Journal of the International Clinical Dental Research Organization

: 2020  |  Volume : 12  |  Issue : 2  |  Page : 102--109

Role of Occlusion as a Risk Factor in Periodontal Disease

Ashutosh Nirola, Priyanka Batra, Kanika Mohindra, Tejasveen Kaur 
 Department of Periodontology and Oral Implantology, Luxmi Bai Institute of Dental Sciences and Hospital, Patiala, Punjab, India

Correspondence Address:
Dr. Ashutosh Nirola
Department of Periodontology and Oral Implantology, Luxmi Bai Institute of Dental Sciences and Hospital, Sirhind Road, Patiala, Punjab


Occlusion can be described in very simple terms as an intercuspal relationship between the set of maxillary and mandibular teeth. It plays an important role in the pathogenesis of periodontal diseases and traumatic lesions are often manifestation of faulty occlusion. Mc neil defined occlusion as the functional relationship between the components of the masticatory system, temporomandibular joint (TMJ), and craniofacial skeleton. From a research point of view, the TMJ serves primarily as a reference from which mandibular movements are duplicated. Most patients function with the built-in discrepancies in occlusion throughout their life. Periodontal treatment modalities may be required when alterations or abnormalities in the occlusal relationship place undue stress on the periodontium and TMJ, thereby causing dysfunction. The role of trauma from occlusion (TFO) in periodontal disease is still controversial. According to American Academy of Periodontology (AAP), the lesion of TFO may occur in conjunction with, or independent of, inflammatory periodontal diseases. Pathologic occlusion has been proposed as a risk factor for periodontitis. In certain cases, traumatogenic occlusion can cause periodontal destruction, and therefore, occlusal adjustment occasionally is indicated as part of periodontal therapy. The present review focuses on TFO as a risk factor and its impact on the periodontium and its treatment.

How to cite this article:
Nirola A, Batra P, Mohindra K, Kaur T. Role of Occlusion as a Risk Factor in Periodontal Disease.J Int Clin Dent Res Organ 2020;12:102-109

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Nirola A, Batra P, Mohindra K, Kaur T. Role of Occlusion as a Risk Factor in Periodontal Disease. J Int Clin Dent Res Organ [serial online] 2020 [cited 2021 Apr 10 ];12:102-109
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Occlusal trauma has been defined as “injury to the periodontium resulting from occlusal forces which exceed the reparative capacity of the attachment apparatus,” i.e., the tissue injury occurs because the periodontium is not able to cope up with the increased stresses it experiences.[1]

Occlusion is the integrated relationship of the teeth, periodontium, neuromusculature, and not just interdigitation.[2] A singular concept of occlusion cannot be applied to all patients. This relationship can exist in a variety of forms, and in a state of normalcy and balance, remains in harmony with the other structures, which make up the dentoalveolar apparatus.

Occlusal discrepancies are often considered as primary or contributory etiologic factors in the initiation of periodontal disease. Apart from the possible relation between trauma from occlusion (TFO) and periodontal disease, destruction of the supporting structure coincident with advanced periodontitis may bring about loss and drifting of teeth and seriously alter the occlusal table.[3] Secondary occlusal trauma develops together with compensatory alterations in the pathway of closure, which may precipitate temporomandibular joint (TMJ) dysfunction.

 Physiology of Temporomandibular Joint

TMJ is one of the most complex joints in the human body. It is a ginglymoarthrodial joint, a term that is derived from ginglymus, meaning a hinge joint, allowing motion only backward and forward in one plane, and arthrodial, meaning a joint which permits a gliding motion of the surfaces of the temporal bone and the mandibular condyle.[4]

TMJ consists of:

Two bones: Temporal and mandibular boneA disk that divides the joint cavity into two spaces: upper and lower compartmentsA joint capsuleLigaments: The lateral ligament, sphenomandibular ligament, and stylomandibular ligamentFour main muscles that create five motions: temporalis, masseter, medial pterygoid, and lateral pterygoid.


