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    Section 5C

    Non-Surgical Pocket Therapy: Dental OcclusionMarlin E. Gher*

    'Private practice, Carlsbad, California

    Question Set1. What evidence exists that establishes a

    relationship between excessive occlusalforcesand the initiation, development, and/or ex-acerbation ofperiodontal diseases?

    2. What evidence exists that occlusal ther-apy can modify the progression ofPeriodon-titis or aid in the treatment ofPeriodontitis?

    3. What are the effects of occlusal forceson wound healingfollowing various periodon-tal surgical procedures; e.g., guided tissueand guided bone regeneration, mucogingivalsurgery, osseous regeneration, etc?

    4. What evidence exists that "preventive"

    occlusal adjustment isjustifiedfor the healthof the periodontium?5. What are the future directions for clini-

    cal practice and research on occlusal therapyin relation to periodontal health?

    Ann Penodontol 1996;1:567-580.

    INTRODUCTION

    The effects of occlusal forces on the pro-gression of Periodontitis have been re-searched and debated for decades.1 36 Earlytheories implicated traumatogenic occlusionas the etiology of Periodontitis.13 When therole of microorganisms as causative agentsin Periodontitis became evident, emphasisswitched to the evaluation of traumatogenicocclusion as a cofactor in the progression ofPeriodontitis.417 Glickman in the early1960s proposed that a traumatogenic occlu-sion could produce a lesion of occlusal

    trauma which could accelerate the progres-sion of Periodontitis and direct the inflam-matory process into the periodontal liga-ment.47 These early papers relied onretrospective analysis of occlusal wear pat-terns, mobility patterns, autopsy material,and patterns of attachment loss and pocketformation to develop the theories that linkedtraumatogenic occlusion and Periodontitis.Later studies by Waerhaug associated thelocation and severity of attachment loss withthe location of the "plaque front" on the

    tooth.1819 These studies questioned the ef-fect of occlusal forces on the progression ofPeriodontitis and suggested that the variouspatterns of attachment loss and intraos-seous defect formation could be explained bythe "down growth of subgingival plaque."

    Controlled prospective studies wereneeded to investigate this controversial issueand substantiate the effects of occlusalforces on the progression of Periodontitis.Due to the ethical questions and difficulty indesigning well-controlled prospective hu-

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    568 Girier

    man studies, animal models were developedto study the effects of traumatogenic occlu-sion on periodontal attachment and boneloss.20 35 The prominent studies of the 1970sand 1980s were published by Poison andZander used squirrel monkeys as their ani-mal model27 35 and by Lindhe, Ericsson, andNyman using beagle dogs as their animalmodel.20 26 In these animal models, the re-searchers could artificially induce experi-mental Periodontitis and superimposing atraumatogenic occlusion to evaluate its ef-fects on bone and attachment loss. Studiesby both Lindhe and Ericsson21 and Perrierand Poison32 presented clinical and histo-logic data which indicated that heavy occlu-

    sal forces, in the absence of Periodontitis,led to increased tooth mobility and boneloss. Bone loss was present principally in theform of widened periodontal ligament spacesand, in a few cases, horizontal loss of crestalbone height.

    These research groups differed in theirfindings, however, when simulated trauma-togenic occlusion was combined with Perio-dontitis. Studies using beagle dogs indicatedthat heavy occlusal forces when combinedwith plaque induced Periodontitis led to ac-

    celerated attachment loss.20'2226 Studiesconducted using squirrel monkeys alsofound bone loss and increased tooth mobil-ity associated with "jiggling forces" used tosimulate a traumatogenic occlusion.27 31 Thesquirrel monkey studies, however, found lit-tle or no effect of traumaticjiggling forces onthe rate of plaque associated attachmentloss. The authors also reported that elimi-nation of traumatic jiggling forces in thepresence of continuing Periodontitis did notlead to bone regeneration or a reduction in

    mobility.30 The resolution of inflammation inthe presence of continuing mobility29 orjig-gling trauma,34 however, led to decreasedmobility and increased bone density, but nochange in attachment level or alveolar bonelevel. The results of these studies led clini-cians to place greater emphasis on the elim-ination of dental plaque, the etiologic agentsresponsible for Periodontitis, and to estab-lish maintenance programs to maintain per-iodontal health.28 Occlusal therapy wasdeemphasized in the treatment of Periodon-

    titis since it appeared to have a minimal rolein maintaining the attachment level onceplaque was eliminated.28

    Human research studies reported from1986-1987 questioned the effect of occlusalforces on the progression of Periodontitis.37 39In a report that evaluated patients with per-iodontal disease and occlusal parafunction,Houston et al. concluded that "...there is noor only weak correlation between periodon-tal disease and bruxism."37 Hakkarainenevaluated the effect of the resolution of in-flammation versus the resolution of occlusaltrauma on sulcular fluid flow.38 He found asignificant decrease in sulcular fluid flow af-ter inflammation was reduced by oral hy-giene instructions and scaling procedures,however, no significant reduction of sulcularfluid flow was detected after the eliminationof occlusal interferences. Pihlstrom et al.evaluated the association between occlusaltrauma, severity of Periodontitis, and radio-graphic bone loss.39 They concluded thatteeth with occlusal contacts in working, bal-ancing, and non-working positions had nogreater severity of Periodontitis than teethwithout these contacts.

