Fig. 6.1

CHAPTER 7

IMPLANT PROSTHETICS AND TEMPOROMANDIBULAR DISORDERS

Daniele Manfredini

Visiting professor, Department of Maxillofacial Surgery, University of Padua

 

Temporomandibular disorders (TMDs) are a heterogeneous group of clinical problems involving the temporomandibular joint (TMJ) and/or masticatory muscles and associated structures (1).

These disorders are the most frequent cause of orofacial pain of non-dental origin, and even though their prevalence is still debated (2), there is evidence that signs and symptoms of TMDs are frequent in the general population (3).

The classical triad of clinical signs characterising TMDs is: pain in temporomandibular joints or masticatory muscles; TMJ sounds; limited or abnormal mandibular movements (4).

Recent studies in the literature suggest that, while the prevalence of TMDs is commonly believed to peak at around 35-45 years of age (5), in clinical populations there exist at least two different, age-related patterns of distribution of TMDs: a predominance of disc displacements associated with TMJ pain in 28- to 35-year-olds, and of symptoms of inflammatory-degenerative joint disorders in subjects aged 50 to 60 years (6).

As regards gender differences, the literature unequivocally demonstrates a strong female preponderance, with female:male ratios found to range from 2.5:1 to 7:1 in various studies involving different ethnicities (7,8).

Over the years, many diagnostic-classification systems have been proposed for TMDs (9).

At present, different standards of reference for framing TMDs are adopted in the clinical and research settings: whereas the guidelines and recommendations of the American Academy of Orofacial Pain (AAOP) (10) and of the European Academy of Craniomandibular Disorders (EACD) (11) are widely used in clinical practice, in research, extensive use is made of the Research Diagnostic Criteria for TMD (RDC/TMD)(12).

The RDC/TMD system, now translated into more than fifty languages in order to encourage its diffusion and multicentre and cross-cultural application, comprises coded criteria allowing a two-axis diagnostic assessment that covers both physical/organic (axis I) and psychosocial (axis II) aspects (Box 7.1).

A fundamental aspect of TMD diagnosis, acknowledged by all the most accredited systems, is the crucial role played by clinical assessment, which can achieve higher levels of diagnostic accuracy and inter-operator calibration than the various currently available electronic instruments (e.g. electromyography, mandibular kinesiography, posturometry) (13-16).

The aetiology of TMDs is recognised as multifactorial.

Numerous factors (psychological, socio-cognitive, parafunctional, skeletal, hormonal, occlusal) can, in ways that are often difficult to decipher, contribute to causing the symptoms in the single individual (17).

Given this lack of understanding of the aetiology of TMDs at single patient level, and also in view of encouraging success rates obtained with a variety of conservative therapeutic approaches, careful management of the clinical symptoms using reversible methods with low biological cost is now the standard of care in clinical treatment settings (18,19).

Over the years, therefore, there has been, both in the literature and in clinical practice, a gradual movement away from the old occlusal conception, according to which all TMD symptoms were due to presumed dental occlusion abnormalities, whose correction through extensive rehabilitation was the sole therapeutic objective.

Nowadays, a TMD is no longer seen as a dental pathology to be approached using dental-based treatments, but rather as a muscular-skeletal disorder that demands a broader, medical-based approach (20).

Notwithstanding this, the translation of correct scientific information into daily clinical practice remains incomplete, with many remnants of old theories still seeming to influence the way occlusion is routinely regarded.

Indeed, the role of occlusion is often exaggerated in many dental specialties, in spite of the absence of evidence demonstrating either the superiority or the iatrogenicity of given occlusal schemes (21,22).

The fact that TMD issues have, for years, been dealt with in association with prosthetic issues, even in the context of university training courses, explains the need to include TMDs in a book on implant prosthetics.

In the light of these opening remarks, it is clear that a discussion of the relationship between implant prosthetics and TMDs cannot fail to include a detailed analysis of the relationship between these disorders and dental occlusion.