Solberg and Seligman (1996) defined occlusion as “the contact relationships of the teeth resulting from neuromuscular control of the masticatory system.”[5] Classic work by Angle and Andrews has established accepted criteria for the normal/ideal functional occlusion. The functional occlusion can be physiologic or nonphysiologic. “Physiologic occlusion exists in an individual who has no signs of occlusion-related pathosis. This implies a range of morphologic variability in the occlusion of the teeth and a sense of physiological and physical comfort. Nonphysiologic occlusion on the other hand is an occlusion judged to be associated with traumatic lesions or disturbances in the supporting structures of the teeth, muscles, and TMJ.”[5]

 Developmental Stages of Occlusal Wear

The earlier stages just as the parameters of periodontal disease (i.e., gingivitis and periodontitis), dental caries (i.e., enamel caries, dentinal caries, and caries involving pulp), and TMJ pathosis (i.e., acute, chronic, and debilitating TMJ disease) are recognized and defined, as must the stages of occlusal/incisal wear be recognized and defined. Preventive and restorative treatments require it.[6]

Using the classic or ideal Angle Class I relation as the norm, we can describe stages of wear [Figure 1] as follows:{Figure 1}

Development stage: Newly erupted dentitionNondisease stage: Adaptive stageStage I: Early occlusal diseaseStage II: Moderate occlusal diseaseStage III: Advanced occlusal diseaseStage IV: Total occlusal disease.

 Trauma from Occlusion

TFO 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. Stillman (1917) defined it as “a condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position.”[7]

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.”[8]

 Etiology of Trauma from Occlusion

There are many factors involved in the etiology of TFO. Broadly, they can be divided into two categories: precipitating factors and predisposing factors. In TFO, the precipitating factors are the destructive occlusal forces. The predisposing factors are those which contribute to the development of TFO indirectly. They include intrinsic and extrinsic factors.

 Precipitating Factors

As already stated, destructive occlusal forces are the precipitating or the primary etiology of TFO. These forces are usually described in terms of magnitude, direction, duration of application, and frequency of application.

Magnitude: When the magnitude of occlusal forces exceeds the normal range of forces for a tooth, due to natural adaptive response, some changes can be appreciated in the periodontal ligament (PDL). There is widening of the PDL space, an increase in the number of PDL fibers, an increase in the width of PDL fibers, and an increase in the density of alveolar boneDirection: The principal fibers of the PDL play an important role in withstanding the occlusal forces and transferring them to the alveolar bone. Normally, they are oriented in such a way that they are best capable of withstanding the occlusal forces. However, if the direction of occlusal forces is changed, these fibers are not able to efficiently bear the occlusal forces, hence injury resultsDuration of force application: If the abnormal occlusal forces are subjected to a tooth for a longer duration of time, they cause injury to the periodontal tooth-supporting structures, which can be seen histologicallyFrequency of force application: Frequent application of abnormal occlusal forces results in more damage to the periodontal tooth-supporting structures than less frequent application.

 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.[8] They can be divided into intrinsic and extrinsic factors.

Intrinsic factors:

The orientation of the long axis of the teeth in relation to the forces to which they are exposedThe morphological characteristics of the roots. The size, shape, and number of the roots determine how occlusal forces are dissipated. In general, short, conical, slender, or fused roots are more vulnerable to TFOThe morphology of the alveolar process, i.e., the quality and the quantity of the alveolar bone play an important role in absorbing the occlusal forces.

Extrinsic factors:

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 claspsNeuroses that result in parafunctional activities, for example, bruxism. These factors are the most prevalent and serious causes of abnormal occlusal stressesLoss of supporting bone: Periodontitis, injudicious bone resection, inadvertent trauma, and systemically related diseases are the chief causative factorsLoss of teeth resulting in overloading of the remaining teeth, for example, posterior bite collapseIatrogenically created functional malocclusion.[9]

 Other Predisposing Factors

Iatrogenic factorsBruxism, abrasion, cracks, fracturesPathologic migration of teethLoss of teethFaulty restorative dentistryInjudicious periodontal surgeryFaulty occlusal adjustmentTMJ dysfunction.