    The subject of occlusal treatment was re-viewed by the World Workshop in ClinicalPeriodontics in 1989.40 After examining theliterature up to that date, the reviewer con-cluded that the role of occlusal trauma inthe pathogenesis of Periodontitis was con-troversial and the influence of occlusion onperiodontal therapy remained unresolved.The 1989 Consensus Report, however, sup-ported the use of occlusal adjustment,splinting, and orthodontic treatment for awide variety of clinical problems faced by thedentist. These included the use of occlusal

    adjustment to reduce mobility and fremitus,encourage repair of the periodontal attach-ment apparatus, treat discomfort duringfunction, treat parafunction, and to achievefunctional relationships in conjunction withrestorative dentistry. Splinting was found tobe indicated for the stabilization of teeth fora variety of restorative and functional needs.Orthodontic treatment was also found to beappropriate for a variety of reasons includingthe facilitation of occlusal and restorativetreatment, to aid in the treatment of gingival

    Annals ofPeriodontology

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    Annals ofPeriodontology

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    Review: Non-Surgical Pocket Therapy: Dental Occlusion 571

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    Review: Non-Surgical Pocket Therapy: Dental Occlusion 573

    ease process or in the tooth mobility identi-fied as a risk factor.

    A retrospective study by Jin and Cao in1992 attempted to relate clinical signs of a

    traumatogenic occlusion with severity ofPeriodontitis in 32 patients with moderate toadvanced chronic adult Periodontitis.59 Thepatients received a complete periodontal ex-amination including radiographs, recordingof probing depths, gingival index, bleedingindex, clinical attachment loss, plaque in-dex, tooth mobility, tooth wear, and an oc-clusal analysis. Abnormal occlusal contacts;i.e., premature contacts in centric relation,non-working contacts in lateral excursions,premature contacts of anterior teeth, and

    posterior tooth contacts during protrusion,were identified. After analyzing the data col-lected, the authors concluded that there wasno significant differences in probing depth,clinical attachment level, or loss of alveolarbone height when comparing teeth with andwithout abnormal occlusal contacts. Teethwith significant mobility, functional mobil-ity, or radiographically widened periodontalligaments were associated with deeper prob-ing depths, more attachment loss, andgreater bone loss. This study could not de-

    termine if tooth mobility and radiographi-cally widened periodontal ligaments wererisk factors for the progression of Periodon-titis or markers of the disease process.

    Other studies have attempted to identify"risk factors" for Periodontitis,60 62 attach-ment loss,63 67 bone loss,68 69 and tooth loss.70Those factors reported as risk factors, listedfrom the most commonly identified to theleast commonly identified by these studies,included: age, race, tobacco use, increasedpercent of sites with plaque, the presence of

    Prevotella intermedius, Bactroides forsythus,bleeding on probing, prior attachment loss,probing depth, lower educational attainment,gender (male), calculus, Porphyromonas gin-givalis, positive BANA test, gingivitis, socio-economic level, diabetes mellitus, systemicdisease, mobility, early loss of the first mo-lar, and the lack of use of dental care. Thesearticles did not clearly distinguish which ofthese factors were true risk factors andwhich were disease markers and thereforecould not establish which were etiologic.

    None of these studies identified occlusion asa risk factor for Periodontitis; however, oc-clusal analysis and mobility measurementswere rarely included in the factors being

    evaluated as risk factors.In a series of papers on prognosis, Mc-Guire and McGuire and Nunn reported ontheir ability to accurately predict futureprognosis from commonly evaluated clinicalfactors.7173 Mobility and parafunctional hab-its were identified as two of several "prog-nostic factors" that correlated with toothloss or with a worsening individual toothprognosis during a 5 to 8 year maintenanceperiod after treatment. In "well maintained"patients, prognostic factors associated witha worsening prognosis for individual teethincluded: deeper initial probing depths,more severe furcation involvement, endo-dontic involvement, smoking, diabetes, mal-posed teeth, unsatisfactory root form, andthe presence of a parafunctional habit withno biteguard.72 Initial tooth mobility was as-sociated with a prognosis that was unlikelyto improve but was not associated with aworsening prognosis.72

    Prognostic factors associated with toothloss during the maintenance period included

    initially greater: probing depths, furcationinvolvement, mobility, and bone loss as wellas poor crown-to-root ratio, poor root form,parafunctional habits without a bite guard,and smoking.73 Tooth loss in this study wasdue to periodontal disease, restorative pur-poses, endodontic involvement, and caries.Unfortunately the authors could not asso-ciate initial prognostic factors with progres-sive attachment loss, the gold standard foradvancing Periodontitis. The inability to as-sociate the prognostic factors of mobility and

    parafunction with advancing attachmentloss; the inclusion of teeth lost due to non-periodontal reasons; and the inability toseparate out other prognostic factors suchas furcation involvement, bone loss, and at-tachment loss inhibit our ability to draw con-clusions about mobility or parafunction inrelation to progressive Periodontitis. The au-thors also noted that these findings relate towell maintained patients and may not applywhen evaluating poorly maintained individ-uals.