OCCLUSION AND TMDs:
EVIDENCE-BASED DATA

The role of occlusion as an aetiological factor in TMDs has, for years, been fiercely debated, even giving rise to what has been called a “clash of cultures”, that is a diatribe between those who do not see occlusion as the aetiological primum movens and those who, instead, consider TMD signs and symptoms to be due to some occlusal abnormality.

Naturally, the most credible scientific position can only be that which is based on the currently available evidence, and actually this evidence throws into question the existence of an association, and certainly of a cause-effect relationship, between the presence of certain occlusal abnormalities and TMDs (20).

In particular, numerous systematic reviews of the literature, some of whose conclusions are summarised in Table 7.1, have confirmed that the available scientific evidence does not support the use of occlusal treatments as a therapeutic approach to TMDs.

 

Historically, theories on the role of occlusion in the aetiology of TMDs date back to the 1930s and the studies of Costen, an otorhinolaryngologist who described a set of ear symptoms which he claimed were caused by a lack of posterior occlusal support (27). Even though the earliest published reports of TMJ disorders appeared in the century before that (28), meaning that Costen was not actually the “discover” of TMDs, the syndrome he described nevertheless took his name and today, seventy-five years on, it is not uncommon to come across the term Costner’s syndrome, even in specialist and medical-legal contexts. Actually, from a historical perspective, the most significant thing these founders of modern gnathology did was to identify dentists as the professionals who should treat patients with TMDs. Over the years, even though some authors had already realised that occlusion could not be the only aetiological factor in TMDs, and that an important role is played by psychoscocial factors (29), research into the relationship between TMDs advanced along two main lines: 1. study of the statistical association between certain occlusal variables and the presence of signs and symptoms of TMDs; 2. attempts to simulate, experimentally, situations of occlusal stress and overloading in order to verify their potential to damage the TMJ and masticatory muscles. A number of occlusal variables have been suggested to have a causal relationship with TMDs, for example, unilateral crossbite, anterior open bite, deep bite, and lack of posterior occlusal support (Fig.s 7.1-7.3), although studies using adequate statistical methods to depict biological models, reappraising the association of these variables with TMJ problems (30) and with muscular disorders (31), have instead suggested that they may simply be the means through which muscle forces developed during parafunctional activities are transmitted to the different structures of the stomatognathic system (32) (Table 7.2).

 

 

 

The most accepted line of evidence is that the presence of occlusal abnormalities in patients with TMDs is actually due to joint degeneration and/or remodelling resulting in an occlusal shift (33) (Fig. 7.4).

As regards experiments exploring the potential of occlusal interferences to provoke TMD signs and symptoms, the evidence produced by the numerous studies conducted on human and on animal models shows that possible iatrogenic interferences (e.g. high occlusal restorations) can, in the worst hypotheses, cause local trauma (26). In short, these interferences demand postural and functional adaptation of masticatory patterns which rarely gives rise to symptoms such as dental and/or masticatory muscle pain. Furthermore, when they do occur, these effects seem to be mainly transitory and easily reversed through removal of the iatrogenic interference. Data from more recent randomised controlled studies suggest that in healthy subjects, the application of an occlusal interference leads to a reduction in the usual electromyographic activity of the masseter muscles (34) and does not significantly affect pressure pain thresholds (35).

Interesting reflections are also prompted by a study which found that subjects with a history of TMDs tended to respond differently to iatrogenic occlusal interferences compared with subjects who had no history of TMDs (36). It seemed that the former have an increased risk of developing muscular pressure pain in response to occlusion abnormalities provoked by dental procedures. These observations should be borne in mind when carrying out occlusal treatments such as prosthetic or orthodontic rehabilitations (based, respectively, on prosthetic and orthodontic indications), which may involve periods of occlusal instability (e.g. temporary restorations, increases in vertical dimension, shifting teeth). Even though the publication of this study gave fresh impetus to those believing occlusion to be the main factor in the aetiology of TMDs (37), it is clearly important to avoid overestimating the importance of these results. First of all, the responses to the placement of the artificial interferences cannot be equated with the presence of TMDs; similarly, an acute occlusal alteration, like the simulated occlusal alterations in the various experimental studies, cannot really be compared to a clinical situation characterised by the presence of “non-ideal” dentition to which the patient, thanks to the exceptional adaptive capacity of the neuromuscular system, has gradually adapted over a period of years (20).

