|Year : 2017 | Volume
| Issue : 2 | Page : 126-132
Trauma from occlusion: The overstrain of the supporting structures of the teeth
Dhirendra Kumar Singh, Md Jalaluddin, Ranjan Rajeev
Department of Periodontics and Oral Implantology, Kalinga Institute of Dental Sciences, KIIT University, Bhubaneswar, Odisha, India
|Date of Web Publication||26-May-2017|
Dhirendra Kumar Singh
Department of Periodontics and Oral Implantology, Kalinga Institute of Dental Sciences, KIIT University, Bhubaneswar - 751 024, Odisha
Source of Support: None, Conflict of Interest: None
Any occlusal force which goes beyond the adaptive capacity of our periodontium causes injury to periodontal structures, and the resultant trauma is called as trauma from occlusion (TFO), several schools of thoughts are there that whether TFO is an etiological factor or cofactor for the occurrence of periodontal diseases. Present review paper is an effort to clear the actual concept of TFO along with its historical background, etiological factors, relevant terminologies, signs and symptoms, and advanced diagnostic methods.
Keywords: Occlusal forces, periodontium, traumatic occlusion
|How to cite this article:|
Singh DK, Jalaluddin M, Rajeev R. Trauma from occlusion: The overstrain of the supporting structures of the teeth. Indian J Dent Sci 2017;9:126-32
|How to cite this URL:|
Singh DK, Jalaluddin M, Rajeev R. Trauma from occlusion: The overstrain of the supporting structures of the teeth. Indian J Dent Sci [serial online] 2017 [cited 2021 Jan 23];9:126-32. Available from: http://www.ijds.in/text.asp?2017/9/2/126/207104
| Introduction|| |
For many years, the role of occlusion and its dynamic interactive impact on the periodontium has been an issue of controversy and extensive debate. Although a variety of occlusal conditions have purportedly been related to this interaction, the central focus has been on occlusal trauma resulting from excessive forces applied to the periodontium.,,, In an attempt to clarify and better understand this condition, early investigators used human necropsy specimens and a variety of animal models as a basis for clinical and histological studies. Findings were often diverse and somewhat contradictory. In the animal studies, factors of concern included differences among animals, forces applied, and lack of controls. Retrospective descriptive observations of the effect of excessive forces on the periodontium were derived from human necropsy materials. The selection of study sites was based on occlusal wear, patterns of pocket formation, and presence of attachment loss leaving some questions as to the presence of ongoing occlusal trauma.
Despite the foregoing concerns, the majority of these early studies agreed that occlusal trauma in and of itself failed to result in pocket formation or loss of connective tissue attachment. It is apparent that the effects of excessive occlusal force and the destructive, adaptive, and reparative response of the periodontium have been complicated by a relative lack of evidence based on well-controlled prospective studies in human beings.,,
This review is based on analysis of 150 papers published in English language till November 2016 in peer-reviewed journals. The search for papers was performed using Medline, Google Scholar, and PubMed by searching keywords such as trauma from occlusion, primary trauma from occlusion, secondary trauma from occlusion, trauma from occlusion, and periodontal diseases. Any discussion related to the trauma from occlusion (TFO) use of in periodontics and implantology was taken into consideration if appropriate for this review.
The present literature review is an attempt to address the histological and clinical effects of abnormal occlusal forces on other teeth and periodontium and to provide diagnosis and clinical aspects for the same.
| Historical Aspects|| |
Karolyi was the first one to start the most controversial issue by introducing in 1901 the concept of bruxism as a significant factor in the pathogenesis of periodontitis. It is known as the “Karolyi effect.”
Talbot did the first comprehensive study of the role of occlusal stress on teeth in relation to periodontal disease was made by Talbot, who pointed out that man is predisposed to disease of the supporting tissues of the teeth because jaw function has been greatly decreased by modern methods of food preparation.
Box et al. did study on sheeps' tooth suggesting that TFO produces vertical bone defect. Stillman  was the first to emphasize traumatic occlusion as a cause of periodontal disease. Repeated abnormal pressures of one tooth on another produce traumatic injury. He pointed out that there are noninfectious changes that are directly produced by traumatic occlusion.