 Signs and Symptoms

Increased tooth mobility is the most important clinical sign of trauma. 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.

Radiographic signs

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 areasVertical destruction of the interdental septum, with the formation of infrabony defectsRadiolucency and condensation of the alveolar boneRoot resorption.

Clinical signs

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 rootRecession of the gingiva, which may be asymmetrical, associated with resorption of the alveolar crestStillman’s clefts – Indentations in the gingival margin, generally on one side of the toothMcCall’s festoons – Discrete semilunar enlargement of the marginal gingiva[9]“Dental mobility in traumatic occlusion is different from the one in periodontitis trough the fact that in occlusion trauma we find 1–2 mobile teeth which have no periodontal pockets”[10]Joint signs – ”Arearthralgia, stiffness of ATM, artrogenahypokinesia, joint noises. Radiological signs are narrowing of the joint space and presence of uneven radiotransparency, irregular osseous contours, deformation of mandibular condyles, atrophy of articular tubercle, osteophytes that transpose an adjusting favorable process. Mandibular condyles lose their oval shape (arthrosis)”[10]Muscular signs – Muscular pathologies are according to the same scheme like joint disorders when the situation occurred is of an occlusion one. Clinical forms are numerous: myositis, myospasm, localised myalgia, and myofibrotic contractions.[10]


Persistent discomfort on eating: The patient complains of persistent discomfort during eating. Due to excessive occlusal forces on a tooth or a group of teeth, the patient is not able to satisfactorily chew the food and the teeth under high occlusion cause discomfortThermal sensitivity: Although the exact effect of occlusal trauma on dental pulp is still not clear, studies have demonstrated that there are changes in the pulp and hence tooth becomes sensitive to thermal changesMuscle hypertonicity: The patient complains of tired jaw, especially after rising in the morning and at the end of the day. It is because of the occlusal interferences causing muscle spasm and discomfort.

 Tissue Response to Trauma from Occlusion

Stages of tissue response. The tissue injury occurs in three stages.

InjuryRepairMorphologic change of periodontium.

Stage 1: Injury

Tissue damage is a result of injurious forces and depends on its severity, frequency, and direction. Slightly excessive pressure leads to osteoclastic resorption of alveolar bone. This in turn leads to widening of the PDL space. This area witnesses numerous blood vessels which are reduced in size. When the pressure is increased, the PDLs are compressed, which leads to thrombosis of the blood vessels and hemorrhage. Subsequently, there is hyalinization and necrosis of ligaments. When the pressure gets severe, undermining resorption takes place.

On slightly excessive tension, the periodontal fibers elongate and there is apposition of alveolar bone. Enlarged blood vessels are present in this area. Severe tension causes widening of PDL, thrombosis, tearing of PDL, and alveolar bone resorption. Temporary depression is seen in the mitotic activity and the rate of proliferation and differentiation of fibroblasts, collagen, and bone formation, which return to normal following dissipation of forces.

Stage 2: Repair

Tissue repair is a continuous process. 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 will continue to remain traumatic as long as the damage produced exceeds the reparative capacity of the tissue. An important feature of reparative process is buttressing bone formation. When the bone is resorbed due to excessive occlusal forces, the thinned trabecular bone is reinforced with the new bone. This attempt to compensate for the lost bone is called buttressing bone formation.

Stage 3: Remodeling of the periodontium

In order to create harmonious structural relationship between the ongoing destruction and repair, the periodontium is remodeled such that the forces are no longer injurious to the tissues. To cushion the impact of the offending forces, the PDL is widened and the adjacent bone is resorbed. The involved teeth become loose. The results are a thickened PDL, funnel-shaped at the crest, and angular defects in the bone. After adaptive remodeling of the periodontium, resorption and formation return to normal.[11],[12],[13],[14]

 Molecular Mechanisms of Bone Resorption Induced by Force Application

Mechanical forces can also induce the production of interleukin-1, a proinflammatory cytokine, and the isoenzyme cyclooxygenase-2, both involved in prostaglandin synthesis.[15]

