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PERIODONTOLOGY 2000
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Fig. 1. Primary occlusal trauma results from excessive occlusal forces applied to a tooth with normal support. Note that the center of rotation is near the middle of the root. (From: T. G. Wilson Jr. et al. Advances in periodontics, 1992. Printed with permission, Quintessence Publishing Co., Inc.).
Fig. 2. Secondary occlusal trauma results from excessive occlusal forces applied to a tooth with reduced support. Note that the center of rotation is in the apical third of the root. (From: T. G. Wilson Jr. et al. Advances in periodontics, 1992. Printed with permission, Quintessence Publishing Co., Inc.).
disease. These early reports created a background for controversy that continues to this day: Is there an association between excessive occlusal forces and the progression of periodontal disease? How are occlusal forces evaluated in a clinical setting and at what point does an occlusal force become ``excessive''? When an occlusal force is detected and the determination is made that it is excessive, when should treatment be initiated and how should this treatment be accomplished? To effectively evaluate the role of occlusal trauma in periodontal disease, it is necessary to review studies that have used human autopsy material or animal models. As previously stated, several early authors felt that occlusal forces were the initiating factor in periodontal disease and led to the ongoing progression of the periodontal lesion. The association between occlusion and periodontal disease was based on clinical observation as opposed to scientic evaluation. In an attempt to demonstrate this relationship, several animal studies on sheep and monkeys were conducted. These studies were an attempt to determine the response of the periodontium to occlusal forces both clinically and histologically (8, 98). The authors of these studies felt that their ndings showed that excessive occlusal forces were a contributing factor in the progression of periodontal disease. By the end of the 1930's, many practitioners felt that excessive occlusal forces (occlusal trauma) were a causative factor in periodontal disease, that occlusal adjustment was a necessary part of periodontal treatment, and that occlusal discrepancies should be prophylactically treated to prevent periodontal disease (9, 60). The role of excessive occlusal forces in the pathophysiology of periodontal disease has been disputed by several researchers. Orban & Weinmann in 1933 (70) and Weinmann in 1941 (109), using human autopsy material, evaluated the effect of excessive occlusal forces on the periodontium. They concluded that there was no relationship between occlusal forces and periodontal destruction and suggested that occlusal forces played no part in periodontal destruction. Instead, they indicated that gingival inammation extending into the supporting bone was the cause of periodontal destruction. During the 1950's and 1960's, further animal research using rats, monkeys, and dogs evaluated the effect of occlusal forces on the periodontium (13, 20, 59, 73, 110). The designs of these studies were more controlled than most of the earlier investigations. The results from these studies did not support
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the concept that excessive occlusal force was a causative agent of periodontal destruction. Further, many of the studies showed no obvious association between occlusal forces and periodontal disease. In contrast to the above noted studies, at approximately the same time Glickman and co-workers published studies based on animal models and human autopsy material. Animal studies using a heavy occlusal contact created by placing a ``high'' restoration were performed utilizing dogs and monkeys (30, 33). While these studies showed no evidence of initiation of periodontal disease by occlusal contacts, the authors felt that a study using rhesus monkeys demonstrated a phenomenon described as an ``altered pathway of destruction'' when excessive occlusal forces were present (31). This altered pathway of destruction was described as a change in the orientation of the periodontal and gingival bers which occurred in the presence of excessive occlusal forces, allowing gingival inammation to extend along the periodontal ligament. The altered pathway of destruction was postulated to cause vertical bony defects due to inammation and bony destruction following the periodontal ligament. Another animal study (34) showed that bone in bifurcation areas was stressed by excessive occlusal force and that bone loss in the furcation area was related to these forces. Glickman and coworkers also reported evidence of an altered pathway of destruction in studies utilizing human autopsy material (30). From these studies, Glickman and co-workers concluded that excessive occlusal forces in the presence of plaque-associated inammation caused a change in the alignment of the periodontal ligaments, allowing an altered pathway of inammation/destruction, resulting in vertical bony defects. Because there were two separate pathologic processes working together to cause bone loss, the process was termed a ``codestructive'' effect. Glickman and coworkers summarized their work in a series of review articles (25, 2729, 32). These papers indicated that excessive occlusal forces (trauma from occlusion) were a codestructive force in the presence of gingival inammation and could lead to vertical osseous defects. Based on these observations, the use of occlusal adjustment was advocated as part of the treatment for existing periodontal disease. Because no evidence existed that excessive occlusal forces initiated periodontal disease, occlusal adjustment to prevent periodontitis was not advocated. Waerhaug (103105) evaluated a large number of human autopsy specimens to determine the relationship of subgingival plaque to the morphology of oss-