Glickman and Smulow ,, proposed the theory in the early 1960s that a traumatogenic occlusion could act as a cofactor in the progression of periodontitis. This theory is known as the “co destructive theory.” Goldman  proved that occlusal trauma was not the cause of soft tissue lesions such as Stillman's clefts and McCall's festoons. Waerhaug , proved the involvement of TFO in the pathogenesis of Infrabony pockets. Polson , used squirrel monkeys as their animal model. Houston et al. concluded that there is no correlation between periodontal disease and bruxism; they seldom occurred in the same individual, and bruxism and occlusal status are not closely associated.
Burgett et al. found no significant difference in the reduction in tooth mobility between the adjusted and the nonadjusted groups. Wolffe et al. stated that “a periodontium remained healthy despite the persistent forces that caused the drifting of the teeth and significant changes in occlusion.”
Ericsson et al. showed that splinting failed to retard attachment loss or to inhibit plaque down growth. He showed that despite healthy gingival tissues, jiggled teeth lost marginal bone and had more probing depth when compared to the nonjiggled.
| Terminologies Used With Trauma from Occlusion|| |
- Occlusal traumatism: The term traumatic occlusion, introduced by Stillman, denoted abnormal stress capable of producing injury to dental or periodontal tissues
- Trauma from occlusion: It is a term used to describe pathologic alterations or adaptive changes which develop in the periodontium as a result of undue force produced by the masticatory muscles
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.” The WHO in 1997 defined TFO as “damage in the periodontium caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaw.” In “Glossary of Periodontics terms” (American Academy of Periodontology 1986), occlusal trauma was defined as “An injury to the attachment apparatus as a result of excessive occlusal force”
- Fremitus: A palpable or visible movement of a tooth when subjected to occlusal forces (also known as functional mobility)
- Occlusal adjustment: Reshaping of the occlusal surfaces of teeth by grinding to create harmonious contact relationships between the upper and lower teeth, or orthodontic movement of the teeth to create more harmonious contact relationship
- Occlusal interference: Any contact that inhibits the remaining occluding surfaces from achieving stable and harmonious contacts
- Occlusal traumatism: The overall process by which a traumatogenic occlusion produces injury in the periodontal attachment apparatus
- Parafunction: Abnormal or perverted function
- Premature occlusal contact: A condition of tooth contact that diverts the mandible from a normal path of closure
- Traumatogenic occlusion: Any occlusion that produces forces those cause an injury to the attachment apparatus
- Occlusal trauma:, An injury to the attachment apparatus as a result of excessive occlusal forces.
| Classification of Trauma from Occlusion|| |
Glickman's classification (1953)
According to duration of cause:
- Acute TFO
- Chronic TFO.
According to nature of cause:
- Primary TFO
- Secondary TFO.
Box defined it as a condition, in which the systems of forces acting upon the tooth during the occlusion are in a state of equilibrium, and they do not and cannot change the normal relationship existing between the tooth and its supporting structures.
The damage produced in the periodontium is due to the overstress produced by the occlusion.
Hamp, Nyman, and Lindhe's classification (1975)
This classification is based on a horizontal component of tissue destruction that has occurred in the interradicular area, i.e., degree of horizontal root exposure or attachment loss.
- Degree I: Horizontal loss of periodontal tissue support not exceeding one-third of the width of the tooth
- Degree II: Horizontal loss of periodontal support exceeding one-third of the width of the tooth
- Degree III: Horizontal through-and-through destruction of the periodontal tissue in the furcation area.
Primary trauma from occlusion
It is generally referred to as a condition resulting from abnormal occlusal forces on relatively sound periodontal structure. In effect, the traumatic forces acting on teeth with normal support are greater than the forces that can be withstood without injury to the periodontium.
Secondary trauma from occlusion
Applied to a condition resulting from physiologic or abnormal occlusal forces, which act on a dentition that is seriously weakened by the loss of supporting alveolar bone. This lack of periodontal support may result not only from effects of periodontal disease but also from injudicious bone resection during periodontal therapy or oral surgery, from accidental trauma or from excessive apical resorption associated with orthodontic or endodontic therapy.
Acute trauma from occlusion
Acute TFO results from an abrupt occlusal impact such as that produced by biting on a hard object (e.g., an olive pit). In addition, restorations or prosthetic appliances that interfere with or alter the direction of occlusal forces on the teeth may induce acute trauma.
