Journal of Clinical Periodontology: 1974: 1: 3-14

Key words: tniunia from occUision — pciiocionlat lifianicnl - jwriodontilin - do^s.Accepted for publication: November 6, 1973.

Influence of trauma from occlusion onprogression of experimental

periodontitis in the beagle dog

JAN LiNDHE AND GUNNAR SX'ANBERG

Department of Periodontology,University of Gothenburg, Gothenburg, Sweden

Abstract. The experiments were performed in six beagle dogs fed a soft diet which alloweddental plaque formation. During a pre-experimental period of 7 weeks, periodon-titis was induced by (1) surgically creating a bony pocket and (2) adapting a copper bandto the exposed tooth surface. Two dogs were sacrificed at the end of this period and tissuesections were prepared for histological examination. In the remaining four dogs, traumafrom occlusion was produced on the left niandibular fourth premolar by the installationof a cap splint and a bar device. The contralateral premolar served as a control.

At the start of, and at regular intervals during, an experimental period of 180 days,tooth mobility, gingival inflammation and plaque accumulation were assessed. After sacri-fice, radiographs were taken of test and control tooth regions and histological sectionsanalysed regarding the width of the marginal periodontal ligament space and the degreeof apical downgrowth of the gingival pocket epithelium.

Only the test teeth showed a gradually increasing horizontal mobility, but gingival in-flammation and Plaque Index scores were similar on test and control sides. Radiographsrevealed (1) horizontal bone loss in both test and control areas, and (2) angular bonedestruction only in test areas. Histological sections showed that the degree of apical pro-liferation of the pocket epithelium was more pronounced in test than in control regions.

Experiments carried out in different labora- may alter the path of spread of gingivaltories have demonstrated that it is possible inflammation and thereby facilitate directin dogs and monkeys to induce a gingival penetration into the periodontal ligamentinflammation which develops into perio- (Macapanpan & Weinman 1954), enhancingdontitis by allowing the accumulation of angular bone resorptioti and infrabonyplaque and calculus (Saxe et al. 1967, pocket formation (Glickman & SmulowLindhe et al. 1973, Kennedy & Poison 1962, 1965).1973). It has been suggested (for review see In animals, periodontal tissue changesPosselt 1966, Glickman 1967) that trauma due to trauma from occlusion resemblefrom occlusion in the presence of perio- those found in human autopsy material (fordontal inflammation may be an important review see Posselt 1966). Objections havecontributory factor in the pathogenesis of been raised, however, concerning the vali-periodontal disease. Thus, occlusal forces dity of conclusions made from autopsy

LINDHE AND SVANBERG

examinations and from experiments whichdo not consider jiggling forces in combina-tion with a progressive periodontal lesion(Wentz et al. 1958, Ramfjord et al. 1966).

The aim of the present investigationswas to assess what effect trauma fromocclusion and permanent tooth hypermo-bility would have on the rate at which ex-perimental periodontitis progresses in thebeagle dog.

Material and Methods

Six beagle dogs, 2-3 years old and weigh-ing around 12 kg, were used. Prior to theexperiments the dogs were fed a dietfavouring gross plaque formation on pre-molars and molars. At the beginning of theexperiments all the dogs showed clinicalsigns of gingivitis in the premolar and molarregions. Throughout the study the animalswere fed a diet allowing plaque and cal-culus formation (Hamp et al. 1973).

Periodontitis was induced according to amodification of the method described bySwenson (1947). On the mesial aspect ofthe fourth lower premolar on both sides (P4and 4P), infrabony pockets were made witha slender diamond cylinder bur. A notchwas made in the root at the level of thebottom of the surgically created pocket.This notch served as a landmark for loss ofattachment measurements performed onhistological preparations in the microscope(see below).

A copper band similar to that used bySwenson (1947) and Hurt (1963) waspunched close to the tooth, with a tongueextending into and carefully adapted to thebase of the notch in the tooth (Fig. 1). Theband was then cemented to the tooth with

* The W. V-B Ames Co., Fremont, Ohio,U.S.A.

•* Unitek 1/4, Monrovia, California, U.S.A.

