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Current concepts of trauma from occlusion - A review
Current concepts of trauma from occlusion - A review
S. Sangeetha, Kiran Mitra, Umesh Yadalam, Sarita Joshi Narayan
Department of Periodontics, Sri Rajiv Gandhi College of Dental Sciences and Hospital, Bangalore, Karnataka, India
Correspondence: Dr. S. Sangeetha, Department of Periodontology Sri Rajiv Gandhi College of Dental Sciences and Hospital, Cholanagar, Hebbal, Bengaluru, Karnataka-560032, India.
Phone: +91-9113851656.
Received: 02 January 2019 ;
Accepted: 12 February 2019
doi: 10.15713/ins.jcri.250
It has been a topic of debate among dental care professionals, if trauma from occlusion is linked with periodontal disease or not. There are several schools of thought related to if trauma from occlusion is an etiological factor or cofactor for the occurrence of periodontal diseases. The present review article discusses historical background, etiological factors, classification, relevant terminologies, tissue response, signs and symptoms, advanced diagnostic methods, and treatment.
Keywords: Occlusal forces, periodontium, traumatic occlusion
How to cite this article: Sangeetha S, Mitra K, Yadalam U,Narayan SJ. Current concepts of trauma from occlusion - Areview. J Adv Clin Res Insights 2019;6:14-19.


The role of occlusal trauma in the initiation and progression of periodontitis remains a controversial subject in periodontology. Occlusal trauma can only be confirmed histologically; its clinical diagnosis completely depends on clinical and radiographic surrogate indicators which make clinical trials difficult. The present review paper discusses the historical background, etiological factors, classification, tissue response, signs and symptoms, advanced diagnostic methods, and treatment.

Historical Aspects

Ever since Karolyi (1901) postulated that an interaction may exist between "trauma from occlusion" (TFO) and "alveolar pyorrhea," different opinions have been presented in the literature regarding the validity of this claim.[1]

In the 1930s, Box (1935) and Stones (1938) reported experiments in sheep and monkeys, the results seemed to indicate that "TFO is an etiologic factor in the production of periodontal disease in which there is vertical pocket formation associated with one or a varying number of teeth" (Stones 1938).[1]

Glickman and Smulow[2] proposed the theory in the early 1960s that a traumatogenic occlusion may act as a cofactor in the progression of periodontitis. This theory is known as the "co destructive theory." Goldman[3] proved that occlusal trauma was not the cause of soft tissue lesions such as Stillman'sclefts and McCall's festoons. Waerhaug[4] proved the involvement of TFO in the pathogenesis of infrabony pockets.

Definition and Terminology

Excessive occlusal force is defined as occlusal force that exceedsthe reparative capacity of the periodontal attachment apparatus, leading to occlusal trauma, and/or causes excessive tooth wear (loss).[5,6]

Occlusal trauma

The injury resulting in tissue changes within the attachment apparatus, including cementum, supporting alveolar bone, and periodontal ligament, as a result of occlusal force(s). A reduced periodontium or an intact periodontium caused by periodontal disease may be affected by occlusal trauma.[7]

TFO was defined by Stillman as "a condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position."[1]

The World Health Organization in 1978 defined trauma from occlusion as "damage in the periodontium caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaw."[1]

In "glossary of periodontic terms" (American Academy of Periodontology 1986), occlusal trauma was defined as "an injuryto the attachment apparatus as a result of excessive occlusalforce."[1]

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Primary occlusal trauma

The injury resulting in tissue changes from excessive occlusalforces applied to a tooth or teeth with normal periodontalsupport.[8] In the presence of normal clinical attachment levels,normal bone levels, and excessive occlusal force(s), primaryocclusal trauma occurs.

Secondary occlusal trauma is injury resulting in tissuechanges from normal or excessive occlusal forces applied toa tooth or teeth with reduced periodontal support.[8] In thepresence of attachment loss, bone loss, and normal/excessiveocclusal force(s), secondary occlusal trauma occurs.


When a tooth is subjected to occlusal forces, a palpable or visiblemovement on the tooth is appreciable, called as fremitus.[7]

Bruxism or tooth grinding

A habit of grinding or clenching of the teeth.[7] Both tooth andattachment apparatus may get damaged by the forces generated.