Chronic trauma from occlusion
Chronic TFO is more common than the acute form and is of greater clinical significance. It most often develops from gradual changes in occlusion produced by tooth wear, drifting movement, and extrusion of teeth, combined with parafunctional habits such as bruxism and clenching, rather than as a sequel of acute periodontal trauma.
| Etiological Factors|| |
Ross has divided the factors causing chronic destructive periodontal disease into two groups:
- Precipitating factors: Precipitating factors are the irritants and the destructive occlusal forces that further destroy the tissues weakened by predisposing factors
- Predisposing factors: Factors which take the place of those contributing to the histopathologic lesion are listed as developmental factors, functional mechanisms, and the systemic component.
They can be divided into intrinsic and extrinsic factors:
- Morphologic characteristics of the roots. Such factors as their size, shape, and number are of prime importance. Teeth with short, conical, slender, or fused roots rather than divergent roots are more predisposed to occlusal traumatism when subjected to prolonged excessive force than are those with normal structure
- The manner in which occlusal surfaces and the roots are oriented in relation to the forces to which they are exposed. Axially inclined forces are more tolerable than are nonaxially inclined forces, which may be functional or parafunctional. When teeth are badly aligned, the effect of excessive force can be deleterious
- Morphologic characteristics of the alveolar processes. If the quantity or quality of alveolar bone is inherently lacking, the effects of prolonged parafunctional forces may result in rapid loss of the remaining support.
Among the extrinsic factors that may seriously increase the rapidity of loss of supporting alveolar bone are the following:
- Irritants: Microbial plaque is implicated as the most serious irritant. Other irritants that may have similar effects are food impaction that results in positive pressure on the tissues, overhanging restorations, poorly contoured crowns and bands, and ill-fitting partial denture clasps
- Neuroses that result in parafunctional activities, for example, bruxism. These factors are the most prevalent and serious causes of abnormal occlusal stresses
- Loss of supporting bone: Periodontitis, injudicious bone resection, inadvertent trauma, and systemically related diseases are the chief causative factors
- Loss of teeth resulting in overloading of the remaining teeth, for example, posterior bite collapse
- Iatrogenically created functional malocclusion.
The terms precipitating and predisposing are equally applicable to the factor causing occlusal traumatism.
| Normal Function Versus Parafunction|| |
Two major categories of activity are performed by the stomatognathic system: normal function and parafunction. Mastication, occlusional light contact during speech, swallowing, coughing, and yawning are regarded as normal functions; all other forms of pressure contact of the teeth are parafunctional.
| Significance of Parafunction|| |
Parafunctional forces have been stressed as the major etiologic factors in occlusal traumatism. The significance of parafunction becomes increasingly greater in mouths that already show signs of alveolar bone loss. Dentitions with moderate-to-severe loss of periodontal support cannot adequately resist parafunctional forces. Alveolar support rapidly deteriorates unless proper therapeutic measures are undertaken. The periodontium must receive additional resistance to normal and parafunctional forces.
| Other Predisposing Factors|| |
Loss of teeth
The early loss of teeth from caries or accident is common and predisposes to occlusal traumatism. A classic example is posterior bite collapse resulting from premature loss of the first permanent molar. The effects of tooth loss are not always restricted to the immediate vicinity of the loss. Changes often take place some distance from missing teeth. As a result of loss of first permanent molars, there are occlusal discrepancies. The discrepancies often cause an increased slide from centric relation occlusion to centric occlusion; the anterior teeth hit each other with increased force during mastication. This functional disharmony causes the anterior teeth to drift labially, thereby resulting in an open contact relationship of the anterior segment. The next phase usually is further bite collapse and loss of alveolar bone.
Faulty restorative dentistry
It is commonly a predisposing factor to acute occlusal traumatism. The traumatism may be transient if the tooth or teeth can drift or rotate into a harmonious occlusal relationship if not, the traumatic situation may become chronic. Therefore, the principles of good functional occlusion must be followed during restorative procedures.
Injudicious periodontal surgery
Loss of alveolar support caused by either periodontal disease or corrective procedures may seriously aggravate occlusal traumatism. In many severe cases, the value of pocket elimination by bone resection must be weighed carefully against this decrease in support. In such circumstances, functional forces previously within a physiologic range may become excessive and irreversible breakdown may occur. Whether bone resection will predispose to occlusal traumatism depends on several factors. The most significant are the amount and location of bone loss around the tooth before surgical intervention. One must relate the degree of loss to the mobility. Significant intrinsic factors to consider are the size, shape, number, and position of roots relative to the alveolar process.
