One of the most immediate dental concerns linked to periodontal disease is tooth mobility, and unlike pocket depth or attachment level, tooth mobility is easily understood by patients. But, what can be done about tooth mobility? Unlike plaque, bleeding on probing, and pocketing, this clinical measure rarely changes with scaling and root planing. This chapter describes the causes of tooth mobility and how it is related to occlusal trauma. While occlusal treatment is a very large topic worthy of its own textbooks and courses, this chapter aims to provide a basic understanding on how tooth mobility develops, the relationship of occlusal trauma to tooth mobility, and how it is related to periodontal disease. This chapter also provides instructions on how to identify occlusal trauma, analyze occlusion, treat minor occlusal discrepancies, and alleviate tooth mobility.
Case
A 62-year old Caucasian male presented to get “everything taken care of” since he complains of several chipped teeth and last had dental treatment 7 years ago.
He has smoked about two packs of cigarettes each day for the last 20 years, and has thought about quitting, but has not done so. He has chronic back pain for which he takes 10-mg Norco as needed, and has hypertension, which is treated with 50-mg Atenolol and 50-mg Nortriptyline once daily. He also takes folic acid 1 mg/day, and has received two IV injection of Denosumab (Prolia) about 2 years and 2 and half years ago for “low bone density.”
Blood pressure is 147/85 mm Hg and pulse is 69/minute.
Extraoral exam findings revealed no abnormal findings for the facial skin, lymph nodes, thyroid gland, cranial nerves, salivary glands, masticatory muscles, and temporomandibular joint other than solar elastosis on his facial skin from his previous work as a construction worker. Intraorally, no mucosal pathology was apparent other than periodontal disease and mild nicotine stomatitis near the soft palate. Several fractured teeth and restorations (teeth nos. 3, 13, 14, and 30) are present along with generalized abfractions (teeth nos. 3, 6, 7, 10 to 12, 19 to 25, and 27 to 30) and moderate attrition. Group function was observed in this Angle Class II Division 1 occlusion. Facial profile is convex. Overjet is 5 mm and overbite is about 50%. The patient reports that his wife told him that he grinds his teeth while he sleeps.
For clinical appearance and radiographs (see Fig. 9.1 Fig. 9.2. Findings in the periodontal chart are as follows.
After scaling, root planing, and extractions, probing depths were as follows:
What can be learned from this case?
What stands out in this case are the signs of occlusal trauma at his initial presentation. In the facial photograph, notice the uneven plane of occlusion with teeth nos. 3, 9, 10, 11, 13, and 14 protruding past the occlusal plane. Also, notice the deep overbite, and that tooth no. 9 is missing a restoration and has a fractured preparation margin at the mesiofacial line angle. Tooth no. 3 is missing a restoration, had recurrent caries, and appears fractured. Multiple teeth have abfraction lesions on the facial surface near the gingival margin, such as teeth nos. 3, 8, 10, 11, 12, 13, possibly nos. 14, 20, 21, 22, 23, 24, 25, 26, 29, and 30. On the occlusal surfaces of maxillary teeth, notice the wear facets that have exposed dentin at teeth nos. 6, 11, 12, and the worn-through porcelain at tooth no. 4. Worn-through occlusal porcelain is significant as this suggests an extreme level of parafunctional chewing movement capable of wearing through a thick layer of durable and otherwise wear-resistant ceramic. Severe attrition is visible on the incisal surfaces of the anterior teeth, which exposes reparative dentin.
Radiographically, the uneven alveolar crest level parallels the uneven occlusal plane, and there are small, funnel-shaped bone defects at teeth nos. 8, 9, 19, 20, 21, and 30. The periodontal ligament is widened at teeth nos. 12, 13, 28, and 29. There may be a fracture line from the post in the mesial root canal extending to the furcation at tooth no. 30.
There are also obvious signs of periodontal disease such as the deep pocketing, bleeding on probing, and the generalized bone/attachment loss. There are also vertical bone defects associated with local factors such as the furcation entrances of teeth nos. 2, 3, 14, 30, and 31; and the radiographic calculus with defect at the distal of tooth no. 31. The implant at the no. 4 site shows signs of bone loss due to periimplant disease, and there are periapical radiolucencies at teeth nos. 7 and 9 suggesting endodontic infections.
All these suggest a compromised dentition that is difficult to restore to health as many teeth show signs of tooth mobility. Moreover, scaling and root planing (SRP), along with tobacco cessation, did not completely resolve the pockets and did not at all change tooth mobility.