Forces During Jaw Movements

During the process of chewing, swallowing, or any parafunctionalhabits, such as bruxism and clenching, the teeth and theirperiodontium are predisposed to functional dynamic loading.

Frequently, in normal healthy adults, tooth-to-tooth contactor near contact occurs during mastication. The lateral guidingcusps (commonly of cuspids and bicuspids) come in contact, andduring closure, the jaw, follows a wide lateral path. Relatively, alow magnitude of forces (averaging 81 N) and short-acting, witha duration of about 20-50 ms, are generated by these contacts.

Forces at final closure in the intercuspal position are muchgreater (averaging 262 N) and are also longer acting with anaverage duration of about 115 ms. An average force of 296 Nand a duration of about 700 ms occur in the intercuspal position,during chewing and swallowing.

Classification OF TFO

Glickman's classification (1953)

According to the duration of cause:[8]
  1. Acute TFO.
  2. Chronic TFO.

Acute TFO

An abrupt occlusal impact, caused by chewing on a hardobject, restorations or prosthetic appliances that may alter theocclusal forces.

Acute trauma may lead to pain, sensitivity, and increasedmobility of the tooth.

Chronic TFO

It is more frequent and has more clinical significance. The gradualchanges in occlusion caused by tooth wear, drifting movement,and extrusion of the teeth along with parafunctional habits leadto chronic TFO.

According to the nature of cause, chronic TFO is classifiedinto: [8]
  1. Primary TFO.
  2. Secondary TFO.
  • Primary TFO: TFO occurs as the result of alterations inocclusal forces.
  • Secondary TFO: It occurs as a result of reduced ability of thetissues to resist the occlusal forces.

Box's classification[9]

Physiologic occlusion

A condition, in which the systems of forces acting on the toothduring the occlusion are in a state of equilibrium, and theydo not and cannot change the normal relationship existingbetween the tooth and its supporting structures, defined bybox.

Traumatic occlusion

The damage produced in the periodontium is due to theoverstress produced by the occlusion.

Hamp, Nyman, and Lindhe's classification (1975)[9]

This classification is based on a horizontal component of tissuedestruction that has occurred in the interradicular area.
  • Degree I: Horizontal loss of periodontal tissue support notexceeding one-third of the width of the tooth.
  • Degree II: Horizontal loss of periodontal support exceedingone-third of the width of the tooth.
  • Degree III: Horizontal through-and-through destruction ofthe periodontal tissue in the furcation area.

Etiological Factors[10]

Precipitating factors

The irritants and the devasting occlusal forces that furtherdestroy the tissues are weakened by the predisposing factors.

Predisposing factors

Factors which take the place of those contributing to thehistopathologic lesion are listed as developmental factors,functional mechanisms, and the systemic component. They canbe divided into:
  1. Intrinsic factors: Consist of the morphology of the roots,alveolar process, and the orientation of the occlusal surfacesand roots to the forces, in which the tooth gets exposed to.
  2. Extrinsic factors: Consist of plaque, parafunctional activities,bone lossor loss of teeth, and malocclusion creatediatrogenically.

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Etiology For Primary TFO[8]
  1. A "high filling;"
  2. Prosthetic replacement which creates undesired forces onabutment and opposite teeth;
  3. Drifting or extrusion of teeth into unreplaced missing teethspace;
  4. Movement of teeth into functionally unacceptable positionsby orthodontic procedures.

Etiology For Secondary TFO[8]

Reduced height of bone with:
  1. Normal periodontium,
  2. Marginal periodontitis.

TFO And Plaque-Associated Periodontal Disease

Analysis of human autopsy material[1]

The assessments made from cadaver specimens have a limitedto questionable value when "cause-effect" relationships betweenocclusion, plaque, and periodontal lesions are to be described.The conclusions drawn from this type of research can becontroversial. This can best be illustrated if "Glickman's concept"is compared with "Waerhaug's concept" of what autopsy studieshave revealed regarding TFO and periodontal disease.

Glickman's concept[11,12]

Glickman (1965, 1967) claimed that, if forces of an abnormalmagnitude are acting on teeth harboring subgingival plaque, thenthe alley of the spread of a plaque-associated gingival lesion canbe altered.