Fig. 1. Copper band cemented on a mandibularfourth premolar. Note that a tongue of theband extends into and is carefully adapted tothe base of the notch made in the tooth. X 3.Fig. 1. Einzenientiertes Kupferband auf einemvierten unteren Prdmolaren. Ein zungenformi-ger Fortsatz des Bandes reicht in cine Kerbeam Zahn und ist dort sorgfidtig angcpasst. X 3.Fig. 1. Bagiie de cuivre cimentee sur une 4cpreniolaire inferieure; a noter une languette quis'etend et est soigncusement adaptee a la basede I'entaille pratiquee duns la dent. X 3.

copper cement*. Three weeks later the cop-per band was removed. To enhance forma-tion of soft deposits a plaque retention bandwas placed around the tooth at the level ofthe cemento-enamel junction. The circum-ference of this rubber band** was equal tothat of the tooth at the cemento-enameljunction.

Four weeks later, two of the dogs weresacrificed and sections of test and controlteeth were prepared for histological ex-amination, as described below. In four ofthe dogs, trauma from occlusion was pro-duced by the installation of cap splints, asdescribed by Svanberg & Lindhe (1973).On the left side of the maxilla the dogswere fitted with a cap splint with an ob-

OCCLUSAL TRAUMA AND PERIODONTITIS

TEST

DAY

POCKETSURGERY

PLAQUECOPPER RETENTION TRAUMA FROMBAND BAND OCCLUSION

END OFEXPERIMENT

I2IDAYS 28DAYS1

TR*180

CONTROL

Fig. 2. Design of the experiment. Trauma from occlusion was introduced 49 days (21 + 28 days)after pocket surgery.Fig. 2. Versuchsplaniing. Die okkhisale Traumatisierung hegaiin 49 Tage (21 + 28 Tage) nacli derchinirgisclu'ii Bilclniig einer Parodontattasche.Fig. 2. Plan de rexperU-iice. Le traiiiuatisnie occlusal jut inlroduit 49 jours (21 + 28 jours) apresla creation chirurgicah' d'line poclic parodoiitale.

lique plane which made primary contactwith the distal surface of the left mandibularfourth premolar (P.i) when the mandiblemoved towards centric occlusion. The in-clination of the oblique plane was such asto exert mainly horizontal forces upon thetest tooth. During chewing movements P4was subjected to excessive horizontal forcesand tilted in mesial direction.

On the left side of the mandible a spring*attached to a lingual bar was introducedthrough a channel in the crown of the testtooth. When not in occlusal contact, P4 wastilted back to its original position by thespring appliance.

The mesial aspect of P,| was designatedthe pressure side. In each dog the contralateral tooth (i.e. 4P) served as a control.In order to attain equal plaque formationon both sides, the right lower jaw (controlside) was fitted with a lingual bar device.However, a soft wire exerting no force upon4P was introduced through the channel inthe crown of the tooth.

The dogs were sacrificed 6 months after

* Dentaurum Ltd., Germany, spring-hard wire0 0.55 mm.

** Whatman Chromatography Paper No. i, W& R Balston Ltd., London, England.

the installation of the cap splint and bardevices.

Immediately after installation of the capsplint and bar devices, i.e. on day TR (Fig.2) and after 30 (TR + 30), 60 (TR + 60),90 (TR 4-90) and 180 (TR-h 180) days,P4 and 4P were studied for the followingclinical features.

I. Tooth mobility. TKIO and Tr,oo wereassessed in accordance with the methoddescribed by Mijhlemann (1954).

II. Gingival inflammation. The state of thegingiva was assessed by measuring (inlTim) the amount of gingival exudateobtainable on chromatography paper**strips inserted into the orifice of themesial gingival pocket of P4 and 4P(Loe & Holm-Pedersen 1965).

III. Plaque. The amount of plaque on themesial surface of P4 and 4P was esti-mated according to the plaque indexsystem (PI I) described by Silness &Loe (1964).

IV. Radiographic bone loss. On day TR +180 the dogs were sacrificed with anoverdose of Pentothal sodium® (Ab-bott, Belgium). The mandible was re-moved and bisected along the midline,and ladiographs of the premolar regionon both sides were taken on a skull

L I N D H E AND S V A N B E R G

table. The central ray was directedperpendicular to the longitudinal axisof the teeth. The focus-to-film distancewas 880 mm and roentgenography wasperformed at 4 kVp and 100 mAs withKodak Ultra Speed film. The verticaldistance between the notch made in theroot surface and the alveolar bone wasmeasured by the aid of a sliding caliper.