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    NON-CONTROLLED CASE STUDIES

    Non-controlled case studies are relativelyunreliable sources of information

    uponwhich to base a philosophy of treatment.Benefits of treatment demonstrated for onepatient may not reliably transfer to other pa-tients and the conclusions drawn from theresults of successful therapy in a few pa-tients under conditions where a multitude ofvariables were either unrecognized or poorlycontrolled may lead the clinician to incorrectconclusions. The following case studies are,therefore, being presented principally to il-lustrate points which have been previously

    presentedin well

    designedstudies.

    Paul et al. reported the treatment of a casediagnosed as rapidly progressive Periodon-titis with localized occlusal trauma involvingtooth #10.74 Treatment consisted of scalingand root planing, microbiological monitor-ing, use of systemic antibiotics, and surgicaltreatment where needed. Six weeks after in-itial therapy, pockets involving tooth #10had been reduced from 8 mm to 3 mm with-out surgical therapy or occlusal adjustment.However, 6 months later, tooth #10 re-mained mobile and

    radiographically appar-ent bone loss remained despite minimalprobing depths. Multiple occlusal adjust-ments over the next year resulted in "re-eruption" of the tooth which reduced thecrown-root ratio, eliminated occlusal inter-ferences, and improved function. This casedemonstrated the ability to reduce probingdepth and eliminate inflammatory periodon-tal disease without occlusal adjustment. Theauthors, however, considered occlusal ad-

    justment to be a valuable treatment to re-duce

    mobilityand

    improveclinical function

    of a tooth with severe attachment loss.Wolffe et al. documented the restorative

    and surgical treatment of a patient with ad-vanced Periodontitis.75 Six months foUowingthe placement of 4 fixed partial dentures(FPD), one in each quadrant, the occlusion re-mained stable. Over the next 2 years, the pa-tient developed a malocclusion due to a shiftof one the FPDs in response to forces gener-ated by the patient's tongue. The authorsstated that the reduced periodontium may

    have contributed to the lack of stability of thesplinted teeth. Occlusal adjustments led to aclinically stable occlusion. The periodontiumremained healthy, with no signs of bleeding,increased sulcus depth, or mobility through-out the reported period despite the persistentforces that caused drifting of the teeth and sig-nificant changes in the occlusion.

    INDIRECT EVIDENCE, ANIMALSTUDIES

    In a beagle dog study, Ericsson et al. eval-uated the effect of splinting on the progres-sion of experimental Periodontitis.76 Fivedogs had their mandibular 2nd and 3rd pre-molars and mandibular 1st molars ex-tracted. Titanium implants were theninstalled in the position of the 1st molar and3rd premolar in the right side of the man-dible. After 3 months of healing, non-resil-ient splints were placed connecting thedental implants to the 4th premolar on theright side. The 4th premolar on the left sideremained unsplinted and served as a controlwith persistent mobility from prior attach-ment loss. Experimental Periodontitis wasinitiated and maintained for 180 days by

    placing a ligature around the premolars. At-tachment loss and down growth of plaquewere evaluated with radiographs and biop-sies after the 180-day test period. The re-searchers found that splinting the testpremolars failed to retard attachment loss orto inhibit the apical down growth of the mi-crobial plaque. They concluded that in-creased tooth mobility at the control toothdid not exacerbate periodontal attachmentloss in this model.

    The effect of jiggling occlusal forces on

    probing depths in beagle dogs with normalperiodontal tissues was evaluated by Neide-rud et al.77 Six beagle dogs had their teethcleaned before entering the study and 3times each week during the study. Each doghadjiggling forces applied to a test premolarwhile a contralateral tooth served as a non-

    jiggling control. Afterjiggling forces had beenapplied for 90 days, a probe was insertedinto the sulcus of the test and control teethand stabilized in position with compositeresin. Biopsies of the sites were obtained

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    and used for histometric and morphometricmeasurements. The measurements revealedthat despite clinically healthy gingival tis-sues, the teeth which had become mobile

    due to the jiggling forces had lost marginalbone. An enlarged "supracrestal connectivetissue compartment" had also developedwhich resulted in significantly greater clini-cal probing depth measurements. This in-creased probing depth was related to a de-crease in collagen density and a morevascular connective tissue that was less re-sistant to probing without loss of connectivetissue attachment.