eous defects and any associations with the presence or absence of excessive occlusal forces. He found that the ``plaque front'' (i.e. the apical border of the subgingival plaque) was always in very close approximation to the epithelial attachment level and always followed the morphology of the bony defect. In addition, the relationship of the plaque level between adjacent teeth (either at the same or different apicocoronal levels) was associated with either horizontal or vertical interproximal bone loss. He also observed that excessive occlusal forces bore no relationship to the underlying bony defect and that vertical defects were found equally around traumatized and nontraumatized teeth. Waerhaug concluded that bone loss was always associated with the downgrowth of plaque and there was no relationship between excessive occlusal forces and vertical bone loss. The use of human autopsy material to study the effect of occlusal forces has the inherent problem that rarely if ever is there a true understanding of the patient's occlusal relationship that existed in life. Some knowledge can be obtained by studying the wear patterns on the teeth but there is no assurance that the teeth actually occluded in the assumed manner or that wear facets represent current and active occlusal trauma. Therefore, any conclusion or observations based on autopsy material concerning the role that occlusal forces may or may not have on the progression of periodontal disease has to be questioned. A single histologic study (95) evaluated the occlusal relationships of four patients prior to the removal of their jaws for cancer therapy. This study did not show a relationship between occlusal forces and periodontal disease. However, it is unclear if excessive occlusal forces existed in these patients. Two extensive animal studies were performed in the 1970s. These studies evaluated the effect of plaque and excessive occlusal forces in the animal models utilized. Unlike most of the earlier investigations, stringent scientic controls and designs were used. One series of studies were conducted by Polson and co-workers (47, 71, 7683) and a different series of studies was performed by Lindhe and co-workers (1719, 5557, 67, 68, 100102). Polson's group used squirrel monkeys and mesialdistal compression forces comparable to orthodontic forces whereas Lindhe's group used beagle dogs and applied buccallingual forces using a high occlusal contact and a nger spring. Both groups investigated excessive occlusal forces in the presence and absence of plaque. These studies yielded similar results despite the different animal models and the different excessive
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occlusal forces used. Excessive occlusal forces in the absence of plaque were found to cause loss of bone density and mobility of the affected tooth but no evidence was found that the occlusal forces alone could cause attachment loss. When the excessive occlusal forces were removed, it was noted that the loss of bone density was reversible. In the presence of plaque, inammation of the gingiva and periodontal supporting structures were noted and in the presence of excessive occlusal forces and plaque together there was an indication that more bone density was lost in both animal models. In the beagle dog model there was evidence of attachment loss when plaque and excessive occlusal forces were both present. These results were not observed in the squirrel monkey model. These two series of studies exhaustively evaluated the relationship of occlusal forces and plaque in an animal model. They both concluded that there was no evidence indicating that excessive occlusal force alone will cause loss of attachment. The studies on beagle dogs showed that under specic circumstances there may be attachment loss when plaque and excessive occlusal forces are both present. Both studies agreed that the removal of plaque and the control of inammation will stop the progression of periodontal disease whether or not excessive occlusal forces are present.
Human studies
Only a few studies have evaluated the effects of excessive occlusal forces in humans. There are many ethical difculties associated with the non-treatment of diagnosed periodontal disease that complicate studying the effect of occlusion on the progression of periodontal disease. The gold standard of clinical research is the randomized controlled clinical trial. These studies require prospective comparisons of different treatment methods on treatment outcomes. However, in order to compare the combined effects of excessive occlusal forces and periodontal disease, it would be necessary to treat one group of patients while leaving the other group untreated. This creates an unacceptable ethical dilemma due to the known deleterious effects of the non-treatment of periodontal disease. The World Workshop in Periodontics stated, ``Prospective studies on the effect of occlusal forces on the progression of periodontitis are not ethically acceptable in humans'' (23). As a result, human studies are limited to retrospective and observational research.