The residual pockets at nos. 1, 3, and 14 are most likely due to the deep furcation involvement of these teeth, and the pocketing around nos. 7, 9, and 10 due to rough tooth surfaces and recurrent caries. The pocketing around tooth no. 31 is most likely due to furcation involvement and deep subgingival calculus. Pocketing around no. 12 is due to mesial root concavity and associated bone defect.
The reason for the tooth mobility is that most teeth have short roots, and severe periodontitis (Stage III, grade C) reduced bone support further. This poor bone support is not changed by SRP, which explains why the tooth mobility has not improved. Given that the patient has a history of bruxing, which produces excessive forces on the teeth, this explains the signs of occlusal trauma and the tooth mobility in this patient.
Recognizing Causes of Tooth Mobility
Tooth mobility is probably the most difficult and intractable periodontal problem, and typically cannot be solved without an interdisciplinary approach. This is because tooth mobility may be caused by other processes than periodontal disease.
Causes of Tooth Mobility
Teeth derive most of their support by periodontal ligament fibers anchored in the surrounding alveolar bone in most patients. The exception to this are patients with severe alveolar bone loss or severely resorbed roots, where a significant amount of tooth support comes from gingival fibers. This then explains the three general causes of tooth mobility (Fig. 9.3).
Fig. 9.3 Causes of tooth mobility and occlusal trauma. With a normal periodontium and normal occlusal forces directed along the long axis of the tooth, there will be little clinically observable tooth mobility. Repeated excessive occlusal forces will cause the periodontal ligament and bone to remodel so that the periodontium can absorb the force. This usually results in a widened periodontal ligament, which allows tooth mobility so that the tooth can move away from the excessive force. Usually, this is seen if there is an interference contact resulting in a sideway force against the tooth. If the periodontium is of normal size, this is called primary occlusal trauma. If periodontal disease has sufficiently reduced the periodontium, even normal forces will cause tooth mobility as there is not enough support to resist movement. This is called secondary occlusal trauma. If there is severe inflammation in the periodontium such as caused by an endodontic infection, the periodontium will widen considerably and allow tooth movement.
Periapical/Periodontal Inflammation
Inflammation produces edema and tissue swelling. With periodontal ligament, severe inflammation caused by certain combinations of pathogenic microorganisms and local factors will cause the periodontal ligament to swell while destroying collagen fibers. Likewise, an endodontic infection will destroy the apical fibers of the periodontal ligament and the fluid-buildup in the periapical tissues will force the tooth slightly coronally as it stretched the other periodontal ligament fibers. In both cases, the loss of fiber support and swelling of the periodontal ligament will allow more tooth movement and occasionally produce the clinical appearance of tooth mobility (Fig. 9.3—damaged periodontium on right).
Reduced Bone Support
This is the cause of tooth mobility seen in patients with severe periodontitis. Consistent periodontal inflammation destroys collagen fibers of the periodontal ligament while a trend toward bone resorption leads to gradual loss of bone covering the tooth roots. At some point, there will be not enough fibers connecting the tooth to the underlying bone to prevent visible tooth movement (Fig. 9.3—reduced periodontium). The point at which this occurs is different for each tooth and depends on root surface morphology. Any root surface feature that increases the root surface area and the number of attached fibers will delay the onset of tooth mobility.
For example, for maxillary central incisors with conical roots, this occurs after about 60% bone loss, but it requires near complete bone loss on maxillary molars for development of noticeable tooth mobility. Also consider that minor tooth mobility is common in mandibular incisors even without periodontal bone loss, mainly because of the narrow size of the tooth roots and thin nature of surrounding alveolar bone.
Occlusal Trauma
It is possible to have tooth mobility in the absence of periodontal or endodontic infection if excessive mechanical forces on the tooth damage the periodontal tissues. In this case, excessive force either ruptures or crushes ligament fibers, leading to immediate loss of fiber support. Or more commonly, continued exposure to excessive forces will trigger remodeling of the periodontal ligament, leading to bone resorption away from the source of occlusal trauma and increased fiber length. Both will allow the tooth to move in response to the excessive force, leading to clinical tooth mobility.
How to Diagnose Causes of Tooth Mobility?
Besides being able to measure tooth mobility, diagnosis of tooth mobility requires evaluation on how inflammation, excessive occlusal force, and loss of support contribute to the observed tooth mobility.