    In a related study, Giargia et al. reporteda reduction of probing depth and mobility af-

    ter removal of plaque retaining ligatures in abeagle dog model.78 This study evaluated theeffect of experimental Periodontitis on thehistologic appearance of the periodontal softtissues, alveolar bone height, and on toothmobility. After 120 days of experimentallyinduced Periodontitis, plaque retaining liga-tures were removed and a supragingival de-bridement was performed. Block sections,taken at the time of ligature removal and 15days and 3 months later, were used for his-tometric and morphometric evaluation. Ex-

    perimental Periodontitis led to the formationof an inflammatory lesion, extensive boneloss, and markedly increased tooth mobility.Removal of the dental plaque led to reducedtooth mobility and a decrease in the inflam-matory lesion, but no regeneration of lostbone. Probing depth which increased due tothe experimental Periodontitis was reducedafter removal of the microbial plaque. Theauthors suggested that the reduced probingdepth was a result of the soft tissue changes,due to resolution of inflammation after

    plaque removal and to reduced mobility ofthe teeth. The authors' comments on the ef-fect of reduced mobility on probing depthchanges appeared to be more related to theirawareness of the results of the prior Neide-rud study than to the results of this study.This study does document an increase inmobility due to periodontal inflammationand a decrease in that mobility as inflam-mation is decreased. This result appeared tobe independent of occlusal forces in this ex-perimental model. It also documented that

    changes in mobility may persist for severalmonths after etiologic factors are reducedand inflammation is resolving.

    In a study in a rat model that evaluated

    the effect of experimental traumatic occlu-sion on periodontal blood flow, Kvinnslandet al. reported an increase in blood flow toboth the pulp and periodontal ligament afterthe initiation of heavy occlusal forces.79 Inthe early stages of the study the experimen-tal "traumatized" side had an increasedblood flow when compared to the controlside. In the later stages of the experiment,both control and experimental sides had in-creased blood flow. This study did not eval-uate the effects of occlusal forces on

    Periodontitis but did demonstrate a physio-logic response of the periodontal tissues toocclusal forces.

    INDIRECT EVIDENCE, LABORATORYSTUDIES

    Photoelastic model and finite elementmodel studies have evaluated the transmis-sion of occlusal forces to the periodon-tium.80 81 Wylie et al. used a photoelasticmodel to simulate the effect of splinting aperiodontally involved tooth to one or moresound teeth when placing a cantileveredfixed partial denture.80 They found that op-timal stress distribution occurred whensplinting the compromised tooth to 2 soundteeth. Increasing the number of splintedteeth, beyond two sound teeth, did not sig-nificantly decrease the stress transmitted tothe periodontium. Cross-arch splinting didnot result in a significant sharing of the oc-clusal forces.

    Using a finite element model, Aydin et al.evaluated the stresses induced by variousloading forces on a mandibular 3-unit fixedpartial denture using a molar and a premo-lar as abutments.81 Loads of 300 N to 600 Napplied in axial and nonaxial directions wereanalyzed. Forces applied in non-axial direc-tions led to an increase the level of stress de-livered to the alveolar bone. The premolarexhibited greater stress distribution to thebone than the molar when non-axial forceswere applied. Stress levels increased, also,when periodontal support was diminished.

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    Studies like these can be used to demon-strate the mechanics of transmission offorces from teeth to the periodontium. Theycan not be used to interpolate results to

    broader and more involved interactions suchas those involving occlusion and inflamma-tory periodontal disease.

    SUMMARY

    Despite decades of debate and multiplepublications that discuss the theory of oc-clusion, occlusal design, and equilibrationtechniques, there have been few well-de-signed human studies that can help answerthe question "does occlusal trauma modify

    the progression of attachment loss due to in-flammatory periodontal disease." The arti-cles reviewed clearly demonstrate thatocclusal forces are transmitted to the perio-dontal attachment apparatus80'81 and thoseforces can cause changes in the bone andconnective tissue.21-27'77-79 These changes caneffect tooth mobility and clinical probingdepth.23,28 74'77 While occlusal forces do notinitiate Periodontitis, results are inconclu-sive on the interactions between occlusionand the progression of attachment loss due

    to inflammatory periodontal disease.While some studies found a relationshipbetween increased attachment loss andtooth mobility,57-59 others found no relation-ship between attachment loss and abnormalocclusal contacts.59 Tooth mobility can be aresult of a variety of factors including loss ofalveolar bone, attachment loss, disruption ofthe periodontal supporting tissues by in-flammation, occlusal forces which lead towidening of the periodontal ligament (phys-iologic adaptation), periodontal ligament at-

    rophy from disuse, or any process whicheffects the supporting periodontal struc-tures. Therefore, any relationship found be-tween tooth mobility and progressing Perio-dontitis does not necessarily indite or defendocclusion as a cofactor in the progression ofinflammatory periodontal disease.

    Periodontitis can be treated and periodon-tal health maintained without occlusal ad-

    justment and despite the obvious presenceof traumatic occlusal forces. 21,29,74,75 How-ever, statistically greater gains in clinical

    periodontal attachment level have been doc-umented when occlusal adjustment was in-cluded as a component of periodontaltherapy.56 The extent to which this is clini-

    cally meaningful in the treatment of Perio-dontitis is unclear. The effects of normalocclusion, parafunctional habits, and toothmobility on wound healing have also notbeen adequately evaluated.