Faulty occlusal adjustment
Therapeutic measure to correct faulty functional occlusion can result in further aggravation if used indiscriminately. Occlusal adjustment procedures resulting in occlusal contact relationships with forces not directed axially cause further trauma.
Temporomandibular joint dysfunction
Some forms of temporomandibular joint (TMJ) affliction can result from minor functional occlusal discrepancies coupled with psychoneurotic habits as well as from major dysfunctional occlusal relationships alone. Often patients demonstrate mandibular deviations that result in bizarre occlusal relationships. Before any occlusal adjustment, one must determine how much of the faulty occlusal relationship is caused by mandibular deviation resulting from myospasm or edema related to posterior encapsulitis. Occlusal correction should not be done during the acute stages of TMJ dysfunction.
Posselt and Maunsbach (1957) basing his observations on the result of three separate studies noted that bruxism and clenching activities are associated with biting forces of over 20 kg/s, and in some instances, intermaxillary contacts for up to 2.5 s.
Tooth malposition or occlusal discrepancies are almost universally present unless the occlusion has to be treated. However, they do not necessarily produce signs or symptoms of occlusal trauma since adaptation is the rule. Adaptation to interferences is dependent on the level of psychic tension or stress to which the individual is subjected. Consequently, the functional impact of an occlusal discrepancy cannot be predicted and could change over time. An overloaded tooth may adapt to the excessive forces by having increased, but not increasing, mobility or by moving away from the excessive force (migration). Under stress, however, the effect of occlusal discrepancy may become significant enough to overcome adaptation and thus become a traumatic interference. The interplay between stress and occlusal interference may trigger the production of bruxism. It is the first manifestation of lack of adaptation to occlusal relationships. It's true detrimental role depends on the degree of adaptation of the particular individual. If well-adapted teeth may depict wear facets, minimal increased mobility, and radiographically a well-defined periodontal support. This represents hyperfunction. If adaptation is overridden, this parafunctional habit may trigger symptomatology and an occlusion dysfunction develops.
Etiologic factors of periodontal occlusal trauma can be divided into four categories:
- Situation that increases the magnitude or frequency of occlusal forces
- Situations that change the direction of occlusal forces
- Circumstances that decrease the resistance of the periodontium to occlusal forces
- Combination of all three factors.
Situation that increases the magnitude or frequency of occlusal forces
- Long sustained occlusal contacts from parafunctional habits such as clenching, bruxism, and chewing on pipe stems
- Parafunctional habits stimulated by occlusal interferences such as centric prematurities and balancing side contacts
- Parafunctional habits and/or the direction of an entire occlusal load onto one or a few teeth triggered by restorative and prosthetic dentistry that does not harmonize with the entire occlusion
- Fixed and removable prosthetic appliances.
Situations that change the direction of occlusal forces
- Tipping forces from occlusal interferences such as centric prematurities and balancing side contacts, which usually occur on inclined planes
- Parafunctional habits in extreme eccentric positions
- Restorative and prosthetic treatment that generate tipping occlusal forces
- Tilting and drifting of teeth.
Circumstances that decrease the resistance of the periodontium to occlusal forces
- Loss of alveolar bone and periodontal ligament (PDL) support
- Loss of a number of teeth, thereby requiring fewer teeth to absorb the entire occlusal load.
Combination of all three factors
All the three, i.e., combination may be found in case of moderate-to-severe periodontitis combined with missing and drifted teeth, occlusal disharmonies, and parafunctional habits.
| Tissue Response to Trauma from Occlusion|| |
Stages of tissue response
The tissue injury occurs in three stages. The first is injury, the second is repair, and third is adaptive remodeling of the periodontium. Tissue injury is produced by excessive occlusal forces. Nature attempts to repair the injury and restore the periodontium. This can occur if the forces are diminished or if the total drifts away from them. However, if the offending force is chronic, the periodontium is remodeled to cushion its impact. The ligament is widened at the expense of the bone; angular bone defects occur without periodontal pockets; and the tooth becomes loose.,,,
Stage I injury
Under the forces of occlusion, a tooth rotates around a fulcrum or axis of rotation that is located in single-rooted teeth, in the junction between the middle third and the apical third of the clinical root. This creates areas of pressure and tension on opposite sides of the fulcrum. Different lesions are produced by pressure and tension although if jiggling forces are exerted they may coexist in the same area.