Histological ExaminationSpecimens containing the distal portion ofPy (,,P), P| (jP) and the mesial portion ofthe first molars (Mj or |M) were fixed in abuffered solution of 10 % formalin inwater, decalcified in a solution of equalamounts of 50% formic acid and 15%sodium formiate, dehydrated and embeddedin paraffin. Mesiodistal sections were cutwith the microtome (Leitz Wetzlar 1300)set at 7 |,im, and stained with haematoxylin-eosin. From each biopsy specimen threesections 50 ^m apart were used for deter-mining the distance between the landmarkin the root surface (i.e. the level of thebottom of the surgically created pocket)and the most apical cells of the pocketepithelium. A mean "loss of attachment"score for each tooth was calculated. Themeasurements were made in the light micro-scope (Leitz Ortoplan).

The periodontal ligament area (PLA) onthe pressure side of P4 and that on thecorresponding side of ,iP were determinedaccording to a technique recently describedby Svanberg & Lindhe (1973). Statisticalanalyses of the data were performed ac-cording to Student's t-test.

Results

Tooth MobilityOn day zero, immediately before traumafrom occlusion was produced, the mobilityof the test and that of the control teethwere similar. Thus, the Tim, and Tsdn values

were 10.0 ± 1.7 and 16.5 ± 2.2 (test) and9.2 ± 1.2 and 17.5 ± 3.7 (control). Afterinstallation of the cap splint and bar devicesthe mobility of the test teeth gradually in-creased (Fig. 3). Tiiiii and Tgno reachedmaximum values at the end of the 180days of the experiment; Tmo = 49.0 ± 8.8;Tn,in =-'- 78.8 ± 18.0. The increase in mobilityof the test teeth was significant (P •< 0.001).In addition, all test teeth clinically exhibiteda pronounced axial mobility. During theentire experiment the mobility of the controlteeth remained practically tmchanged.

Gingival InflamtnationThe mean gingival exudate scores of thetest and control teeth on day zero were4.9 ± 0.9 and 3.1 ± 0.8 respectively, thedifference not being significant. Neither inthe test tooth areas nor in the control onesdid any significant alteration of the gingivalexudation occur during the experimentalperiod (Table 1).

Table I. Amount of gingival exudate (in mm)obtained on chromutography paper stripsplaced in the orifice of the mesial gingivalpocket of test and control teethTabelle 1. Menge des Sulcusexudates, gemes-sen in nun. Das Exudat wiirde auf Chromalo-griipliie-Papicrslreifeii, welche an den Eingangder niesialen Zahnfleischtasche des KontroU-iind Iraiinuilisierlen Zahnes gclegt warden, ge-saminelt

Tableau 1. Qiiaiilile d'exsiidal gingival (en mm)ohfenu siir des langaellcx de papier a chromo-tographie placees a I'orifice da cul-de-sac gin-gival mesial des dents test et controle.

Day TestX ± s.e.

ControlX ± s.e.

0306090

180

4.94.53.34.03.2

0.90.70.50.80.9

3.13.73.92.54.3

0.80.90.90.60.6

O C C L U S A L T R A U M A A N D P E R I O D O N T I T I S

Toil

Control

90 180 Doyi 0 60 90 180 Doyi

Fig. 3. Alterations in tooth mobility (Tioo and T500) during 180 days of combined trauma fromocclusion and experimental periodontitis.Fig. 3. Veninderungen der ZcihnbewegUchkeit (Tjoo und Tsoo) iin Verlauf von 180 Tagen am Test-zahn durch die Koinbination dcr okkhisalen Traumatisieruiig mit der experimenlellen Parodon-titis. Der KonlroUzahn weist luir letztere aiif.Fig. 3. Alterations dans la mohilite dentaire (Tioo et T500) durant ISO jours de traiiinatisme oc-cliisal combine a la parodontite experimentale.

Plaque IndexAt all examinations, from day zero to day180, the Plaque Index scores of both thetest and the control teeth were 3, i.e. thegingival third of the tooth surfaces as wellas the gingival pockets exhibited abundantsoft deposits. At the examinations after 60,90 and 180 days of the experiment, miner-alized deposits were present on the test aswell as on the control teeth.

Radiographic Bone LossAt the end of the experiment radiographsof the regions of the control tooth in allfour dogs revealed pronounced horizontalloss of marginal periodontal bone. Fig. 4is a radiograph of the control side of dogII at the end of the experiment. The meandistance between the notch of the controlteeth and the alveolar bone, as measured inthe roentgenograms, was 2.1 ±0 .1 mm(Table 2).