It has been reported that patients who have occlusal discrepancies have no more severe periodontal destruction than do patients without occlusal discrepancies (46, 51, 74, 84, 85, 94). However, it has also been reported that molars with furcation invasion and mobility have greater probing depths than molars that are clinically nonmobile (106). The increased mobility noted in this study may have been due to occlusal factors or to greater loss of bony support associated with the furcation involvement. Due to the inability to determine whether occlusal factors or bone loss was initially present, it is impossible to draw a clear relationship between occlusal discrepancies, mobility, and probing depths from this study. Other studies reported that patients who received occlusal adjustment as part of their periodontal therapy had greater attachment gain than patients who did not receive occlusal adjustment (10, 21). These studies suggest that occlusal adjustment should be performed, where indicated, as a part of periodontal treatment. A report on risk factors for periodontal destruction indicated that mobility and parafunctional habits that are not treated with a biteguard are associated with increased attachment loss, worsening prognosis, and tooth loss (61). This study seems to indicate that untreated (i.e. no biteguard) parafunctional habits may contribute to increased periodontal breakdown. Another study has shown that mobile teeth treated with regenerative surgery did not respond as well as nonmobile teeth (14). However, no association was drawn between mobility and occlusal forces. In a series of retrospective reports, private practice patients were evaluated who were diagnosed with advanced periodontal disease and had a comprehensive treatment plan recommended that included surgical treatment. Occlusal adjustment was recommended if signicant occlusal discrepancies were detected. Some of these patients self-selected to not have any periodontal treatment performed (untreated group). Other patients had only nonsurgical periodontal treatment performed (partially treated group). Others followed through with all recommended periodontal treatment including surgery (fully treated group). The effect of occlusal discrepancies was studied in each of these groups using the individual tooth as the experimental unit (40, 41, 66). This means that the progression of periodontal destruction or the improvement of the periodontium for each tooth was followed over time. This study design allowed for the evaluation of teeth with occlusal discrepancies versus teeth without occlusal discrepancies rather than comparing patients with
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occlusal discrepancies vs. patients without occlusal discrepancies. This experimental approach differs from most past studies where the patient was the experimental unit and the changes in probing depth or attachment levels were expressed as the ``patient mean.'' Using the patient mean may tend to mask changes that are occurring at the more active sites and, thereby, give results that do not reect what is actually occurring during localized disease progression. These studies found that teeth with occlusal discrepancies had deeper presenting probing depths and worse prognoses than those teeth that did not have occlusal discrepancies. Further, when teeth with occlusal discrepancies were followed over time, a signicant increase in probing depth and a worsening of prognosis was noted when compared to teeth without occlusal discrepancies. Additionally, teeth in the partially treated group that had received occlusal adjustment showed a slowing of the progression of periodontal destruction when compared to teeth with occlusal discrepancies from the same group that had not had occlusal adjustment. It was concluded that occlusal discrepancies appear to be a signicant risk factor that contribute to more rapid periodontal destruction and that treatment of occlusal discrepancies seemed to slow periodontal destruction. The authors postulated that the reason for the difference in their ndings and those of previous studies was the use of the individual tooth as the experimental unit, which they felt yielded a more accurate assessment of the effect of occlusal discrepancies on the periodontium (40, 41, 66). In summary, animal and human studies have indicated some association between occlusal discrepancies/occlusal trauma and changes in the periodontal supporting structures. Extensive animal studies have shown that occlusal trauma does have an effect on the periodontal supporting structure but does not initiate breakdown of the attachment apparatus with resulting measurable attachment loss. The human studies have indicated that treating occlusal discrepancies may lead to better results following periodontal treatment. A study using a more contemporary statistical analysis and utilizing individual sites as the basis for comparison, has shown a strong association between occlusal discrepancies and deeper pockets (66). Furthermore, existing research does not establish a cause-and-effect relationship between occlusion and periodontal disease. However, there are strong data to indicate that occlusion is a potential risk factor for periodontal breakdown and that controlling this
risk factor may slow the progression of periodontal destruction and improve the results of periodontal treatment outcomes. As is the case with all risk factors such as smoking, oral hygiene, and systemic factors, the effect of occlusion on periodontal disease needs to be minimized by recognizing the risk, diagnosing the existence of the risk factor, and minimizing the risk by the use of various treatment modalities such as selective grinding, orthodontics, and/or occlusal appliances.