Loss of supporting bone is the simplest identifiable cause of tooth mobility. If there is severe radiographic bone loss that results in a poor crown-to-root ratio worse than 1:1 then some of the observed tooth mobility is likely due to reduced bone support. Usually, incisors will begin to display significant mobility if more than half of bone is lost, whereas maxillary molars require almost complete bone loss to show mobility greater than Miller grade I. Generally, severe tooth mobility (i.e., Miller grade III) is almost always caused by near complete bone loss.
Relatively simple to diagnose is inflammation as a cause of tooth mobility. Swelling in the periodontal ligament due to severe inflammation can cause minor tooth mobility (grade I), and should be suspected for teeth surrounded by severely swollen, red gingiva that bleeds profusely when probed with little pressure. Alternatively, minor tooth mobility may be caused by periapical inflammation in response to endodontic disease, which will become apparent in the form of a periapical radiolucency or radiographic widening of the apical periodontal ligament on fully erupted teeth. The ultimate test of inflammation as a source of tooth mobility is treating the inflammation (i.e., SRP and root canal treatment) and observing a reduction in tooth mobility.
Excessive occlusal force as a source of tooth mobility is more difficult to diagnose as it involves some degree of occlusal analysis and close observation of teeth and radiographs for signs of occlusal trauma (see Section 9.4.4 on how to identify occlusal trauma). Typically, occlusal trauma in the absence of periodontal inflammation and bone loss produces minor tooth mobility (Miller grade I).
How to Treat Tooth Mobility?
Treating tooth mobility depends on the initial diagnosis of the three causes of tooth mobility (Fig. 9.4). In general, if there is any significant periodontal or endodontic inflammation, it must be treated first.
Fig. 9.4 Treatment of tooth mobility. If a tooth is found to be mobile during the exam, check first if there is either periodontal or endodontic inflammation, and treat this with appropriate treatment. If mobility persists and there is evidence of occlusal issues, analyze the occlusion and adjust where necessary. If tooth mobility persists because of reduced bone support, a decision has to be made based on patient comfort, the risk and importance of the problematic tooth. If the tooth is neither a treatment hazard or bothersome, it can be maintained as is, as mobility will not get worse in absence of inflammation or occlusal trauma. If the tooth is bothersome, the symptom of tooth mobility can be removed with a splint as long as the tooth is not a hazard and the patient wants to hold on the tooth. Alternatively, if a patient is receiving a partial or complete denture, bone support can be improved by severely shortening the tooth and using the remaining “stump” as an overdenture abutment where it provides added denture support. For all other situations, the most predictable treatment for mobile teeth is removing them and replacing them with a prosthesis. Endo, Endodontic; Occ, Occlusal; Perio, Periodontal.
Once periodontal and endodontic inflammation has been diminished with treatment, tooth mobility needs to be evaluated again. Often, minor tooth mobility (Miller grade I) connected to severe periodontal inflammation connected with heavy plaque and calculus deposits in a patient with mild periodontal disease and no occlusal trauma resolves completely with thorough SRP.
However, tooth mobility is most often caused by a combination of reduced bone support and excessive occlusal force. Since it is often easier to accomplish, the focus is on eliminating any occlusal trauma. Occlusal analysis can suggest ways to eliminate occlusal trauma on a mounted model, and if feasible, this can then be replicated in a patient’s mouth through occlusal adjustment. Occlusal adjustment may be as simple as removing a few tenths of millimeters of enamel or restorative material from a few “high” occlusal spots in limited occlusal adjustment, or may require the complete reshaping of most occlusal surfaces with a complete occlusal adjustment (see Section 9.5.2 on how to perform an occlusal analysis and adjustment).
It is possible that occlusal adjustment will not eliminate tooth mobility since there is either loss of bone or poor root surface morphology (i.e., a short, thin, and conical tooth root). In this case, it may be decided to leave the tooth “as is” if the patient is not bothered by tooth mobility and the tooth does not present an acute hazard to the patient. A tooth should not be removed simply because of tooth mobility, unless restoration is not possible or there is caries or periodontal infection that is not treatable. If the patient is bothered by tooth mobility and there is no other reason to remove the offending tooth, splinting can relieve the discomfort associated with tooth mobility while maintaining the tooth. A splint connects a mobile tooth or teeth to surrounding teeth that are not mobile, which then eliminates the feeling of tooth mobility if done correctly.