    Once periodontal health is established,occlusal therapy can be an aid to help re-duce mobility, regain some bone lost dueto traumatic occlusal forces, and to treat avariety of clinical problems related to oc-clusal instability and restorative needs.40 71Based on the literature, it appears that a

    clinician's decision whether or not to useocclusal adjustment as a component ofperiodontal therapy should be related to anevaluation of clinical factors involving pa-tient comfort and function and not basedon the assumption that occlusal adjust-ment is necessary to stop the progressionof Periodontitis.

    FUTURE RESEARCH

    Prospective studies on the effects of occlu-sal forces on the progression of Periodontitisare not ethically acceptable in humans.Double-blind controlled prospective humanstudies to determine the effects of occlusalforces and mobility on wound healing follow-ing periodontal therapy are possible and arebadly needed. These studies could answerquestions concerning the effects of occlusionand mobility on regenerative periodontaltherapy such as guided tissue regenerationand periodontal plastic surgery.

    Studies that attempt to identify risk fac-tors for Periodontitis should also include oc-clusal analysis in the study parameters toevaluate this variable. These studies are,however, retrospective in nature and there-fore may find it difficult to establish causeand effect relationships. Animal studiescould help to define the effects of occlusalforces on peri-implant bone loss and to de-termine if excessive occlusal forces can effectthe progression of plaque induced peri-im-plantitis.

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    GLOSSARY OF TERMS

    Attachment apparatus: The cementum,periodontal ligament, and alveolar bone

    which function as a unit to support theteeth.Bruxism: A habit of grinding, clenching,

    or clamping the teeth. The forces so gener-ated may damage both the tooth and the at-tachment apparatus.

    Co-factor: An aspect of personal behavioror life-style, an environmental exposure, oran inborn or inherited characteristic whichby itself does not cause a disease processbut which can modify the course or expres-sion of a disease process.

    Disease markers: Factors that are indic-ative of the disease, but that are not thoughtto be etiologic or may be historical measuresof the disease or disease progression.

    Fremitus: A palpable or visible movementof a tooth when subjected to occlusal forces,(also referred to as functional mobility)

    Mobility, tooth: A visually perceptiblemovement of the tooth away from its normalposition when a light force is applied. (Thismovement may be within physiologic limitsor beyond physiologic limits.)

    Occlusion: The contact of opposing teeth.Occlusal adjustment: Reshaping the oc-cluding surfaces of teeth by grinding to cre-ate harmonious contact relationships be-tween the upper and lower teeth ororthodontic movement of the teeth to createa more harmonious occlusal relationship.

    Occlusal forces: Forces that are gener-ated and transmitted to the supportingstructures of the teeth when the teeth arebrought into contact.

    Occlusal interference: Any contact that

    inhibits the remaining occluding surfacesfrom achieving stable and harmonious con-tacts..

    Occlusal trauma: An injury to the attach-ment apparatus or tooth as a result of ex-cessive occlusal forces.

    Occlusal traumatism: the overall processby which a traumatogenic occlusion pro-duces injury in the periodontal attachmentapparatus.

    Parafunction: abnormal or pervertedfunction, as in bruxism.

    Premature occlusal contact: A conditionof tooth contact that diverts the mandiblefrom a normal path of closure.

    Primary occlusal trauma: Injury result-

    ing from excessive occlusal forces applied toa tooth or teeth with normal periodontalsupport.

    Secondary occlusal trauma: Injury re-sulting from normal occlusal forces appliedto a tooth or teeth with inadequate periodon-tal support.

    Traumatogenic occlusion: Any occlu-sion that produces forces that cause an in-

    jury to the attachment apparatus.

    REFERENCES

    1. Stillman PR. The management of pyorrhea. DentCosmos 1917;59:405-414.

    2. Box HK. Experimental traumatogenic occlusion insheep. Oral Health 1935;29:9-15.

    3. Leof M. Clamping and grinding habits: Their rela-tion with severity of periodontal disease. J Am DentAssoc 1944;31:184-194.

    4. Glickman I, Smulow JB. Alterations in the pathwayof gingival inflammation into the underlying tissuesinduced by excessive occlusal forces. J Periodontol1962;33:7-13.

    5. Glickman I, Smulow JB. Effect of excessive occlusalforces upon the pathway of gingival inflammation inhumans. J Periodontol 1965;36:141-147.

    6. Glickman I, Smulow JB. Further observations onthe effects of trauma from occlusion. J Periodontol1967;38:280-293.

    7. Glickman I, Smulow JB. Adaptive alterations in theperiodontium of the rhesus monkey in chronictrauma from occlusion. J Periodontol 1968;39:101-105.

    8. Akiyoshi M, Mori K. Marginal Periodontitis-

    A his-tological study of the incipient stage. J Periodontol1967;38:45-52.

    9. Macapanpan LC, Weinmann JP. The influence of in-

    jury to the periodontal membrane on the spread ofgingival inflammation. J Dent Res 1954;33:263-272.