The periodontal structures can be divided into:
  1. The zone of irritation.
  2. The zone of codestruction.

The zone of irritation consists of the marginal and interdentalgingiva. The soft tissue zone is surrounded by the hard tissue(the tooth) on one side and has no impact by occlusal forces.This means that gingival inflammation cannot be initiated byTFO but rather due to irritation from plaque.

The zone of codestruction consists of the periodontal ligament,cementum, and alveolar bone and is coronally delineated by thetransseptal and the dentoalveolar collagen fiber bundles.

In contrast to the co-destructive theory, Waerhaug andGlickman, both had examined autopsy specimens, but Waerhaugalso measured the distance from the subgingival plaque to theperiphery of the associated inflammatory cell infiltrate in thegingiva and the adjacent alveolar bone surface. He came to theconclusion that angular bony defects and also infrabony pocketsoccur equally often at periodontal sites which are unaffected byTFO like in traumatized teeth.[4]

Various animal studies using the Squirrel Monkey[13-15] andBeagle Dog[16-20] evaluated the excessive jiggling force's effects inthe experimentally induced periodontitis.

The conclusions of these studies are as follows:
  1. Occlusal trauma does not induct gingival inflammation.
  2. A traumatogenic occlusion will lead in increased mobility,widening of PDL, and crestal bone loss along withbone volume but no attachment loss in the absence ofinflammation.
  3. When gingival inflammation was present, excess jigglingforces did not cause increased attachment loss in squirrelmonkeys, but accelerating occlusal forces may increaseattachment loss in beagle dogs.
  4. Although there will be no difference in attachment level, aftertreating the inflammation in the existence of mobility, it willat least decrease the mobility of teeth and help in gainingbone density.

Tissue Response To TFO[8]

There are three stages of tissue response: Injury, repair, andadaptive remodeling of the periodontium.

Stage I Injury[8]

Immoderate pressure initiates resorption of the alveolarbone, along with widening of the periodontal ligament space.Immoderate tension leads to elongation of the periodontalligament fibers and alveolar bone apposition. In areas of excessivepressure, there are numerous blood vessels which are reduced insize; in areas of excessive tension, they are expanded. Greaterpressure leads to changes in the PDL, such as compression of thefibers, producing hyalinization.

Stage II Repair[8]

In the normal periodontium, repair occurs persistently, andincreased reparative activity is stimulated due to TFO. Whendue to excessive occlusal forces, bone is resorbed, the bodyreinforces the bony trabeculae which is thinned, with new bone.This process of compensating for the lost bone is termed as"buttressing bone formation."

Buttressing bone formation occurring within the jaw is calledcentral buttressing and on the bony surface is called "peripheralbuttressing."

A shelflike thickening of the alveolar margin or an evidentbulge in the facial and lingual bone may be produced byperipheral buttressing which is called as "lipping."

Stage III Adaptive remodeling of the periodontium[8]

If the destruction due to the occlusion surpasses the repairprocess, the periodontium is remodeled so that it can maintaina structural relationship. This leads to thickening of the PDL,which will be funnel shaped at the crest and angular defects inthe junctional epithelium without any pocket formation. Theinvolved teeth become mobile. There will also be an increase invascularization.

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Clinical signs
  1. Mobility and periodontal ligament widening Positivefremitus test
  2. in the apical region and in bifurcationareas, lamina durathickening can be seen.
  3. Occlusal prematurities.

Radiographic signs[8,22,23]
  1. Periodontal ligament widening, mostly with lamina durathickening along the root's lateral aspect, apical region, andbifurcation.
  2. Vertical destruction of the interdental septum.
  3. Radiolucency and alveolar bone condensation.
  4. Resorption of root.
  5. Migration of tooth.
  6. Tooth fracture.
  7. Thermal sensitivity.