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Fig. 3. (a) Initial contact in centric relation. (b) Centric slide between centric relation and centric (acquired centric; habitual) occlusion. (c) Centric (acquired centric;
habitual) occlusion, demonstrating maximum intercuspation or contact of the teeth of the opposing arches. (Courtesy Dr. J. Y. Cho).
a retruded position of the mandible but on a clinical basis, an attempt is made to guide the mandible into a position where both right and left condyles are rmly placed in the fossa of the temporomandibular joint. This position is one that is felt by the practitioner rather than conrmed by any type of device or instrument and is therefore subjective in nature. Once the practitioner feels that a retruded position has been achieved, the patient is asked to close until the patient feels the rst contact between the teeth (Fig. 3a). This contact point is veried by the examiner either by eye, inked marking paper or ribbon, or both. This initial contact in a retruded position has been described as contact in ``centric relation''. Following the establishment of the initial contact, the patient is asked to continue to close the jaws together until maximum contact between the teeth is achieved. The jaw position of maximum tooth contact is often termed ``centric occlusion''. The position of maximum tooth contact is assumed to be the position that the patient will naturally move to as the most comfortable or habitual position (Fig. 3b,c). The distance that the patient moves between the retruded initial contact and the point of maximal tooth contact is termed the slide between the positions of centric relation and centric occlusion. This slide is often described as the ``centric relation/centric occlusion slide'' or ``CR/CO shift''. This slide is usually recorded as the length of the slide in the anterior, vertical, and lateral planes (26). No direct correlation with histologic evidence of trauma from occlusion has been shown between the presence of a slide between the contacts in centric relation and the contacts in centric occlusion. However, indirect clinical evidence of a more rapid progression of periodontal destruction as evidenced by increased probing depths has been shown to occur in patients with untreated periodontal disease (40, 41, 66). While this nding cannot be directly correlated with animal research showing histologic evidence of
inammation and bone rarefaction in the presence of experimental occlusal stress and, in beagle dogs, the loss of attachment when plaque is present in addition to the experimental occlusal stress, there is a likelihood that a similar process is occurring in humans as in the beagle dog model. If this assumption is true, then at least in certain cases the histologic lesion of occlusal trauma is likely to be present in periodontal patients who have occlusal interferences. Other clinical ndings that have been associated with trauma from occlusion are tooth mobility and wear patterns on the occlusal surface of the teeth (Table 1). These clinical ndings are extremely difcult 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. In the case of occlusal wear patterns, it is often impossible to determine whether they are caused by functional or parafunctional habits that are occurring at present or whether they may be associated with episodes of bruxism that have occurred in the past. If bruxism has occurred in the past, what if any part did it play in the current clinical evidence of periodontal breakdown? The practitioner must evaluate and record all of these ndings so that a picture of the occlusal stresses being placed on the periodontium can be assessed and to help form an assumption of the occurrence of trauma from occlusion.
Table 1. Clinical indicators of occlusal trauma
Clinical indicators of occlusal trauma may include one or more of the following: 1. Fremitus 2. Mobility (progressive) 3. Occlusal discrepancies 4. Wear facets in presence of other indicators 5. Tooth migration 6. Fractured tooth/teeth 7. Thermal sensitivity
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What's abfraction and are there data to support a role of occlusion in its development?
Abfraction has been dened as the ``pathological loss of hard tooth substance by biomechanical loading forces'' (37). The lesions have been described as angular or wedge-shaped defects that occur at the cementoenamel junction of affected teeth as a result of exure and eventual fatigue of enamel and dentin (7) (Fig. 4). The prismatic structure of enamel is strong in compression, but vulnerable in areas of tension, accounting for the resultant morphology of the proposed lesion (52). It is further noted that occlusal loads which generate cervical exure may disrupt hydroxyapatite crystal bonds, and result in microfracture and eventual loss of associated enamel (53). Noncarious hard-tissue cervical lesions (NCLs) have been classied as abrasive, erosive, corrosive, abfractive or combined (38). In contrast to abfraction, abrasion represents a pathologic loss of tooth substance resulting from biomechanical wear and is exemplied by improper or overzealous toothbrushing. This condition is generally accompanied by marginal tissue recession and may affect one or more teeth (75) (Fig. 5). Erosion is a chemically induced loss of tooth substance that occurs primarily through acid dissolution (44) (Fig. 6). Attrition is dened as the physiologic wearing away of a substance or structure, such as the teeth (3). This typically affects the occlusal and incisal surfaces of the teeth and may result from functional or parafunctional wear, manifesting as facets (7). These highly polished surfaces may appear on marginal, transverse and oblique ridges, and on cusps and restored surfaces (Fig. 7).
