JICDRO is a UGC approved journal (Journal no. 63927)

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REVIEW ARTICLE
Year : 2020  |  Volume : 12  |  Issue : 2  |  Page : 102-109

Role of Occlusion as a Risk Factor in Periodontal Disease


Department of Periodontology and Oral Implantology, Luxmi Bai Institute of Dental Sciences and Hospital, Patiala, Punjab, India

Date of Submission11-Aug-2020
Date of Acceptance05-Sep-2020
Date of Web Publication14-Dec-2020

Correspondence Address:
Dr. Ashutosh Nirola
Department of Periodontology and Oral Implantology, Luxmi Bai Institute of Dental Sciences and Hospital, Sirhind Road, Patiala, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jicdro.jicdro_44_20

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   Abstract 


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.

Keywords: Coronoplasty, occlusal adjustment, occlusion, peri-implant bone loss, trauma from occlusion


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;12:102-9

How to cite this URL:
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 Jan 22];12:102-9. Available from: https://www.jicdro.org/text.asp?2020/12/2/102/303406




   Introduction Top


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 Top


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 bone
  • A disk that divides the joint cavity into two spaces: upper and lower compartments
  • A joint capsule
  • Ligaments: The lateral ligament, sphenomandibular ligament, and stylomandibular ligament
  • Four main muscles that create five motions: temporalis, masseter, medial pterygoid, and lateral pterygoid.



   Occlusion Top


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 Top


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: developmental stages of occlusal wear given by Lytle, J.D. (1990)

Click here to view


  • Development stage: Newly erupted dentition
  • Nondisease stage: Adaptive stage
  • Stage I: Early occlusal disease
  • Stage II: Moderate occlusal disease
  • Stage III: Advanced occlusal disease
  • Stage IV: Total occlusal disease.



   Trauma from Occlusion Top


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 Top


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 Top


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 bone
  • Direction: 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 results
  • Duration 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 histologically
  • Frequency 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 Top


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 exposed
  • The 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 TFO
  • The 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 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.[9]



   Other Predisposing Factors Top


  • Iatrogenic factors
  • Bruxism, abrasion, cracks, fractures
  • Pathologic migration of teeth
  • Loss of teeth
  • Faulty restorative dentistry
  • Injudicious periodontal surgery
  • Faulty occlusal adjustment
  • TMJ dysfunction.



   Signs and Symptoms Top


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

  1. 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
  2. Vertical destruction of the interdental septum, with the formation of infrabony defects
  3. Radiolucency and condensation of the alveolar bone
  4. Root resorption.


Clinical signs

Box and Stillman considered TFO to be the causative factor for the following signs of incipient periodontal disease:

  1. Traumatic crescent – A crescent-shaped bluish red zone of gingiva confined to about one-sixth of the circumference of the root
  2. Recession of the gingiva, which may be asymmetrical, associated with resorption of the alveolar crest
  3. Stillman’s clefts – Indentations in the gingival margin, generally on one side of the tooth
  4. McCall’s festoons – Discrete semilunar enlargement of the marginal gingiva[9]
  5. “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]
  6. 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]
  7. 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]


Symptoms

  • 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 discomfort
  • Thermal 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 changes
  • Muscle 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 Top


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

  1. Injury
  2. Repair
  3. Morphologic 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 Top


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: (a) molecular mechanisms of bone rosorption induced by force application. (b) Flowchart depicting molecular mechanisms of bone loss folowing force application

Click here to view



   Is Traumatic Occlusion Reversible? Top


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 Top


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: bone loss seen around implant due to trauma from occlusion

Click here to view



   Treatment of Trauma from Occlusion Top


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

  1. To reduce traumatic forces to teeth that display:


    1. Increasing mobility or fremitus to encourage repair within the periodontal attachment apparatus
    2. Discomfort during occlusal contact or function.


