodantal tissues became adapt-ed ta the altered functianal demands; theperiodantal ligament was wider than narmalbut cantained a normal amaunt of bloodvessels. The vessels did nat display signs afaltered permeability, the bane surface of theperiodontal ligament presented anly fewosteoclasts, and there was no loss af connec-tive tissue attachment. When the same exper-iment was repeated in dogs with experi-mental periodontitis, similar jiggling forcesproduced an extended phase of progressive,

i.e. increasing tooth mobility. During theentire period of jiggling, the periodontal tis-sues were unahle to adjust to the abnormalacclusal load. Hence, throughout 6 monthsaf abservation, the gradually increasingtooth mability was accompanied by an in-crease in size of the periodontal ligamentarea. In addition, the periodontal ligamenttissues contained an increased number ofosteoclasts and an increased number of ves-sels which displayed signs af altered perme-ability. In these dags trauma from occlusionwas accompanied by an iticreased rate ofattachment loss and dawngrawth of packetepithelium.

It may be argued that the co-destructiveeffect (Glickman 1963) of the jiggling farcesin dogs with experimental periadontitis wasthe consequence of an initially reducedheight of the periadontium rather than thepresence of a chronic inflammatory lesionin the tissues caused by plaque. Recently,however, Ericsson & Lindhe (1977) studiedthe effect of jiggling farces in dogs withmarkedly reduced but non-inflamed perio-dontium and reported that occlusal traumaacting an teeth with a healthy but reducedperiodontium produced increased tooth mo-bility and angular bany defects but did notcause attachment lass and epithelial down-grawth. It seems therefore reasonable tosuggest that jiggling farces may operate asco-destructive factors only in situationscharacterized by an ongoing plaque-induceddestruction of the periadontal tissues.

Meitner (1975) suggested that infrabonydefects may favour a ca-destructive factoreffect of occlusal trauma an periodontitisand Glickman (1967) postulated that trau-ma from occlusion was an etiologic factorin the formation of infrahany packets andcrater-like defects. In the present studythere was neither in test nor cantral toothregions signs af infrahony pocket formation.Since the jiggled premolars displayed moreloss of attachment than the non-jiggled'


teeth, this observation implies that the pre-sence of infrabony defects can neither beregarded as a prerequisite for a detrimentaleffect of jiggling trauma on progressive pe-riodontitis nor as an exclusive sign of trau-ma from occlusion. In most respects there-fore, the present findings seem to validatethe assumption made by Glickman (1967)that "identification of trauma from occlu-sion combined with inflammation as factorsresponsible for infrabony pockets and os-seous defects does not imply that there can-not be suprabony pockets and horizontalbone loss around teeth in instances of trau-ma".

When ligatures are placed around theneck of premolars in dogs, large amountsof plaque wiii rapidly accumulate and aphase of periodontal tissue breakdown-. periodontitis - soon results fSchroeder &Lindhe 1975). Periodontitis produced inthis manner is characterized by the presenceof a collagen-poor, inflammatory cell-richinfiltrate (ICT) in the gingival tissues closeto the bacterial plaque. The inflammatorylesions cause loss of connective tissue at-tachment to the tooth, resorption of alveo-lar bone and cementum, apical proliferationof the junctional epithelium, the coronalportion of which becomes transformed intoa pocket epithelium, and often recession ofthe marginal gingiva. According to the datapresented by Schroeder & Lindhe (1975),the inflammatory cell infiltrate, producedby ligature placement at the buccal aspectsof premolars, never reached the alveolarbone crest which always seemed to be cov-ered by a layer of non-infiltrated connectivetissue. Jn the present study, the repeatedexchange and replacement of ligatures in asubgingival position caused an extremelyrapid loss both of connective tissue attach-ment and alveolar bone. Thus, after 330days of the experiment, around 50 % of theattachment around the lower third andfourth premolars had been destroyed. At

the end of the experiment, 33 days later, anadditional 146 ^m of tissue support for thecontrol teeth was lost. This means that alsoduring the final phase of the experimentthere was an active breakdown of the peri-odontal tissues. In the controls the distancebetween the apical border of the infiltratedconnective tissue (ICT) and the bone crestwas around 250 ,am, thus confirming thefinding by Schroeder & Lindhe (1975) thatnon-inflamed connective tissue is present ina zone immediately above the alveolar bone.When teeth with aetive periodonta] diseasewere subjected to jiggling forees, within afew weeks there was a marked additionalloss of connective tissue attachment (621^m test vs. 146 /./m control) and alveolarbone (1399 fun test vs. 883 am control). Inaddition, in the jiggled tooth regions in com-parison to the controls, the ICT area ex-tended around 600 /am further in an apicaldirection (Table 1), still leaving, however,around 150 /im of connective tissue withapparently normal Sharpey's fibers insertinginto the eementum covering the bone crest.The question arises how jiggling forces mayhave established conditions which favouredmarked extension of the ICT area and pro-liferation of the pocket epithelium in anapical direction. The findings made in thisstudy do not answer this question. However,since the distance between the apical borderof the mierobial plaque and the apical bor-der of ICT was similar in test and controltooth regions, it seems reasonable to suggestthat the jiggling forces and the progressivelyincreasing tooth mobility in one way or an-other favoured an apical proliferation of themicrobia! plaque. This in turn may havecaused further destruction of the supportingapparatus.