Table 2. Distance between the notch in the rootsurface and the marginal alveolar bone level(control) or bottom of osseous pocket (test).The measurements were performed on radio-graphs (mm)Tabelle 2. Distanz zwischen der Kerbe in derWurzeloberfUiche und der Hohe des alveoldrenKnochens (Kontrolle) oder Fundus der Kno-chentasche (Traumatlsierter Testzahn). DieMessiingen wurden aiif Rontgenbildern vorge-nommen, mm. Die Versuchshunde sind mit ro-mischeii Ziffern bezeichnet

Tableau 2. Distance entre I'entaille radiculaireet d'iine part la Crete de I'os atveolaire mar-ginal (controle) et d'autre part le fond du cul-de-sac infraosseux (test). Les mesures furent ef-fectuees sur des radiographies (mm).

Dog

111IIIIVX ± s.e.

Test

4.55.54.55.0

4.9 ± 0.24

ToothControl

2.02.52.02.0

2.1 ± 0.12

Diff.

2.53.02.53.0

2.7 + 0.14

L I N D H E AND S V A N B E R G

Fig. 4. Radiograph of controltooth at the end of the experimentshowing marked iiorizontal alveo-lar bone loss (;» 50 %). X 4.Fig. 4. Rontgetibild des Kontroll-z.ahnes bei Versuchsabschluss.Aiisgepriigter liorizontaler Kno-chensciiwiind von ca. 50 %. X 4.Fig. 4. Radiographie d'nne dentcontrole a la fin de I'experienceinontrant utie perte osseuse alveo-taire hori7,ontate marquee(^ 50%). X 4.

\i\ the region of the test teeth there wasnot only a pronounced horizontal bone lossbut also, on the pressure side, a markedcone-shaped widening of the periodontalligament space. In addition, the periapicalperiodontai ligament space was markedlywidened. Fig. 5 is a radiograph of the testside of dog 11 at the end of the experiment.Note the angular bony defect arid the in-frabony pocket on the pressure side, as wellas tbe radiolucent zone around the apices.The mean distance between the notch ofthe test teeth and the marginal alveolar bone(i.e. the bottom of tbe mesial bony pocket)was 4.9 ± 0.2 mm (Table 2).

Histological FindingsDay 0. Tissue sections obtained from twodogs 7 weeks after the induction of experi-mental periodontitis (corresponding to day 0

of the trauma from occlusion experiment)revealed that tbe four epithelialized pockets(on the mesial aspects of P,| and jP in eachanimal) extended to tbe level of or slightlyapical to «100(, im) tbe notch made inthe cementum. The connective tissue sub-jacent to the pocket epithelium was in-filtrated with round ceils. In all four biopsyspecimens the inflammatory cell infiltrationcomprised most of the supra alveolar con-nective tissue.

Day 180. Sections from the regions of thecontrol teeth representing day 180 of theexperirnent consistently showed an apicaldowngrowth of epithelium from the notchin the root surface (= the bottom of thesurgically created pocket). Adjacent to thegingival pocket were dilated vessels in aconnective tissue heavily infiltrated with

O C C L U S A L T R A U M A A N D P E R I O D O N T I T I S

Fig. 5. Radiograph of test tooth atIhe end of the experiment. In ad-dition to marked horizontal alveo-lar bone loss («» 50 %), an angu-lar bony defect is seen on thepressure of the test tooth. X 4.Fig. 5. Rontgenhild des Iraiinwti-sierten Zahnes bei Versuchseiule.Ueber den aiisgeprcigten horizoii-talen Parodontalknochenscliwundvon ungefiihr 50 % hat sicli aiifder Dnickseite eine schihselfdr-niige verlikalc Knochenatrophiegebildct. X 4.

Fig. 5. Radiographie d'line dentIraiinuitisee a In fin de I'experi-ence. En plus de la perte osseusealveolaire liorizontale marquee(f^ 50 %) on observe un defautosseux vertical triangulaire a I'en-droit oi'i le desniodonte est traii-nwtixe. X 4.

leucocytes. Within the peiiodontal ligamentleucocytes were seen only occasionally (Fig.6a).

Sections of regions of the test teeth (Fig.6b) showed more extensive proliferation ofthe pocket epithelium. The leucocyte in-filtration area seemed to extend furtherapically than in corresponding sections ofthe regions of the control teeth. Markedlydilated vessels were seen within a supra-alveolar connective tissue which was heavilyinfiltrated with leucocytes. The periodontalligament, however, was not infiltrated withinflammatory cells. On the bone surface ofthe alveolus, a few osteoclasts could beseen.