Diagnosis of TFO[21,22]

For the correct diagnosis of TFO, proper clinical history takingand clinical examination of the patients are vital.
  1. Cardinal manifestation of primary TFO is increased toothmobility. The mobility can be assessed by mechanical andelectronic instrument. Subjective assessments of mobility aredone as in Miller classification assigned from 0 to 3 score.
  2. Tilting and migration of individual teeth or of completesegments. The percussion of teeth on tapping with a bluntinstrument changes from a resonant note with a healthysupporting structure to a dull note if there is primary TFO inattachment apparatus.
  3. Careful palpation of the muscles of mastication to ascertainwhether there is hypertrophy or sign of hypertonicity withpossible spasm of one group of muscle.
  4. Palpation of TMJ and observation of any deviation of themandible in various paths of closure.
  5. Fremitus test: [23,24] Measures the vibratory patterns of theteeth during contact positions and during movements.

The following classification system is used:
  • Class 1: Mild vibration or movement detected.
  • Class II: Easily palpable vibration but no visible movement.
  • Class III: Movement visible with the naked eye.

Goals And Treatment Considerations[25]

TXTreatment considerations that must be considered includeone or more of the following: [25]
  1. Occlusal adjustment of the tooth.
  2. Correction of parafunctional habits.
  3. Temporary, provisional, or long-term stabilization of mobileteeth with appliances.
  4. Orthodontic corrections.
  5. Occlusal readjustments.
  6. Extraction of indicated teeth.

Occlusal adjustment

Occlusal adjustment means, setting up of functional relationshipsappropriate to the periodontium by: Coronoplasty, dentalrestorations, tooth removal or by orthognathic surgery.[26]

Indications and contraindications for occlusal adjustment

Given by World Workshop in Periodontics (1989)[27]

  1. To fortify repair within the periodontal attachment apparatusby reducing traumatic forces to teeth that exhibit increasedmobility or fremitus.
  2. To obtain functional association and masticatory effectivenessalong with restorative treatment, orthodontic, orthognathicsurgery, or jaw trauma.
  3. As an adjunct, reducing the damage from parafunctionalhabits.
  4. To recontour teeth, responsible for causing soft tissue injury.

  1. Prophylactic adjustment.
  2. As a treatment of primary, microbial-induced inflammatoryperiodontal disease.
  3. Based on a patient history, correction of bruxism, withoutexact evidence of damage, pathosis, or pain.
  4. When the patient's emotional state impedes a satisfactoryresult.
  5. When severe extrusion, mobility or malpositioning of teeth ispresent where occlusal adjustment would not be sufficient.

Management of parafunctional habits

The perfect diagnosis of bruxism can be acheived by takingproper history and by assessing the clinical features of the patient.Methods by which the patient with bruxism can betreated:Electromyographic biofeedback[28,29] a physical therapy course,medications aimed at altering sleep arousal or anxiety level andthe appliances for maxillary stabilization.


A splint is an appliance used for immobilization or stabilization.[30]Splinting is stabilization, achieved by joining two or more teethto increase resistance to the forces applied. The types being theshort-term splint, the provisional or long-term splint.

Indications and Contraindications for Splinting

Given by World Workshop in Periodontics (1989)[27]

  1. To stabilize the teeth with increased mobility that have notbeen corrected by occlusal adjustment and periodontaltreatment.
  2. When there is an interference with the normal functioningand patient discomfort.
  3. Splinting extremely mobile teeth, before periodontalinstrumentation and occlusal adjustment procedures,facilitating the treatment.
  4. To prevent tipping or drifting and extrusion of teeth.
  5. Following orthodontic movement to stabilize the teeth.
  6. To create enough occlusal stability while replacing themissing teeth.
  7. Following acute trauma.

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  1. If the treatment of inflammatory periodontal disease has notbeen done.
  2. If occlusal adjustment for the reduction of trauma and/orinterferences has not been addressed previously.

Occlusal reconstruction

In cases where no other treatment could achieve occlusalequilibration, occlusal reconstruction has to be done. It consistsof recontouring the occlusal contacts by providing crowns,bridges, or implant-supported prosthesis.


A tooth which has a poor prognosis and by the extraction ofwhich, the prognosis of the remaining teeth improves, then thetooth in question should be extracted.


Inconclusive evidence based on well-controlled prospectivehuman studies has led to the unsure treatment of periodontiumaffected with TFO. Removal of the anomalous occlusal forcesand stabilization of the affected tooth/teeth is the most relevanttherapy for teeth affected by TFO.


I would like to thank all the contributors of this review and theinstitutions. The authors declare that there is no conflict ofinterests.

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