Zusammenfassung

Die Einwirkung progressiver Zahnmobilildl aufdie destruktive Parodontitis beim Hunde


Die vorliegende Studie untersucht am Hunde,inwieweit bei vorhandener destruktiver Paro-dontitis, traumatisierende Krafte in Grossenord-nungen die Zahnlockerung verursacben konnen,imstande sind den Verlauf der destruktiven Pa-rodontitis zu beeinflussen.

Die Versuche wurden an 5 Hunden vorge-nommen, die mit einer Diat emahrt wurden,die die Ansammlung dentaler Plaque ermog-Iichte.

Die Auflosung der parodontalen Gewebe umden dritten und vierten Pramolaren herum (4P,3P und P3, P4) wurde durch Befestigung pla-qneretinierender Ligaturen an den Zahnhalseninduziert. Als nacb 330 Tagen etwa 50 % derStlitzgewebe verloren gegangen war, wurdenmukoperiostale Lappen um die vier Pra.molarenherum mobilisiert und dann in Hohe der mar-ginalen Begrenzung des alveolaren Knochensan den bukkalen Oberflacben der Wurzeln Ker-ben prapariert. Die Kerben dienten als Fest-punkte fiir spatere Messungen an bistologischenPraparaten. Die Lappen wurden wieder in Situresuturiert und neue plaqueretinierende Ligatu-ren um die Wurzeln der vier Zahne herum ap-pliziert.

Eine Woche spater (Tag 0) wurden P.̂ undP4 (Testzabne) in bukko-lingualer Richtungdurch einen Elevator hin- und ber kippenden(jiggling) Kraften ausgesetzt. Das Hin- undHerkippen (jiggling) dauerte 30 Sekunden undwurde an den Tagen 4, 8, 12 und 16 wieder-holt und so vorgenommen, dass die Zahnmo-bilitat wahrend der Versucbsperiode zunabm.Die Tiere wurden am Tage 26 geopfert und die4P, 3P sowie P.̂ , P4 enthaltenden Sektionen wur-den zur Durchmusterung im Lichtmikroskopvorbereitet.

Die Ergebnisse dieser Studie zeigten, dasshin- und herkippenden Krafte, die imstandewaren die Zabnmobilitat zu erbohen, bei Hun-den mit fortscbreitender Auflosung des Paro-dontalgewebes zu gesteigerter Destruktion desHalteapparates beitrugen.

Action de la mobilite dentaire progressive surla parodonpathie destructrice chez le chienLe but de la presente etude a ete d'etablir dansquelle mesure des forces traumatisantes quiprovoquent une mobilite dentaire augmentantprogressivement infiuencent une parodontopa-thie destructrice en evolution.

Les experiences ont ete pratiquees sur 5

chiens recevant un regime qui permettait l'ac-cumulation de plaque dentaire. Une destructionparodontale a ete provoquee autour des troisie-mes et quatriemes premolaires inferieures (4P,aP et P3, P4) en posant autour du collet desdents des ligatures assurant la retention de laplaque microbienne. 330 jours plus tard, quandenviron 50 % des tissus de soutien avaient eteperdus, des lambeaux muco-periostes ont etereclines autour des quatre premolaires et desrainures ont ete preparees sur les faces vesti-bulaires des racines a la limite marginale dei'os alveolaire. Les rainures servaient de re-peres pour les mesures faites plus tard sur Iescoupes histologiques. Les lambeaux ont ete su-tures en place et de nouvelies ligatures assurantla retention de la plaque microbienne ont eteplacees autour des racines des 4 dents.

Une semaine plus tard (Jour 0), P3 et Pi(dents experimentales) ont ete soumises a desforces de va-et-vient (jiggling) en directionvestibuio-linguale a I'aide d'un elevateur. Ceprocede, d'une duree de 30 secondes, a ete re-pete aux Jours 4, 8, 12 et 16, et guide de tellesorte que la mobilite des dents aille en aug-mentant pendant la periode experimentale. Lesanimaux furent sacrifies au Jour 26, et descoupes de 4P, 3P et P3, P4 ont ete prepareespour l'examen au microscope optique.

Les resultats de cete etude ont mis en evi-dence le fait que les forces de va-et-vient quiproduisent une augmentation progressive de lamobilite, determinaient une augmentation de laVitesse de destruction de Tappareil de soutienchez des chiens presentant une destruction destissus parodontaux en evolution.

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Address:Department of PeriodontologyEaculty of OdontologyUniversity of GothenburgGothenburgSweden

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