The marginal part of the periodontalligament space on the pressure side of thetest teeth showed an angular widening and,according to the planimetrie data, the perio-

dontal ligament area (PLA) was 3.3 (s.e. ±± 0.60) times that of the controls. Thebone surface of the alveolus was markedlyundulated. The periodontal ligament ap-peared less dense than in the controls andwide communications between the perio-dontal space and the marrow spaces werepresent. The periapical periodontal ligamentspace of the test teeth was extremely wideand bordered by an alveolar bone, the sur-faee of which was undulated. The tissuewithin the periapical portion of the perio-dontal ligament was characterized by thepresence of a large number of small vesselsand the absence of inflammatory cells.

The histologic measurements revealedthat the distance between the notch in theroot and the most apical cell of the pocketepithelium ("loss of attachment") on thepressure side of the test teeth was 2.2 ±

10 LtNDHE AND SVANBERG

Fig. 6. Sections from control and test teeth at the end of the experiment showing a more extensiveapical proliferation of pocket epithelium on the pressure side of the test tooth (Fig. 6b) than onthe control side (Fig. 6a). Haematoxylin-eosin, orig. magn. obj. X 1.N: Notch in root surface (= bottom of surgical pocket).P: Localization of the most apical cells of the pocket epithelium.L: Loss of attachment (from induction of experimental periodontitis to the end of the traumafrom ocelusion experiment).Fig. 6. Gewebsschnitte des traunmtisierten Zahncs (Fig. 6b) und dcs Kontrottzabnes (Fig. 6a). Dertraumatisicrte Zabn zcigt im Vcrglcicb mit dcm Kontrollzabn (Fig. 6a) cine ticfer greifende api-kalc Proliferation des Tascbenepithcls auf der Druckseite (Fig. 6b). Hamatoxylin-Eosin. Orig.Vergr. 1 X,A'; Kerbe in der WurzcloberfIdcbe = Fundus dcr chirurgiscb gehildeten Parodontaltasche.P: Apikalste Stctlc dcr Tasclicnepitbelzctlen.L: Gewebsloslosuug (Attacbmcnt-Vcrtust) vom Beginn dcr Erzeugung der cxpcrimeutcllen Paro-dontitis bis zum Abschltiss der kiinstlichen okklusalen Traumatisierung.Fig. 6a, b. Coupes de deuts traumatisecs et coutrote a la fin de I'experiencc montraut une pro-liferation apicale de repithetiunr du cul-de-sac plus etcndue du cote traumatise (Fig. 6b). Heniato-xylinc-eosinc, magn. orig. X 1.N: entaille dans la surface radiculaire ("= fond du cul-de-sac chirurgical).P: localisation dcs cellules lcs plus apicales de t'epitbelium du cut-de-sac.L: perte d'attacbcinent (de t'induction de la parodontite cxperimentale a la fin de I'experience detraumatismc occtusal).

O C C L U S A L T R A U M A A N D P E R 1 O D O N T I T 1 S 11

± 0.47 tntn. The corresponditig distancefor the control side was 0.8 ± 0.13 mm. Thedifference is significant (P < 0.05).

Discussion

The presetit experiments have demonstratedthat it is possible to produce pathologicalpocket formation in the beagle dog by (1)surgical creation of a local osseous defect,(2) prevention of initial reattachment, and(3) promotion of gross plaque formation byapplication of a non-elastic rubber bandaround the tooth at the level of the ce-mento-enamel junction.

Seven weeks after surgery the gingivaeshowed marked clinical signs of inflamma-tion. Biopsy specimens from this periodrevealed the presence of an epithelializedgingival pocket extending down to the bot-tom of the surgical defect. The connectivetissue subjacent to the epithelium washeavily infiltrated with leucocytes. Thesefindings are in agreement with those pub-lished by Swenson (1947) and Ramfjord(1951). They used a similar method forproducing a periodontal lesion and reporteddeveloping gingivitis and downgrowth ofepithelium to the bottom of the surgicalpocket.