Slightly excessive pressure stimulates resorption of the alveolar bone, with a resultant widening of the PDL space. Slightly excessive tension causes elongation of PDL fibers and opposition of alveolar bone. In areas of increased pressure, the blood vessels are numerous and reduced in size, in areas of increased tension they are enlarged. Greater pressure produces a gradation of changes in the PDL, staring with compression of the fibers, which produces areas of hyalinization. Subsequent injury to the fibroblasts and other connective tissue cells leads to necrosis of areas of the ligament.,,,
Stage II repair
Repair is constantly occurring in the normal periodontium. During TFO, the injured tissues stimulate increased reparative activity. The damaged tissues are removed, and new connective tissue cells and fibers, bone, and cementum are formed in an attempt to restore the injured periodontium. Forces remain traumatic only so long as the damage produced exceeds the reparative capacity of the tissues. Cartilage-like material sometimes develops in the PDL space as an aftermath of the trauma. Formation of crystals from erythrocytes has also been shown. When bone is resorbed by excessive occlusal forces, nature attempts to reinforce the thinned bony trabeculae with new bone. This attempt to compensate for lost bone is called buttressing bone formation and is an important feature of the reparative process associated from TFO. It also occurs when bone is destroyed by inflammation or osteolytic tumors.
Stage III adaptive remodeling of the periodontium
If the repair process cannot keep pace with the destruction caused by the occlusion, the periodontium is remodeled in an effort to create a structural relationship, in which the forces are no longer injurious to the tissues. This result in a thickened PDL, which is funnel shaped at the crest and angular defects in the junctional epithelium with no pocket formation. The involved teeth become loose. An increase in vascularization had also been reported.
The three stages in the evolution of traumatic lesions have been differentiated histometrically by means of the relative amounts of periodontal bone surface undergoing resorption or formation. The injury phase shows an increase in areas of resorption and decrease in bone formation, whereas the repair phase demonstrates increased formation and decreased resorption. After adaptive remodeling of the periodontium, resorption and formation return to normal.,,
| Signs and Symptoms|| |
The most important clinical sign of trauma is increased tooth mobility. Tooth mobility produced by TFO occurs in two phases. The initial phase is the result of alveolar bone resorption increasing the width of the PDL and reducing the number of periodontal fibers. The second phase occurs after repair of the traumatic lesion and adaptation to the increased forces, which results in permanent widening of the PDL space.
Presence of occlusal wear which can note attributed to any abnormality of patient diet and is not commensurate with patient's age.
Tilting and migration of individual teeth or of complete segments.
- Widening of the PDL space, often with thickening of the lamina dura along the lateral aspect of the root in the apical region and in bifurcation areas
- Vertical rather than horizontal destruction of the interdental septum, with the formation of infrabony defects
- Radiolucency and condensation of the alveolar bone
- Root resorption.,,
Box and Stillman considered TFO to be the causative factor for the following signs of incipient periodontal disease:
- Traumatic crescent – a crescent-shaped bluish red zone of gingiva confined to about one-sixth of the circumference of the root
- Recession of the gingiva, which may be asymmetrical, associated with resorption of the alveolar crest
- Stillman's clefts – indentations in the gingival margin, generally on one side of the tooth
- McCall's festoons - discrete semilunar enlargement of the marginal gingiva
- Absence of stippling – interpreted as evidence of edema secondary to trauma.
None of these changes have been shown conclusively to be associated with trauma to the periodontium.
| Clinical Features of Occlusal Trauma|| |
- No periodontitis
- Tooth wear (mild faceting or marked attrition)
- Fractures of the enamel or restorations
- Occlusal interferences (either from the retruded contact position to intercuspal position (ICP) or in lateral excursions/protrusive movements)
- Ridging of buccal mucosa
- Indentations in lateral border of the tongue
- Reddening of the tip of the tongue.
| Radiographical Features|| |
- Secondary dentin laid down in the pulp chamber.
| Diagnosis|| |
Because TFO is defined and diagnosed on the basis of histologic changes in the periodontal supporting structure, diagnosis is impossible without block section biopsy. Often Angle's classification is a part of occlusal analysis. However, the Angle's classification was designed to classify the skeletal relationship between the mandible and maxilla and the little bearing on the occlusal relationship that exists between various cusp surfaces. Therefore, it is the relationship between opposing cusps that is the most important aspect of occlusion. The tooth mobility and wear patterns are extremely difficult to correlate with occlusal contacts. In the case of mobility, many other factors such as loss of attachment can affect the presence and severity of the mobility.