Fig. 5. Note the generalized loss of cervical tooth substance and accompanying marginal tissue recession. The patient admitted (and demonstrated) aggressive horizontal toothbrushing.
Fig. 6. The maxillary right central incisor shows erosion as a result of chemically induced loss of enamel. (Courtesy Dr. Terry D. Rees).
Is there evidence for a role of occlusal loading in the genesis of noncarious cervical tooth loss?
The presence of lesions consistent with those described as abfraction have been reported to increase in size and depth with age of affected individuals (54). In a study of 913 subjects, 23% presented with such defects. Sixty-ve percent of the affected individuals had conrmed parafunction as compared to 35% who did not (35). Another study reported that 96% of teeth with noncarious cervical lesions also presented evidence of occlusal discrepancies (86). In comparing canine-guidance with group-function occlusal relationships, abfractionlike lesions were observed six times more often in the latter group, suggesting that increased occlusal tooth contact during lateral excursion favored the occurrence of these lesions (87).
Fig. 4. Maxillary right rst premolar presents a well-delineated noncarious hard-tissue cervical lesion consistent with abfraction.
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Fig. 7. The mandibular rst molar presents facets on the mesiobuccal and distobuccal cusps and on the amalgam restoration at the mesiolingual surface.
evaluated for occlusal correction or bite-splint therapy to address interferences that may contribute to tooth exure (75). In a separate case study of 52 modern human skulls, occlusal ndings failed to provide evidence for abfraction (43). There is a strong contention that NCLs represent a multifactorial phenomenon. It has been proposed that the presence of occlusal stresses in combination with acidic substances may result in greater damage than either alone (39). However, one clinical question remains Why does abfraction occur on the buccal/ facial surfaces, with only rare reports of lingual lesions? In summary, available evidence suggests a plausible explanation for abfraction. It is equally apparent that this diagnosis is not absolute. In cases where the therapist is confronted with NCLs, toothbrushing habits and occlusal relationships should be thoroughly evaluated. Restorative and/or periodontal plastic surgical intervention should be preceded by control of any habits and/or untoward occlusal loading which may adversely affect predictable long-term treatment outcome.
In addition to clinical observations, evidence suggesting a role of occlusal loading in development of abfraction-like lesions comes from various stress and strain studies. These include articulated study models, strain-gauge studies, nite element stress analysis and photoelastic stress analysis (88). Such studies have shown that controlled loading (500 N) applied to inner inclines of the buccal and lingual cusps of mandibular premolars resulted in stress values exceeding the failure stress of enamel (89). This loading corresponds to that anticipated during excursive contacts in group-function occlusal relationships. These studies are principally in vitro investigations that fail to take into account the role of the periodontal ligament and bone during the course of occlusal loading. It is important to note that in a strain gauge study of maxillary incisors in healthy volunteers, large cervical surface strains were observed (65). In a clinical investigation of the characteristics and prevalence of abfraction-like lesions in a U.S. population with 103 noncarious cervical lesions, the vast majority of the lesions were strongly suspected as being the result of toothbrush abrasion. A small subset (i.e. 15 lesions) was deemed the result of some other phenomenon. Six (40%) of these teeth manifested premature occlusal contacts. Compared to control teeth without NCLs, affected teeth did not signicantly differ in terms of wear facets or occlusal contacts. No NCLs were reported on lingual surfaces. However, the authors cautioned that teeth with noncarious wedge-shaped lesions should be carefully
Fig. 8. One way to assess tooth mobility is by using two instrument handles applied to the tooth and applying alternating luxating force orofacially.