Mechanical stimuli on teeth generate free proteins within PDL that can cause degranulation of mast cells present in PDL, releasing histamine and free nerve endings neuropeptides.[16] These processes result in contraction, vasodilatation, and increased vascular permeability of endothelial cells, leading to leukocyte leakage from blood vessels through interendothelial cell junctions.[17]

It has been demonstrated that traumatogenic occlusion resulted in increased expression of both RANKL and osteopontin, probably related to the increase in the number of activated osteoclasts. It has also suggested that the maintenance of a physiological occlusal state is achieved primarily by inhibition of bone apposition in response to the occlusal forces, rather than the equilibrium between continuous deposition of apical tissue and the corresponding resorption of bone tissue. Inhibition of alveolar bone apposition by occlusal forces was considered to be an important mechanism for controlling occlusal height, which might work in synergy with RANKL-induced bone resorption to maintain normal occlusion.[18]

Bone and cementum portray structurally and histologically similar characteristics. Densitometric analysis revealed increased background levels of osteopontin in the resorptive lacunae of roots in the test group, suggesting that increased expression of osteopontin is associated with root resorption induced by orthodontic tooth movement. As TFO can elicit the same response as orthodontic tooth movement, it can be assumed that the resorptive processes of roots in teeth under traumatogenic occlusion could be mediated through the same mechanism[19] [Figure 2]a and [Figure 2]b.{Figure 2}

 Is Traumatic Occlusion Reversible?

Occlusal disease is comparable to periodontitis in that it is generally not reversible (an exception for periodontitis might be osseous grafting). Occlusal disease, however, like periodontitis, is often maintainable. It does lend itself to treatment and when restorative dentistry is utilized, it becomes, in that sense, reversible.

TFO is known to cause several changes in the periodontal tissues. Forces caused by occlusal trauma could decrease perfusion of the PDL, resulting in ischemia and necrosis of the PDL cells when the adaptive capacity of the PDL is exceeded. In this case, bacterial inflammation of the periodontium could progress faster because of the lower tissue resistance or tissue integrity. Hence, TFO might be a catalyst for the destructive processes initiated by bacterial periodontal inflammation.[20],[21]

 Trauma from Occlusion Around Implants

The injuries resulting from occlusal trauma, besides affecting the periodontal tissues (in the case of natural teeth), can affect the peri-implant region. It is established that the obtainment and maintenance of balanced occlusal relationships is important both in natural dentition and in rehabilitation with osseointegrated implants. Nevertheless, the actual role that the occlusal trauma plays in the installation and/or worsening of periodontal/peri-implant disease remains controversial.[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36]

The peri-implant bone loss has two major etiological factors: inflammation caused by microorganisms and occlusal overload. A study was conducted in order to verify the correlation between occlusal trauma and peri-implant bone loss that compromised osseointegration. The authors concluded that there is not sufficient evidence to confirm the correlation between occlusal overload and peri-implant bone loss.

Assessing the occlusal ability to detect occlusal interferences, it was found that the perception of interference on natural teeth and implants with antagonists was approximately 20 and 48 mm, respectively.[37] In another study, it was detected values of tactile perception for implants 8.75 times higher (100.6 g) than for natural teeth (11.5 g). These results demonstrate that dental implants, without the receivers of the PDL, may be more susceptible to occlusal overload [Figure 3], which is justified by its low adaptive capacity and of distribution of forces.[38]{Figure 3}

 Treatment of Trauma from Occlusion

The treatment of TFO involves removal of the excessive occlusal forces and bringing the tooth/teeth in comfortable position. Many treatment modalities have been advised to treat TFO. These include:

Coronoplasty, dental restorations, tooth movements, tooth removal, and orthognathic surgery.

Indications of occlusal adjustment

To reduce traumatic forces to teeth that display:

Increasing mobility or fremitus to encourage repair within the periodontal attachment apparatusDiscomfort during occlusal contact or function.