- Cardinal manifestation of primary TFO is increased tooth mobility. The mobility can be assessed by mechanical and electronic instrument. Subjective assessments of mobility are done as in Miller classification assigned from 0 to 3 score
- Tilting and migration of individual teeth or of complete segments. The percussion of teeth on tapping with a blunt instrument changes from a resonant note with a healthy supporting structure to a dull note if there is primary TFO in attachment apparatus
- Careful palpation of the muscles of mastication to ascertain whether there is hypertrophy or sign of hypertonicity with possible spasm of one group of muscle
- Palpation of TMJ and observation of any deviation of the mandible in various paths of closure
- Fremitus test:, Fremitus is a measurement of the vibratory patterns of the teeth when the teeth are placed in contacting positions and movements. A dampened index finger is placed along the buccal and labial surfaces of the maxillary teeth, and patient is asked to tap the teeth together in the maximum ICP and grind systemically in the lateral, protrusive, and lateral protrusive contacting movements and positions. The teeth that are displaced by the patient in these jaw positions are then identified. In general, this is limited to the maxillary teeth; however, in cases of edge-to-edge occlusion or when there is little overlap of the teeth, mandibular teeth can also be assessed.
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.
| Conclusion|| |
Despite decades of debate and multiple publications that discuss the theory of occlusion, occlusal design, and equilibration techniques, there have been few well-designed human studies that can help answer the question “does occlusal trauma modify the progression of attachment loss due to inflammatory periodontal disease?” The articles reviewed clearly demonstrate that occlusal forces are transmitted to the periodontal attachment apparatus, and those forces can cause changes in the bone and connective tissue. These changes can affect tooth mobility and clinical probing depth. While occlusal forces do not initiate periodontitis, results are inconclusive on the interactions between occlusion and the progression of attachment loss due to inflammatory periodontal disease.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Lascala NT, Moussalli NH. Contemporary of periodontal therapeutics. 2nd
ed. São Paulo: Artes Médicas; 1995.
Carranza FA. Clinical Periodontology. 9th
ed. Rio de Janeiro: Guanabara Koogan; 2004.
Hallmon WW, Harrel SK. Occlusal analysis, diagnosis and management in the practice of periodontics. Periodontol 2000 2004;34:151-64.
Lindhe J. Clinical Periodontology and Implant Dentistry. 3rd
ed. Rio de Janeiro: Guanabara Koogan; 2004.
Gher ME. Changing concepts. The effects of occlusion on periodontitis. Dent Clin North Am 1998;42:285-99.
Harrel SK. Occlusal forces as a risk factor for periodontal disease. Periodontol 2000 2003;32:111-7.
Reinhardt RA, Killeen AC. Do mobility and occlusal trauma impact periodontal longevity? Dent Clin North Am 2015;59:873-83.
Stillman PR. The management of pyorrhea. Dent Cosmos 1917;59:405.
Glickman I, Smulow JB. Alterations in the pathway of gingival inflammation into the underlying tissues induced by excessive occlusal forces. J Periodontol 1962;33:7-13.
Glickman I, Smulow JB. Further observations on the effects of trauma from occlusion in humans. J Periodontol 1967;38:280-93.
Glickman I, Smulow JB. Adaptive alterations in the periodontium of the rhesus monkey in chronic trauma from occlusion. J Periodontol 1968;39:101-5.
Goldman HM. Gingival vascular supply in induced occlusal traumatism. J Oral Surg 1956;9:939-41.
Waerhaug J. The angular bone defect and its relationship to trauma from occlusion and downgrowth of subgingival plaque. J Clin Periodontol 1979;6:61-82.
Waerhaug J. The infrabony pocket and its relationship to trauma from occlusion and subgingival plaque. J Periodontol 1979;50:355-65.
Polson AM. Interrelationship of inflammation and tooth mobility (trauma) in pathogenesis of periodontal disease. J Clin Periodontol 1980;7:351-60.
Polson AM. The relative importance of plaque and occlusion in periodontal disease. J Clin Periodontol 1986;13:923-7.
Houston F, Hanamura H, Carlsson GE, Haraldson T, Rylander H. Mandibular dysfunction and periodontitis. A comparative study of patients with periodontal disease and occlusal parafunctions. Acta Odontol Scand 1987;45:239-46.