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3.
cations of this index are used extensively throughout dentistry, and especially periodontics (11, 20). Clinical assessments of tooth mobility derived by this means are somewhat arbitrary and dependent on examiner subjectivity and interpretation. As a result, they do not usually discriminate well between small mobility increments (99). Consequently, a means of more precise and objective measurement of tooth mobility has been pursued and includes mechanical, electronic and optical devices, and laser Doppler vibrometry (12, 64, 69, 72, 92). Despite objective approaches striving to standardize tooth mobility evaluation, such devices by and large have not been well accepted for use in clinical practice. More recently, the Periotest1 (Gulden-Medizintechnik, Bensheim, Germany), a device resembling a dental handpiece, has gained favor in evaluating and monitoring tooth mobility and clinical success of dental implants (6, 93). The instrument is applied orthoradially to the center of the anatomic crown, delivering a standardized percussive force. Recorded values range from 0 to 100, and correspond to time in milliseconds taken for the supporting structure(s) to respond to impact deceleration, thus assessing rebound dynamics and damping characteristics of the periodontium (42, 58, 91, 108). It is interesting to note that no signicant change in numeric Periotest1 values has been observed when comparing baseline values with those recorded after the initial phase of periodontal therapy (16). This would suggest that Periotest1 mobility evaluation relates primarily to the amount of bone loss (i.e. support) about teeth being evaluated and may not be directly related to traditional tooth mobility. Contraindications to use of this instrument include acute inammation, traumatic subluxation and dental implants in the initial phases of healing (91). One of the diagnostic challenges confronting the clinician is to determine the associative cause of the observed tooth mobility. It is widely recognized that some degree of tooth mobility is always present in the healthy dentition. This has been termed physiologic (normal) tooth mobility, in contrast to
pathologic (abnormal) mobility. Factors that have been associated with tooth mobility include periodontal status of the teeth (e.g. inammation, loss of clinical attachment/bone), periodontal surgery, occlusal trauma, pregnancy, and pathologic processes affecting the jaws/teeth (22, 24, 36, 49, 50). More recently, it has been proposed that the designators ``pathologic tooth mobility'' and ``adaptive tooth mobility'' may be helpful in addressing mobility status and thus, facilitate management and maintenance approaches in affected patients (4). Stability of tooth mobility appears acceptable in the absence of confounding variables, but progressive mobility is a concern and should be addressed by controlling inammation, occlusal adjustment and considering a stabilization appliance or splinting as indicated. The long-term therapeutic objective is to maintain the health, stability, comfort and function of the patient's natural dentition (or implants).
Of what value are assessments of tooth mobility in the management of patients with periodontitis?
A limited number of human studies have suggested that tooth mobility may be associated with greater attachment loss, probing depth and bone loss when compared to nonmobile teeth (45, 46, 106). It is difcult to determine from these studies whether tooth mobility was a result of the associated periodontal disease process or if, in some way, it contributed etiologically. Two studies reported that teeth exhibiting a combination of furcation invasion and tooth mobility were at risk of sustaining greater attachment loss as compared to nonmobile teeth or teeth with furcation invasion alone (45, 106). In a longitudinal study by McGuire & Nunn (62), tooth mobility was associated with non-improving prognoses of affected teeth. Other studies have examined the effects of tooth mobility on periodontal treatment outcomes. In an 8-year follow-up study in which patients received scaling, oral hygiene instruction, occlusal adjustment, periodontal surgery (subgingival curettage, modied Widman ap or pocket elimination) and 3-month maintenance, baseline and annual assessments were made of probing depth, attachment level and tooth mobility. Results indicated that pockets associated with mobile teeth did not respond as positively (i.e. clinical attachment level gain) to therapy as rm teeth. This inuence was observed by the end of the rst year and became more pronounced by the second year, with only minor
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changes occurring throughout the duration of the 8year clinical trial. It should be noted that although clinically mobile teeth could be effectively treated and maintained, better responses (i.e. clinical attachment level gain) were generally observed in association with rm teeth (21). In a randomly controlled clinical trial examining clinical outcomes and postoperative morbidity in regenerative treatment of deep infrabony defects, tooth mobility was assessed as a covariate. Among clinical parameters evaluated in the study were clinical attachment level, probing depth, recession, tooth mobility, full-mouth plaque scores, and full-mouth bleeding scores. These were assessed immediately, prior to surgery and at 1-year post-treatment. Tooth mobility was evaluated with a purpose-built electronic device (Periotest1). Baseline tooth mobility was signicantly associated with a reduction in anticipated amounts of clinical attachment level gain. Based on the results of this study, the authors suggested that clinicians may want to consider reducing tooth mobility prior to attempting periodontal regenerative therapy to facilitate therapeutic success (14). Other studies have examined the effect of splinting on tooth mobility after initial therapy and after osseous surgery. In the initial therapy study, there was a reduction in tooth mobility over the 17-week period, but there was no difference between the splinted and non-splinted sites. The reduction in mobility observed in both study groups was attributed to reduction of inammation and occlusal adjustment accompanying initial therapy (49). No difference was observed between splinted and non-splinted teeth receiving osseous surgery, indicating that splinting had no lasting effect on tooth mobility. Mobility predictably increased following surgery, but returned to baseline presurgical levels after 6 months (22). In summary, although a signicant role has been suggested regarding the effect of tooth mobility on treatment results, it is clear that controlled intervention studies will be necessary in order to clarify the effect of reducing baseline tooth mobility on periodontal treatment outcomes. Until such studies are conducted, it would appear prudent, based on available data, to consider reduction/control of tooth mobility as an integral part of periodontal therapy.