The experiments also showed that thetechnique used can induce a rapidly pro-gressing periodontal disease around a singletooth; the lesion included further apicalshift of the pocket epithelium and extensivealveolar bone loss. Thus, about 8 monthsafter the beginning of the experiment some50 % of the alveolar bone around thecontrol teeth had been lost. This observationis largely in agreement with findings byCollings (1957) and Collings & Redden(1959). They created an initial bony lesionsurgically, allowed gross plaque formation,and reported that a periodontal lesionresembling rapidly progressing periodontitisin humans could be produced in the dog.

Similar findings have been reported by, e.g.Zander et al. (1971), Caton & Crigger(1972), and Kennedy & Poison (1973) fromexperiments in the monkey.

Immediately prior to the introduction ofjiggling forces, i.e. after 7 weeks of theexperiment, tooth mobility of the test teethand control teeth was similar. It should beobserved, however, that the T]oo and T500values obtained were about seven times ashigh as those of posterior premolars in dogswith non-inflamma':ory gingivae, as reportedby Svanberg & Lindhe (1973). After theinstallation of cap splints the test teethshowed a very pronounced and graduallyincreasing mobility throughout the observa-tion period. On "Day T R + 1 8 0 " thejiggling teeth were found to be extremelyloose and mobile both transversely andlongitudinally. In contrast, the mobility ofthe contralateral control teeth remainedpractically unchanged during the final 6months of the experiment (Fig. 3).

The microscopic examination of sectionsfrom the pressure side of the test teeth ob-tained 6 months after the onset of "traumafrom occlusion" revealed an extremely wideperiodontal ligament space, bordered by anundulated alveolar bone surface and acementum with resorption lacunae in someareas. The PLA scores showed that thewidth of the periodontal ligament space ofthe test teeth was about three times that ofthe controls. This finding is in close agree-ment with data presented by Wentz et al.(1958), who studied periodontal tissue reac-tions to the jiggling type of trauma inmonkeys with normal gingiva. After 3- and6-month experiments they observed a widen-ing of the periodontal ligament space from,on the average, 0.19 mm (at start) to 0.65mm. In the present material after 6 months'jiggling of the teeth, the periodontal tissuesshowed /((, marked signs of active resorptionof bone or cementum, necrosis, vascularthrombosis or pronounced inflammatory cell

12 L I N D H E AND S V A N B E R G

infiltration. This means that at this stage thetest teeth and their periodontal tissues musthave become almost but not entirely adaptedto the altered occlusal function. Such aconclusion is in agreement with resultspublished by Wentz et al. (1958) andSvanberg & Lindhe (1973). They reportedinitial tissue reactions, e.g. bone resorptionand granulation tissue formation, followingexposure of the teeth to jiggling forces.After some months of experiment, however,the periodontal tissues appeared normalexcept for a widening of the periodontalspace.

The radiographs of the test tooth regionsobtained at necropsy, i.e. after 6 months ofjiggling and continued plaque formation,displayed not only advanced horizontalbone loss but also angular or crater-likeosseous defects. The bony defects were mostpronounced in the pressure areas. The de-fects in the bone resembled the lesion fre-quently described by Glickman and collabo-rators (for review see Glickman 1967) asthe result of trauma from occlusion.

The radiographs also revealed obviouszones of bone resorption around the rootapices; especially around those of the mesialroots. The microscopical analyses confirmedthe x-ray findings, viz. markedly widenedapical periodontal spaces. These spaces con-tained richly vascularized tissue, but nosigns of vascular thrombosis, or inflamma-tory cell infiltration. The pulp tissue in theapical region did not harbour inflammatorycells. The cementum showed resorptionlacunae and the bordering bone was undu-lated, both of which are indications ofprevious active bone resorption. The peri-apical alterations must therefore be regar-ded as adaption of the tissue to increasedfunctional requirements.

Though the Plaque Index scores and thedegree of gingival exudation of the testand control teeth were similar throughoutthe experimental period, the test teeth

showed an apical shift of the pocket epi-thelium which was three times that of thecontrols. In dogs with no clinical inflamma-tion of the gingiva or with well establishedgingivitis, trauma from occlusion by thesame method as that used in this experimentdid not result in an apical shift of thejunctional epithelium (Svanberg 1974). Inthe study referred to, the most apical epi-thelial cells were always located at thecemento-enamel junction (CEJ), and theconnective tissue subjacent to CEJ wasconsistently free from inflammatory cellinfiltrates. Similar results have been ob-tained by Wentz et al. (1958) in monkeyswith overt gingivitis. It may therefore besuggested that any effect of ocelusal traumaon the attachment level requires the pres-ence of a plaque-induced inflammatorycell lesion in the supra-alveolar connectivetissue. In Ihe present experiment, whichallowed abundant plaque formation, deep-ening of the gingival pocket and loss offibre attachment occurred at a faster rateon teeth subjected to jiggling tissue trauma.Henee it may be suggested that trauma fromocclusion in dogs may accelerate progres-sion of experimental periodontitis.