    10. Goldman HM. Gingival vascular supply in inducedocclusal traumatism. J Oral Surg 1956;9:939-941.

    11. Ramfjord SP, Kohler CA. Periodontal reaction tofunctional occlusal stress. J Periodontol 1959;30:95-112.

    12. Muhlemann H, Herzog H. Tooth mobility and mi-croscopic tissue changes produced by experimentalocclusal trauma. Helv OdontolActa 1961;5:33-39.

    13. Yuodelis RA, Mann WV. The prevalence and possi-ble role of non-working contacts in periodontal dis-ease. Periodontics 1965;3:219-223.

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    14. Comar MD, Kollar JA, Garglulo AW. Local irritationand occlusal trauma as co-factors in the periodon-tal disease process. JPeriodontol 1969;40:193-200.

    15. Stahl SS. The responses of the periodontium tocombined gingival inflammation and occluso-func-

    tional stresses in four human surgical specimens.Periodontics 1968;6:14-22.

    16. Ramfjord SP, Ash MM. Significance of occlusion inthe etiology and treatment of early, moderate andadvanced Periodontitis. J Periodontol 1981 ;52:511-517.

    17. Nascimento A, Sallum AW. Periodontal changes indistant teeth due to trauma from occlusion. J Per-iodont Res 1975;10:44-48.

    18. Waerhaug J. The infrabony pocket and its relation-ship to trauma from occlusion and subgingivalplaque. JPeriodontol 1979;50:355-365.

    19. Waerhaug J. The angular bone defect and its relation-

    shipto trauma

    from occlusion and down growth ofsubgingival plaque. J Clin Periodontol 1979;6:61-82.20. Lindhe J, Svanberg G. Influence of trauma from oc-

    clusion on progressive experimental Periodontitis inthe beagle dog. J Clin Periodontol 1974;1:3-14.

    21. Lindhe J, Ericsson I. Influence of trauma from oc-clusion on reduced but healthy periodontal tissuesin dogs. J Clin Periodontol 1976;3:110-122.

    22. Ericsson I, Lindhe J. Effect of longstandingjigglingon experimental Periodontitis in the beagle dog. JClin Periodontol 1982;9:497-503.

    23. Lindhe J, Ericsson I. The effect of elimination ofjig-gling forces on periodontally exposed teeth in thedog. JPeriodontol 1982;53:562-567.

    24. Ericsson I, Lindhe J. Effect of longstandingjigglingon experimental marginal Periodontitis in the bea-gle dog. J Clin Periodontol 1982;9:497-503.

    25. Ericsson I, Lindhe J. Lack of significance of in-creased tooth mobility in experimental Periodonti-tis. JPeriodontol 1983;55:447-452.

    26. Nyman S, Lindhe J, Ericsson I. The effect of pro-gressive tooth mobility on destructive Periodontitisin the dog. J Clin Periodontol 1978;5:213-225.

    27. Poison AM, Meitner SW, Zander HA. Trauma andprogression of marginal Periodontitis in squirrelmonkeys. III. Adaptation of interproximal alveolarbone to repetitive injury. J Periodont Res 1976; 11:279-289.

    28. Poison A. The relative importance of plaque and oc-clusion in periodontal disease. J Clin Periodontol1986;13:923-927.

    29. Poison AM, Kantor ME, Zander HE. Periodontal re-pair after reduction of inflammation. J PeriodontRes 1979;14:520-525.

    30. Poison AM, Meitner SW, Zander HA. Trauma andprogression of marginal Periodontitis in squirrelmonkeys. IV. Reversibility of bone loss due totrauma alone and trauma superimposed upon Per-iodontitis. J Periodont Res 1976;11:290-297.

    31. Kantor M, Poison AM, Zander HA. Alveolar bone re-generation after the removal of inflammatory trau-matic factors. JPeriodontol 1976;47:687-695.

    Annals ofPeriodontology

    32. Perrier M, Poison A. The effect of progressive andincreasing tooth hypermobility on reduced buthealthy periodontal supporting tissues. J Periodon-tol 1982;53:152-157.

    33. Poison AM, Zander HA. Effect of periodontal trauma

    upon intrabony pockets. J Periodontol 1983;54:586-592.34. Poison AM, Adams RA, Zander HA. Osseous repair

    in the presence of active tooth hypermobility. J ClinPeriodontol 1983;10:370-379.

    35. Poison AM. Trauma and progression of marginalPeriodontitis in squirrel monkeys. II. Co-destructivefactors of Periodontitis and mechanically producedinjury. J Periodont Res 1974;9:146-152.

    36. Knowles J, Burgett F, Morrison E, Nissle R, Ra-mfjord S. Comparison of results following three mo-dalities of periodontal therapy related to tooth typeand initial pocket depth. J Clin Periodontol 1980;7:32-47.

    37. Houston F, Hanamura H, Carlsson GE, HaraldsonT, Rylander H. Mandibular dysfunction and Perio-dontitis. A comparative study of patients with per-iodontal disease and occlusal parafunctions. ActaOdontol Scand 1987;45:239-246.