between centric relation and centric occlusion contribute to the progression of periodontal destruction and that the presence of mobility will negatively affect the outcome of periodontal treatment. What part each of these actually plays in periodontal destruction, whether these ndings are related to each other or play separate roles, and whether either or both of these ndings are associated with the classic histologic denition of occlusal trauma is unknown. Furthermore, due to ethical considerations, it is unlikely that these questions will ever be satisfactorily answered. However, when periodontal disease and destruction are present, the currently available evidence appears to support the need for occlusal treatment that will minimize occlusal interferences and help decrease tooth mobility. The treatment of occlusion usually involves either a reversible approach consisting of some type of bite appliance (i.e. ``night guard'') and/or the selective grinding of the occlusal surfaces of the teeth (Fig. 9). Orthodontic therapy is also an effective method of changing occlusal relationships and minimizing
Fig. 9. (a) Hard acrylic occlusal nightguard in place. As the patient's jaw moves into a left lateral excursion, note the disclusion of the teeth in the anterior and right side. (b) Note the smooth, highly polished occlusal surface and the presence of ball clasps between the second premolar and the rst molar to facilitate retention.
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occlusal forces between opposing teeth. However, orthodontics is rarely used during the active phase of periodontal therapy and selective grinding of the contacting surfaces is usually necessary following orthodontic therapy. Appliance therapy has the advantage of causing no permanent changes to the occlusal surfaces and is therefore fully reversible. However, appliance therapy is only effective in controlling occlusal forces when the appliance is worn by the patient. Selective grinding involves the nonreversible reshaping of occlusal surfaces but has the advantage of minimizing occlusal forces at all times. The selection of the treatment modality for treating occlusal stresses must take into consideration operator skill and condence in selective grinding, the presence or absence of parafunctional habits, the presence or absence of muscle splinting, and the patient's psychological state. Measurement of the outcomes from occlusal therapy usually cannot be readily achieved. In cases where the patient is experiencing discomfort from occlusal contact, the relief of heavy occlusal pressure by selective grinding may elicit immediate relief of the patient's symptoms. In most cases, however, the changes are subtle and can only be measured in terms of decreased mobility and long-term favorable results to periodontal therapy. Due to the fact that other treatments routinely performed during periodontal therapy will also tend to improve mobility and contribute to long-term favorable outcomes, it is difcult to determine to what extent occlusal treatment has played a role in any clinical improvements observed. However, just as periodontal disease results from a combination of risk factors and contributing causes, long-term favorable outcomes and decreases in mobility are probably due to the elimination or relief of multiple risk factors. The treatment of periodontal disease consists of attempting to control the risk factors for the disease such as bacterial plaque and the deeper pockets, which harbor reservoirs of plaque bacteria, ameliorate negative habits such as smoking, and controllable systemic factors such as diabetes. The treatment of occlusal discrepancies/occlusal trauma should also be viewed in the context of the control of one of the risk factors contributing to periodontal disease. The successful treatment of periodontal disease requires the control of all controllable risk factors. If occlusal discrepancies exist in the presence of periodontal disease, the occlusal factors should be controlled by the minimization of the occlusal forces. In other words, occlusal treatment should be performed, where indicated, as a routine part of periodontal therapy.
References
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