To achieve functional relationships and masticatory efficiency in conjunction with restorative treatment, orthodontic treatment, orthognathic surgery, or jaw trauma when indicatedAs adjunctive therapy, that might reduce the damage from parafunctional habitsTo reshape the teeth, which are contributing to soft tissue injuryTo adjust marginal ridge relationships and cusps that are contributing to food impaction.

Contraindications for occlusal adjustment

Occlusal adjustment lacking careful pretreatment study, documentation, and patient educationProphylactic adjustment without evidence of occlusal traumaAs the primary treatment of microbial-induced inflammatory periodontal diseaseTreatment of bruxism without evidence of damage, pathosis, or painWhen the emotional state of the patient impedes satisfactory resultInstances of severe extrusion, mobility, or malpositioning of teeth that would not respond to occlusal adjustment alone


It is defined as the selective reduction of occlusal areas with the primary purpose of influencing the mechanical contact conditions and the neural pattern of sensory output”. It is the direct and irreversible change of occlusal scheme (Krogh-Poulsen, 1968). The principle behind performing coronoplasty is to remove the detrimental occlusal forces that cause tissue damage and tooth mobility and it should be done by mechanically eliminating all occlusal supracontacts which are in function and parafunction.[39]

 Indications for Coronoplasty in Periodontal Therapy

Coronoplasty is based on the premise that tissue damage and excessive tooth mobility caused by occlusal forces are resolved when undesirable occlusal forces are corrected. A second premise is that realigning occlusal forces by creating unobstructed functional contacts provides trophic stimulation beneficial to the periodontium, the muscle, and the TMJ. In general, coronoplasty is not often indicated in periodontal therapy, except when a patient has an occlusion weakened by bone loss.

 Treatment Planning and Technique

Objectives of coronoplasty

Change in the pattern and degree of afferent impulsesLessening of excessive tooth mobilityMultiple simultaneous contact spread over the occlusal scheme to effect occlusal stabilization (i.e., decrease need for muscular stabilization)Beneficial change in the pattern of chewing or swallowing functionVerticalization of occlusal forces on implants.

Steps for coronoplasty

Coronoplasty can be attained using a variety of different sequences, particularly if the area to be corrected involves only a few teeth.[39]

Retrusive prematurities are eliminated.This step is to eliminate the supracontacts that interfere with posterior border closure of the mandible to a stable bilateral retruded contact position using chin grasp technique and Dawson’s technique. The retrusive ranger adjustment is complete only when:

Contact pattern is bilateral with multiple pointed contactsDeflective shift with lateral thrust from Retruded Contact Position (RCP) to Intercuspal Position (ICP) has been eliminatedBoth the RCP and ICP approach have the same vertical dimensions of occlusionThe pathway from RCP to ICP should be in sagittal direction.[40]

Adjust intercuspal position to achieve stable, simultaneous contacts: The purpose is to achieve a stable Intercuspal position and to refine occlusal anatomical relationships. Identification of supracontacts without the guidance of the operator’s hand is the main feature of this step. The goal of Intercuspal position adjustment is to achieve occlusal stabilityTest for excessive occlusal contact on the incisors in intercuspal position. According to Mac Donald et al., the incisor teeth should be slightly out of contact or in light contact over the maximum no. of teethElimination of posterior protrusive contacts. The objective of this step is to attain bilateral well distributed contact on the incisal edges in the maxillary and mandibular incisor teethReduce mediotrusive prematurities; it is very essential to identify the mesiotrusive interference arising from RCP and ICP. According to Helsing et al., the probability of mediotrusive supra contacts is about 84.2% of healthy individuals, which is routinely observed as an oblique facets on first and second molar teethLaterotrusive prematurities in healthy adults, the lateral guidance is dominated by the canine and first premolar. The canine tooth is most frequently involved. The lack of adequate guidance in the canine area increases the risk of single tooth molar supracontacts that may produce trauma in functional and parafunctional movementsGross occlusal disharmonies [Figure 4]Recheck Contact relationshipsPolish all depressed surfaces.{Figure 4}

 Other Treatment Modalities

Management of parafunctional habitsTemporary, provisional, or long-term stabilization of mobile teeth with removable or fixed appliancesOrthodontic tooth movementOcclusal reconstructionExtraction of selected teeth.[41]


One of the major functions of the dentition is mastication and since the periodontium constitutes the supporting mechanism which enables the teeth to fulfill this function, consideration of the interrelation between occlusal forces and the periodontium is basic in periodontology. Periodontal disease has multifactorial etiology, among them is TFO.