Identifying Occlusal Trauma
Any periodontal exam should include checking a patient’s dentition for signs of occlusal trauma.1
Signs of Occlusal Trauma
What are the signs of occlusal trauma? Clinical signs of occlusal trauma include the following:
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Fremitus means tooth movement that can either be observed or felt as a patient occludes. Presence of fremitus is diagnostic for occlusal trauma, and fremitus needs to be eliminated as part of initial, nonsurgical periodontal treatment.
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Tooth mobility not explainable by inflammatory processes or loss of bone support.
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Percussion sensitivity in the absence of pulpal disease. Percussion sensitivity usually indicates inflamed periapical tissue, which may be caused by pulpal disease, and also by irritation triggered by excessive occlusal force.
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Wear facets and attrition, which is excessive for a patient’s age and diet pattern, may suggest the presence of occlusal trauma. Some loss of enamel is typical with increasing age, but occlusal dentin should not appear in nongeriatric patients eating mostly soft, cooked, and processed foods. Wear and attrition should not be confused with erosion caused by acidic foods and medical conditions. Erosion can be distinguished from attrition if the erosion process leaves restorative margins higher than the surrounding tooth structure.
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Abfractions may suggest occlusal trauma. Abfractions are wedge-shaped noncarious cervical lesions that may be caused by high occlusal loads.2 When evaluating abfractions, it is important to check how the patient uses a toothbrush on this tooth as brushing can cause abfraction-type lesions as well. Similarly, abfraction should not be confused with abrasion, where a mechanical agent such as a gritty dentifrice or smokeless tobacco wears away exposed dentin.
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Tooth and restoration fracture may suggest occlusal trauma, although these can also be related to predisposing restorative factors such as root canal treatment or the presence of large direct restorations.3
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Development of exostoses, although other factors such as genetics can also favor the development of exostoses.
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A history of bruxism (tooth grinding) or clenching may suggest the presence of occlusal trauma if there are signs of damage to teeth such as fractures and significant attrition.
Radiographic signs of occlusal trauma include the following:
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Vertical bone defects not attributable to other factors such as furcation entrances and calculus. Usually, these defects will appear as narrow, funnel-shaped bone defects on teeth with significant occlusal wear.
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Widened periodontal ligament near the alveolar crest.4 A widened periodontal ligament due to occlusal trauma should correspond to clinically observable tooth mobility. Since a widened periodontal ligament can also be caused by rare medical conditions such as scleroderma and osteosarcomas,5 thorough medical history taking and oral cancer screening must rule out these conditions when widened periodontal ligament is observed.
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Root fractures can be related to occlusal trauma or other predisposing factors.
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Pulpal necrosis and development of periapical radiolucencies in absence of caries, failed restorations, and tooth fractures.
The following case (Fig. 9.5) illustrates that occlusal trauma can manifest itself in different ways within the same mouth.
Fig. 9.5 Occlusal trauma may cause different effects on each opposing tooth. Here, there is an interference contact between the first molars caused by the uneven occlusal plane. Bitewings show a bone level mostly parallel to the CEJ of teeth, but the maxillary molar has a large periapical radiolucency related to coronal leakage under a loose crown with strong occlusal wear. The mandibular molar has furcation bone loss and isolated crestal bone loss on the mesial surface. In contrast, the molars on the right side lack occlusal interferences and lack any significant radiographic findings (not shown).
A 60-year-old Caucasian female presents for a consultation requesting a “second opinion on her gum issue.” She reports that her dentist recommended gum surgery on the lower right side, which feels fine to her. She is more concerned about the persistent ache on the upper left side and points to tooth no. 14. She recalls that she had a root canal and a crown made for this tooth 10 years ago, and it never felt quite right after that. However, within the last few months, pain developed at this site and it is bothering her more and more. She reports a history of hypertension, for which she takes 100-mg losartan once a day. She has hypothyroidism after surgical removal of an “overactive node,” and takes 50-mg levothyroxine to supplement her now low thyroid hormone levels. She also takes 100-mg gabapentin for chronic nerve pain in her right foot. Blood pressure is 117/80 mm Hg and the pulse is 84/min.
There are no remarkable extraoral findings, and there is no intraoral soft tissue pathology other than periodontal disease. Temporomandibular joints (TMJs) function normally with no pain or restriction in mouth opening, but there was some tenderness in the temporalis muscle on the left side upon palpation.
Findings in the periodontal chart are as follows (see Fig. 9.5, for clinical appearance and radiographs):
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