    38. Hakkarainen K. Relative influence of scaling androot planing and occlusal adjustment on sulcularfluid flow. JPeriodontol 1986;57:681-681.

    39. Pihlstrom B, Anderson KA, Aeppli D, Schaffer EM.Association between signs of trauma from occlusionand Periodontitis. J Periodontol 1986;57:1-6.

    40. Proceedings of the World Workshop in Clinical Peri-odontics. Chicago: The American Academy of Per-iodontology; 1989:111/1.

    41. Chasens AI. Controversies in occlusion. Dent Clin

    North Am 1990;34:111-123.42. Rosenbaum RS. The possible effect of periodontal

    diseases on occlusal function. Curr Opin Periodontol1993;2:163-169.

    43. Keough B. Occlusal considerations in periodontalprosthetics. Int J Periodontics Restorative Dent1992;12:359-371.

    44. Devlin H. Ferguson MW. Alveolar ridge resorptionand mandibular atrophy. A review of the role of lo-cal and systemic factors. BrDentJ 1991;170:101-114.

    45. Burgett F. Trauma from occlusion. Periodontal con-cerns. Dent Clin North Am 1995;39:301-311.

    46. Rosenbaum RS. The possible effect of periodontal

    diseases on occlusal function. Curr Opin Periodontol1993:163-169.47. Seaton P. Mechanics of tensile and shear stress

    generation in fixed partial denture retainers. JProsthetDent 1994;71:237-244.

    48. Mericske-Stern R, Hofmann J, Wedig A, GeeringAH. In vivo measurements of maximal occlusalforce and minimal pressure threshold on overden-tures supported by implants or natural roots. Acomparative study. Part 1. IntJ Oral Maxillofac Im-plants 1993;8:641-649.

    49. Randow K, Detand T. On functional strain in fixedand removable partial dentures. An experimental invivo study. Acta Odontol Scand 1993;51:333-338.

  • 8/8/2019 Annals.1996.1.1 Occlusion

    13/14

    Review: Non-Surgical Pocket Therapy: Dental Occlusion 579

    50. Ogata K, Okunishi M, Miyake T. Longitudinal studyon forces transmitted from denture base to retain-ers of lower distal-extension removable partial den-tures with conus crown telescopic system. J OralRehabil 1993;20:69-77.

    51. Carlsson BR, Carlsson GE, Helkimo E, YontchevE.Masticatory function in patients with extensivefixed cantilever prostheses. J Prosthet Dent 1992;68:918-923.

    52. Ogata K, Miyake T, Okunishi M. Longitudinal studyon forces distributed in lower distal-extension re-movable partial dentures with circumferencialclasps. J Oral Rehabil 1992;19:585-594.

    53. Ogata K, Ishii A, Nagare I. Longitudinal study ontorque transmitted from a denture base to abut-ment tooth of a distal-extension removable partialdentures with circumferencial clasps. J Oral Reha-bil 1992;19:245-254.

    54. Yang HS, Thompson VP. A two-dimensional stress

    analysis comparing fixed prosthodontics ap-proaches to the tilted molar abutment. Int JProsthet 1991;4:416-424.

    55. Laureil L, Lundgren D. Influence of occlusion onposterior cantilevers. J Prosthet Dent 1992;67:645-652.

    56. Brgert FG, Ramfjord SP, Nissle RR, Morrison EC,Charbeneau TD, Caffesse RG. A randomized trial ofocclusal adjustment in the treatment of Periodon-titis patients. J Clin Penodontol 1992;19:381-387.

    57. Wang H, Brgert F, Shyr Y, Ramfjord S. The influ-ence of molar furcation involvement and mobility onfuture clinical periodontal attachment loss. J Per-iodontol 1994;65:25-29.

    58. Ismail AI, Morrison ED, Burt BA, Caffessee RG, Ka-vanagh MT. Natural history of periodontal diseasein adults: Findings from the Tecumseh periodontaldisease study. J Dent Res 1990;69:430-435.

    59. Jin L, Cao C. Clinical diagnosis of trauma from oc-clusion and its relation with severity of Periodonti-tis. J Clin Periodontol 1992;19:92-97.

    60. Horning GH, Hatch CL, Cohen ME. Risk indicatorsin a military treatment population. J Periodontol1992;63:297-302.

    61. Locker D, Leake JL. Risk indicators and risk mark-ers for periodontal disease experience in olderadults living independently in Ontario, Canada. JDent Res 1993;72:9-17.

    62. Beck JD. Methods of assessing risk for Periodon-titis and developing multifactorial models. J Peno-dontol 1994;65:468-478.

    63. Kallestal C, Matsson L: Periodontal conditions in agroup of Swedish adolescents (II). Analysis of data.J Clin Periodontol 1990; 17:609-612.

    64. Beck JD, Koch GG, Rozier RG, Tudor GE. Preva-lence and risk indicators for periodontal attach-ment loss in a population of older community-dwelling blacks and whites. J Periodontol 1990;61:521-528.