Zusammenfassung

Die vorliegende Arbeit wurde ausgefuhrt, umden Einfluss von traumatisierenden Kraften(Jiggling) auf das Fortschreiten einer vorbe-standenen experimentellen marginalen Parodon-titis festzustellen.

Die Versuche wurden an sechs Beagle Hun-den durchgeflihrt. Plaqueablagerungen auf denZahnen wurden durch eine weiche Diat gefor-dert. Vor der Traumatisierung wurde wahrend7 Wochen eine marginale Parodontitis naeh derMethode von Swenson (1947) erzeugt und anzwei Hunden histologisch verifiziert. Die ubri-gen vier Tiere erhielten am linken unterenvierten Praemolaren eine Vorrichtung, die wlih-rend der Kaufunktion abnorme Krafte im Sinnedes Jiggling ausubte. Der kontralaterale Zahndiente als Kontrolle. Zu Beginn und in gleichenAbstanden wahrend der 180 Tage dauerndenTraumatisierung des Parodonts wurden Zahn-

O C C L U S A L T R A U M A A N D P E R I O D O N T t T I S 13

beweglichkeit, Zahnfleischentzundung und Pla-queanhiiufung gemessen. Nach Opferung derTiere wurden Rontgenbilder von der Test- undKontrollseite angefertigt. Histologische Schnittewurden im Hinblick auf die Breitc des Desmo-dontalspaltes und des Ausmasses der Tiefen-wucherung des Taschenepithels untersuclit. Dietraumatisierten Zahne zeigten eine allmiililichansteigende horizontale Beweglichkeit im Ver-gleieh zu den Kontrollen. Der Grad der Zahn-fleischentzi'indung und Plaqueanhiiufung warjedoch auf beiden Seiten gleieli.

Radiologisch war auf der Seile des okklusa-len Traumas, wie aueh auf der Kontrollseite

. horizontaler Knochenschwund vorhanden. Vcr-tikale Einbrliche konnten nur auf der Trauma-seite festgestellt werden. Die Tiefenwucherungdes Taschenepithels war auf der Testseite aus-gesprochener.

Zusammenfassend schien die Progression dervorbestandenen marginalen Parodontitis durchdie Traumatisierung, gemessen an der Zahn-beweglichkeitserhohung, gefordert zu werden.

Resume

Cette recherche fut entreprise pour analyserl'effet de forces occlusales traumatisantes deva-et-vient (jiggling) sur la progression de laparodontite marginale experimentale. Six bri-quets re9urent une diete molle permettant laformation de plaque dentaire. Durant une pe-riode pre-experimentale de 7 semaines, uneparodontite marginale fut introduite par unemethode chirurgicale; a la fin de cette periodedeux des chiens furent sacrifies en vue d'exa-mens histologiques. Chez les quatre chiens re-stants le traumatisme occlusal fut produit sur la4>' premolaire gauche inferieure (P4) par l'in-stallation d'une attelle a bagues et d'un dispo-sitif a barre. 4P servit de controle.

La mobiiite dentaire, l'inflanimation gingivaleet l'accumulation de plaque furent evaluees audebut et a intervales reguliers durant une pe-riode experimentale de 180 jours. Apres sacri-fice, on radiographia les dents testes et controleset on analysa les coupes histologiques quant ala largeur du desmodonte et au degre de proli-feration apicale de l'epithelium du cul-de-sac.

Seule la dent test montra une mobilite hori-zontale augmentant graduellement et significa-tivement tandis que l'inflammation gingivale etles resultats de l'index de plaque furent simi-laires pour les cotes test et controle. Les radio-graphies revelerent 1) une perte osseuse hori-zontale dans le parodonte traumatise et de

controle; 2) une destruction osseuse verticale,du type triangulaire seulement dans le paro-donte test. En plus, les coupes histologiquesmontrerent une proliferation apicale de l'epithe-lium du cul-.de-sac plus prononcee dans le paro-donte test que dans le controle.

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Address:Department of PeriodontologyFaculty of OdontologyFackS-400 33 Goteborg 33Sweden