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


Contraindications for occlusal adjustment

  1. Occlusal adjustment lacking careful pretreatment study, documentation, and patient education
  2. Prophylactic adjustment without evidence of occlusal trauma
  3. As the primary treatment of microbial-induced inflammatory periodontal disease
  4. Treatment of bruxism without evidence of damage, pathosis, or pain
  5. When the emotional state of the patient impedes satisfactory result
  6. Instances of severe extrusion, mobility, or malpositioning of teeth that would not respond to occlusal adjustment alone



   Coronoplasty Top


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 Top


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 Top


Objectives of coronoplasty

  1. Change in the pattern and degree of afferent impulses
  2. Lessening of excessive tooth mobility
  3. Multiple simultaneous contact spread over the occlusal scheme to effect occlusal stabilization (i.e., decrease need for muscular stabilization)
  4. Beneficial change in the pattern of chewing or swallowing function
  5. Verticalization 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]

  1. Retrusive prematurities are eliminated.
  2. 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:


    1. Contact pattern is bilateral with multiple pointed contacts
    2. Deflective shift with lateral thrust from Retruded Contact Position (RCP) to Intercuspal Position (ICP) has been eliminated
    3. Both the RCP and ICP approach have the same vertical dimensions of occlusion
    4. The pathway from RCP to ICP should be in sagittal direction.[40]


  3. 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 stability
  4. Test 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 teeth
  5. Elimination 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 teeth
  6. Reduce 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 teeth
  7. Laterotrusive 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 movements
  8. Gross occlusal disharmonies [Figure 4]
  9. Recheck Contact relationships
  10. Polish all depressed surfaces.
Figure 4: schematic diagram showing gross adjustment and elimination of occlusal disharmonies

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   Other Treatment Modalities Top


  1. Management of parafunctional habits
  2. Temporary, provisional, or long-term stabilization of mobile teeth with removable or fixed appliances
  3. Orthodontic tooth movement
  4. Occlusal reconstruction
  5. Extraction of selected teeth.[41]



   Conclusion Top


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.”

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Davies SJ, Gray RJ, Linden GJ, James JA. Occlusal considerations in periodontics. Br Dent J 2001;191:597-604.  Back to cited text no. 1
    
2.
Harrel 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.  Back to cited text no. 2
    
3.
Thompson 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.  Back to cited text no. 3
    
4.
Stallard RE. Relation of occlusion to temporomandibular joint dysfunction: The periodontic viewpoint. J Am Dent Assoc 1969:79:142-4.  Back to cited text no. 4
    
5.
Solberg W, Seligman D. Dental occlusion. In: Carranza FA, Newman MG, editors. Clinical Periodontology. 8th ed.. Philadelphia: WB Saunders Company; 1996. p. 173.  Back to cited text no. 5
    
6.
Lytle JD. The clinicians index of occlusal disease: Definition, recognition and management. Int J Periodontics Restorative Dent, 1990;10:102-23.  Back to cited text no. 6
    
7.
Stillman PR. The management of pyorrhea. Dent Cosm 1917;59:405.  Back to cited text no. 7
    
8.
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.  Back to cited text no. 8
    
9.
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.  Back to cited text no. 9
  [Full text]  
10.
Stanciu L, Fratila A, Boitor C, Pangica A, Sabau M. Occlusion traumatic and iatrogenic factors. In: DAAAM International Scientific Book 2010;9:779-87.  Back to cited text no. 10
    
11.
Carranza FA. Clinical Periodontology. 9th ed.. Rio de Janeiro: Guanabara Koogan; 2004.  Back to cited text no. 11
    
12.
Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant Dentistry. 3rd ed.. OxfoardOX4 2QD, UK: Munksgaard; 1997. p. 279.  Back to cited text no. 12
    
13.
Goldman HM. Periodontia. 2nd ed.. St. Louis: C. V. Mosby Co.; 1949.  Back to cited text no. 13
    
14.
Wilson TG, Kornman KS. Fundamentals of Periodontics. Carol Stream IL.: Quintessence Publishing Co. Inc.; 1996.  Back to cited text no. 14
    