    65. Oliver RC, Brown LJ, Le H. Variations in the prev-alence and extent of Periodontitis. J AmDentAssoc1991;122:43-48.

    66. Haffajee AD, Socransky SS, Lindhe J, Kent RL,Okamoto H, Yoneyama T. Clinical risk indicatorsfor periodontal attachment loss. J Clin Periodontol1991;18:117-125.

    67. Grossi SG, Zambon JJ, HO AW, et al. Assessmentof risk for periodontal disease. I. Risk indicators forattachment loss. J Periodontol 1994;65:260-267.

    68. Wheeler TT, McArthurWP, MagnussonI, etal. Mod-eling the relationship between clinical, microbiolog-ical, and immunologic parameters and alveolarbone levels in an elderly population. J Periodontol1994;65:68-78.

    69. Grossi SG, Genco RJ, Machtei EE, et al. Assess-ment of risk for periodontal disease. II. Risk indi-cators for alveolar bone loss. J Periodontol 1995;66:23-29.

    70. Burt BA, Ismail AI, Morrison EC, Beltran ED. Riskfactors for tooth loss over a 28-year period. J DentRes 1990;69:1126-1130.

    71. McGuire MK. Prognosis versus actual outcome. Along-term survey of 100 treated periodontal pa-tients under maintenance care. J Penodontol 1991;62:51-58.

    72. McGuire MK, Nunn ME. Prognosis versus actualoutcome II. The effectiveness of commonly taughtclinical parameters in developing an accurate prog-nosis. J Periodontol 1996;67:658-665.

    73. McGuire MK, Nunn ME. Prognosis versus actualoutcome III. The effectiveness of commonly taughtclinical parameters in accurately predicting toothsurvival. J Periodontol 1996;67:666-674.

    74. Paul BF, Leupold RJ, Towle HJ. Occlusal trauma:

    A case in perspective. J Am Dent Assoc 1995; 126:94-98.75. Wolffe GN, SpanaufAJ, Brand G. Changes in occlu-

    sion during the maintenance of a patient treatedwith combined periodontal/prosthetic therapy: Acase report. Int J Periodontics Restorative Dent1991;11:49-57.

    76. Ericsson I, Giargia M, Lindhe J, Neiderud AM. Pro-gression of periodontal tissue destruction atsplinted/non-splinted teeth. An experimental studyin the dog. J Clin Periodontol 1993;20:693-698.

    77. Neiderud A-M, Ericsson I, Lindhe J. Probing pocketdepth at mobile/nonmobile teeth. J Clin Periodontol1992;19:754-759.

    78. Giargia M, Ericsson I, Lindhe J, Berglindh T, Nei-derud A-M. Tooth mobility and resolution of exper-imental Periodontitis. Am experimental study in thedog. J Clin Periodontol 1994;21:457-464.

    79. Kvinnsland S, Kristiansen AB, Kvinnsland I, Heye-raas KJ. Effect of experimental traumatic occlusionon periodontal and pulpal blood flow. Acta OdontolScand 1992;50:211-219.

    80. Wylie RS, Caputo AA. Fixed cantilever splints onteeth with normal and reduced periodontal support.J Prosthet Dent 1991;66:737-742.

    81. Aydin AK, Tekkaya AE. Stresses induced by differ-ent loadings around weak abutments. J ProsthetDent 1992;68:879-884.

    Vol. 1, No. 1, November 1996

  • 8/8/2019 Annals.1996.1.1 Occlusion

    14/14

    580 Gher

    82. Gher ME, Vernino AR. Root anatomy: A local factorin inflammatory periodontal disease. IntJ Periodon-tics Restorative Dent 1981;l(5):53-63.

    83. Gher ME, Vernino AR. Root morphology-

    Clinicalsignificance in pathogenesis and treatment of peri-odontal disease. J Am Dent Assoc 1980; 101:627-633.

    84. Mafia JI, Bissada NF, Maybury JE, Ricchetti P. Ef-ficiency of scaling of the molar furcation area withand without surgical access, frit J Periodontics Re-storative Dent 1986;6(6):25-35.

    85. Vacek JS, Gher ME. Cementum anomalies of the

    dentogingival junction. Int J Periodontics Restora-tive Dent 1993;13:443-449.

    86. Hermann D, Gher ME, Dunlap R, Pelleu G. The po-tential attachment area of the maxillary first molar.JPeriodontol 1983;54:431-4.

    87. Gher ME, Vernino AR. Root Morphology - Clinicalsignificance in pathogenesis and treatment of peri-odontal disease. J Am Dent Assoc 1980; 101;627-33.

    88. Bower RC. Furcation morphology relative to perio-dontal treatment. Furcation root surface anatomy.JPeriodontol 1979;50:366-374.

    89. Bower RC. Furcation morphology relative to perio-dontal treatment

    -

    Furcation entrance architecture.JPeriodontol 1979;50:23-27.


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