Thus, pathologic occlusion has been proposed as a risk factor for periodontitis. It is hypothesized that in certain cases, traumatogenic occlusion can exacerbate periodontal destruction, and therefore, occlusal adjustment occasionally is indicated as part of periodontal therapy. Every individual tooth should be investigated, diagnosed, and subsequently treated for TFO.

This philosophy is best summed up by Ramfjord and Ash, who stated that “the need for adjustment should be based on a definite diagnosis of a traumatic lesion rather than the location of some occlusal interferences which may be of no significance.”

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Conflicts of interest

There are no conflicts of interest.


1Davies SJ, Gray RJ, Linden GJ, James JA. Occlusal considerations in periodontics. Br Dent J 2001;191:597-604.
2Harrel SK, Nunn ME, Hallmon WW. Is there an association between occlusion and periodontal destruction? Yes – Occlusal forces can contribute to periodontal destruction. J Am Dent Assoc 2006;137:1380, 1382, 1384 passim.
3Thompson RH, Geiger AM, Wasserman BH, Turgeon LR. Relationship of occlusion and periodontal disease Part III – Relation of periodontal status to general background characteristics. J Periodontol 1972;43:540-6.
4Stallard RE. Relation of occlusion to temporomandibular joint dysfunction: The periodontic viewpoint. J Am Dent Assoc 1969:79:142-4.
5Solberg W, Seligman D. Dental occlusion. In: Carranza FA, Newman MG, editors. Clinical Periodontology. 8th ed.. Philadelphia: WB Saunders Company; 1996. p. 173.
6Lytle JD. The clinicians index of occlusal disease: Definition, recognition and management. Int J Periodontics Restorative Dent, 1990;10:102-23.
7Stillman PR. The management of pyorrhea. Dent Cosm 1917;59:405.
8Schluger 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.
9Singh DK, Jalaluddin M, Rajeev R. Trauma from occlusion: The overstrain of the supporting structures of the teeth. Indian J Dent Sci 2017;9:126.
10Stanciu L, Fratila A, Boitor C, Pangica A, Sabau M. Occlusion traumatic and iatrogenic factors. In: DAAAM International Scientific Book 2010;9:779-87.
11Carranza FA. Clinical Periodontology. 9th ed.. Rio de Janeiro: Guanabara Koogan; 2004.
12Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant Dentistry. 3rd ed.. OxfoardOX4 2QD, UK: Munksgaard; 1997. p. 279.
13Goldman HM. Periodontia. 2nd ed.. St. Louis: C. V. Mosby Co.; 1949.
14Wilson TG, Kornman KS. Fundamentals of Periodontics. Carol Stream IL.: Quintessence Publishing Co. Inc.; 1996.
15Passanezi E, Sant’Ana AC. Role of occlusion in periodontal disease. Periodontol 2000 2019;79:129-50.
16McCulloch CA, Lekic P, McKee MD. Role of physical forces in regulating the form and function of the periodontal ligament. Periodontol 2000 2000;24:56-72.
17Albrektsson T. Bone tissue response. In: Bränemark PI, Zarb GA, Albrektsson T, editors. Tissue Integrated Prostheses: Osseointegration in Clinical Dentistry. Chicago, IL: Quintessence; 1985. p. 129-43.
18Walker CG, Ito Y, Dangaria S, Luan X, Diekwisch TG. RANKL, osteopontin, and osteoclast homeostasis in a hyper-occlusion mouse model. Eur J Oral Sci. 2008;116:312-8.
19Seifi M, Jessri M, Vahid-Dastjerdi E. Identification of a novel root resorptive function of osteopontin gene. J Dent 2008;5:142-9.