15.
Passanezi E, Sant’Ana AC. Role of occlusion in periodontal disease. Periodontol 2000 2019;79:129-50.  Back to cited text no. 15
    
16.
McCulloch 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.  Back to cited text no. 16
    
17.
Albrektsson 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.  Back to cited text no. 17
    
18.
Walker 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.  Back to cited text no. 18
    
19.
Seifi M, Jessri M, Vahid-Dastjerdi E. Identification of a novel root resorptive function of osteopontin gene. J Dent 2008;5:142-9.  Back to cited text no. 19
    
20.
De 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.  Back to cited text no. 20
    
21.
Wadhwa S, Kapila S. TMJ disorders: Future innovations in diagnostics and therapeutics. J Dent Educ 2008;72:930-47.  Back to cited text no. 21
    
22.
Junqueira 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.  Back to cited text no. 22
    
23.
Davies SJ, Gray RJ, Linden GJ, James JA. Occlusal considerations in periodontics. Br Dent J 2001;191:597-604.  Back to cited text no. 23
    
24.
Hallmon WW, Harrel SK. Occlusal analysis, diagnosis and management in the practice of periodontics. Periodontol 2000 2004;34:151-64.  Back to cited text no. 24
    
25.
Gross MD. Occlusion in implant dentistry. A review of the literature of prosthetic determinants and current concepts. Aust Dent J 2008;53:S60-8.  Back to cited text no. 25
    
26.
Asikainen 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.  Back to cited text no. 26
    
27.
Jin LJ, Cao CF. Clinical diagnosis of trauma from occlusion and its relation with severity of periodontitis. J Clin Periodontol 1992;19:92-7.  Back to cited text no. 27
    
28.
Kim 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.  Back to cited text no. 28
    
29.
Hürzeler 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.  Back to cited text no. 29
    
30.
Meyer G, Fanghänel J, Proff P. Morphofunctional aspects of dental implants. Ann Anat 2012;194:190-4.  Back to cited text no. 30
    
31.
Sakka S, Baroudi K, Zakaria M. Factors associated with early and late failure of dental implants. J Investig Clin Dent 2012;3:25861.  Back to cited text no. 31
    
32.
Wan 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.  Back to cited text no. 32
    
33.
Cibirka RM, Nelson SK, Lang BR, Rueggeberg FA. Examination of the implant-abutment interface after fatigue testing. J Prosthet Dent 2001;85:268-75.  Back to cited text no. 33
    
34.
Khraisat 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.  Back to cited text no. 34
    
35.
Foz AM, Artese HP, Horliana AC, Pannuti CM, Romito GA. Occlusal adjustment associated with periodontal therapy – A systematic review. J Dent 2012;40:1025-35.  Back to cited text no. 35
    
36.
Liu 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.  Back to cited text no. 36
    
37.
Jacobs R, van Steenberghe D. Comparison between implant-supported prostheses and teeth regarding passive threshold level. Int J Oral Maxillofac Implants 1993;8:549-54.  Back to cited text no. 37
    
38.
Hämmerle 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.  Back to cited text no. 38
    
39.
Singh M. Coronoplasty: An unexplored treatment modality in periodontal therapy. Int J Curr Res 2018;10:72253-6.  Back to cited text no. 39
    
40.
Malathi K, Anand AJ, Karthikeyan R, Garg S. Coronoplasty. IOSR J Dent Med Sci 2014;13:64-7.  Back to cited text no. 40
    
41.
Sanadi 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.  Back to cited text no. 41
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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  In this article
    Abstract
   Introduction
    Physiology of Te...
   Occlusion
    Developmental St...
    Trauma from Occl...
    Etiology of Trau...
    Precipitating Fa...
   Predisposing Factors
    Other Predisposi...
   Signs and Symptoms
    Tissue Response ...
    Molecular Mechan...
    Is Traumatic Occ...
    Trauma from Occl...
    Treatment of Tra...
   Coronoplasty
    Indications for ...
    Treatment Planni...
    Other Treatment ...
   Conclusion
    References
    Article Figures

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