Burgett FG, Ramfjord SP, Nissle RR, Morrison EC, Charbeneau TD, Caffesse RG. A randomized trial of occlusal adjustment in the treatment of periodontitis patients. J Clin Periodontol 1992;19:381-7.
Wolffe GN, Spanauf AJ, Brand G. Changes in occlusion during the maintenance of a patient treated with combined periodontal/prosthetic therapy: Report of a case. Int J Periodontics Restorative Dent 1991;11:48-57.
Ericsson I, Giargia M, Lindhe J, Neiderud AM. Progression of periodontal tissue destruction at splinted/non-splinted teeth. An experimental study in the dog. J Clin Periodontol 1993;20:693-8.
Neiderud AM, Ericsson I, Lindhe J. Probing pocket depth at mobile/nonmobile teeth. J Clin Periodontol 1992;19:754-9.
Schluger S, Yuodelis R, Page RC, Johnson RH. Periodontal Diseases: Basic Phenomena, Clinical Management and Occlusal & Restorative Interrelationships. 2nd
ed. Philadelphia, London: Lea and Febiger; 1990.
Macmillan HW. The case against traumatic occlusion. J Am Dent Assoc 1930;17:1996.
Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant Dentistry. 3rd
ed. OxfoardOX4 2QD, UK: Munksgaard; 1997. p. 279.
Lindhe J, Nyman S, Ericsson I. Trauma from occlusion. Clinical Periodontics and Implant Therapy. 2nd
ed., Ch. 8. Oxfoard, UK: Blackwell Publishing Ltd, 9600 Garsington Road, 1996. p. 279.
Box HK. Traumatic occlusion and traumatogenic occlusion. Oral Health 1930;20:642-6.
Wentz FM, Jarabak J, Orban B. Experimental occlusal trauma imitating cuspal interferences. J Periodontol 1958;29:117.
Posselt U, Maunsbach O. Clinical and roentgenographic studies of trauma from occlusion. J Periodontol 1957;28:192-6.
Gratzinger M. Dynamic irritation as a cause of periodontal disease and the means for its elimination. Am Psychol 1948;3:294-310.
Lundquist GR. Connective tissue changes associated with variable occlusal stresses. J Am Dent Assoc 1937;24:1577.
Leonard HJ. The occlusal factor in periodontal disease. J Periodontol 1946;17:80-91.
Goldman HM. Periodontia. 2nd
ed. St. Louis: C.V. Mosby Co.; 1949.
Wilson TG, Kornman KS. Fundamentals of Periodontics. Carol Stream IL.: Quintessence Publishing Co. Inc.; 1996.
Orban B, Weinmann J. Signs of traumatic occlusion in average human jaws. J Dent Res 1933;13:216.
Breitner C. Tooth-supporting apparatus under occlusal changes. J Periodontol 1942;13:72.
Hallmon WW. Occlusal trauma: Effect and impact on the periodontium. Ann Periodontol 1999;4:102-8.
Pihlstrom BL, Anderson KA, Aeppli D, Schaffer EM. Association between signs of trauma from occlusion and periodontitis. J Periodontol 1986;57:1-6.
|This article has been cited by|
||Pediatric Stainless-Steel Crown Cementation Finite Element Study
| ||Ahmed S. Waly,Yasser R. Souror,Salah A. Yousief,Waleed M.S. Alqahtani,Mohamed I. El-Anwar |
| ||European Journal of Dentistry. 2020; |
|[Pubmed] | [DOI]|
||Inhibition of yes-associated protein dephosphorylation prevents aggravated periodontitis with occlusal trauma
| ||Wei Wei,Lili Xue,Liangyu Tan,Jie Liu,Qin Yang,Jiajia Wang,Bing Yan,Qiaoling Cai,Li Yang,Yuan Yue,Liang Hao,Min Wang,Jinle Li |
| ||Journal of Periodontology. 2020; |
|[Pubmed] | [DOI]|
||Cavitas electrochemical sensor toward detection of N-epsilon (Carboxymethyl)lysine in oral cavity
| ||Bianca Ciui,Mihaela Tertis,Claudia Feurdean,Aranka Ilea,Robert Sandulescu,Joseph Wang,Cecilia Cristea |
| ||Sensors and Actuators B: Chemical. 2018; |
|[Pubmed] | [DOI]|