20De Boever JA, Carlsson GE, Klineberg IJ. Need for occlusal therapy and prosthodontic treatment in the management of temporomandibular disorders. Part I. Occlusal interferences and occlusal adjustment. J Oral Rehabil 2000;27:367-79.
21Wadhwa S, Kapila S. TMJ disorders: Future innovations in diagnostics and therapeutics. J Dent Educ 2008;72:930-47.
22Junqueira RB, Guilherme de Siqueira F, De Macedo NL. Considerations about the relation between occlusal trauma and periodontal/peri-implant disease. Braz Dent Sci 2015;18:9-14.
23Davies SJ, Gray RJ, Linden GJ, James JA. Occlusal considerations in periodontics. Br Dent J 2001;191:597-604.
24Hallmon WW, Harrel SK. Occlusal analysis, diagnosis and management in the practice of periodontics. Periodontol 2000 2004;34:151-64.
25Gross MD. Occlusion in implant dentistry. A review of the literature of prosthetic determinants and current concepts. Aust Dent J 2008;53:S60-8.
26Asikainen P, Klemetti E, Vuillemin T, Sutter F, Rainio V, Kotilainen R. Titanium implants and lateral forces. An experimental study with sheep. Clin Oral Implants Res 1997;8:465-8.
27Jin LJ, Cao CF. Clinical diagnosis of trauma from occlusion and its relation with severity of periodontitis. J Clin Periodontol 1992;19:92-7.
28Kim Y, Oh TJ, Misch CE, Wang HL. Occlusal considerations in implant therapy: Clinical guidelines with biomechanical rationale. Clin Oral Implants Res 2005;16:26-35.
29Hürzeler MB, Quinones CR, Kohal RJ, Rohde M, Strub JR, Teuscher U, et al. Changes in peri-implant tissues subjected to orthodontic forces and ligature breakdown in monkeys. J Periodontol 1998;69:396-404.
30Meyer G, Fanghänel J, Proff P. Morphofunctional aspects of dental implants. Ann Anat 2012;194:190-4.
31Sakka S, Baroudi K, Zakaria M. Factors associated with early and late failure of dental implants. J Investig Clin Dent 2012;3:25861.
32Wan HY, Sun HQ, Sun GX, Li X, Shang ZZ. The early phase response of rat alveolar bone to traumatic occlusion. Arch Oral Biol 2012;57:737-43.
33Cibirka RM, Nelson SK, Lang BR, Rueggeberg FA. Examination of the implant-abutment interface after fatigue testing. J Prosthet Dent 2001;85:268-75.
34Khraisat A, Hashimoto A, Nomura S, Miyakawa O. Effect of lateral cyclic loading on abutment screw loosening of an external hexagon implant system. J Prosthet Dent 2004;91:326-34.
35Foz AM, Artese HP, Horliana AC, Pannuti CM, Romito GA. Occlusal adjustment associated with periodontal therapy – A systematic review. J Dent 2012;40:1025-35.
36Liu H, Jiang H, Wang Y. The biological effects of occlusal trauma on the stomatognathic system – A focus on animal studies. J Oral Rehabil 2013;40:130-8.
37Jacobs R, van Steenberghe D. Comparison between implant-supported prostheses and teeth regarding passive threshold level. Int J Oral Maxillofac Implants 1993;8:549-54.
38Hämmerle CH, Wagner D, Brägger U, Lussi A, Karayiannis A, Joss A, et al. Threshold of tactile sensitivity perceived with dental endosseous implants and natural teeth. Clin Oral Implants Res 1995;6:83-90.
39Singh M. Coronoplasty: An unexplored treatment modality in periodontal therapy. Int J Curr Res 2018;10:72253-6.
40Malathi K, Anand AJ, Karthikeyan R, Garg S. Coronoplasty. IOSR J Dent Med Sci 2014;13:64-7.
41Sanadi RM, Chelani LR, Bhakkand SR, Sheth JK. Role of trauma from occlusion in periodontal disease – A controversy. IOSR-J Dent Med Sci 2016;15:118-22.