In the light of these remarks, it is legitimate to ask ourselves how much importance should be attached to occlusal considerations in the planning of extensive rehabilitations using prosthetic implants. In short: 1. Does carrying out rehabilitations using prosthetic implants increase a patient’s risk of developing signs and symptoms of TMDs? 2. Are there any particular indications that should be followed when performing such rehabilitations (for prosthetic, aesthetic, or other reasons) in patients affected by TMDs?

IMPLANT PROSTHETICS AND TEMPOROMANDIBULAR DISORDERS

In medicine, the best method for broaching any given medical topic is to search the available relevant literature in PubMed, a database of all the main publications appearing in journals submitted to editorial quality control.

The results of a PubMed search for publications identified by combining the key words “dental implants” and “temporomandibular joint disorders” were rather discouraging (Table 7.3).

In particular, of the 35 publications identified, only two set out, as their main aim, to assess the prevalence of signs and symptoms of TMDs in patients previously submitted to oral implant surgery.

A study conducted to analyse and quantify the prevalence of sensory and affective aspects of orofacial pain in patients undergoing dental implant treatment found no significant associations between dental implantology procedures and pain in the TMJ and masticatory muscles (38). Another study, more detailed and better designed, was conducted to establish the prevalence of the appearance of TMJ osteoarthritis in patients wearing implant dentures; similarly, this study found no association between degenerative TMJ disease and dental implants after a mean follow up of over five years (39).

Obviously the evidence that can be drawn from such studies is extremely limited and a discussion of the relationship between implant prosthetics and TMDs must thus be based on several considerations of a biological nature that are actually applicable to all types of prosthetic rehabilitation, both those based on natural teeth and those using dental implants.

Theoretically, the results of the experiments on occlusal interferences, considered in a wider context, seem to suggest that any perturbation of a stomatognathic system that works, and works in the absence of TMD symptoms, should be avoided.

The stomatognathic system has extraordinary powers of adaptation, both to “natural” dental-skeletal abnormalities (40) and to iatrogenic modifications of the system (41).

In the different stages of the planning and execution of extensive rehabilitations using prosthetic implants, the primary objective, in order to protect the stomatognathic system against the appearance of symptoms of TMDs, is not to provoke modifications that demand an adaptation that exceeds the system’s own capacity for accommodation. In short, it is never advisable to perform rehabilitations according to predetermined occlusal schemes (Fig. 7.5) and according to preconceived ideas of interarch relations that fail to take into account the muscle engrams that the neuromuscular system of a patient with no TMD symptoms have developed naturally. In this regard, it is worth highlighting a few aspects and clinical considerations relating to the concepts of centric relation and vertical dimension.

CENTRIC RELATION IN THE PHYSIOPATHOLOGY OF MASTICATION

Centric relation (CR) has, for decades, been a controversial and much debated concept. Indeed, its definition has been changed on many occasions, even in the prestigious Glossary of Prosthodontic Terms, evolving from a retruded, postero-superior condyle position to an anterior-superior position of the condyle, which lies against the wall of the articular eminence (42) (Box 7.2).

Over the years, there has been a considerable reduction in the importance given to centric relation as a key reference position and, to some extent, as a “therapeutic” position; in the same way, it has been found that there is no real evidence to support the affirmation that in ideal conditions centric relation should coincide with the position of maximum intercuspation (MI) (44).

Furthermore, even though some studies have described a weak association between CR-MI slides and TMJ disorders, it is probable that such occlusal slides are actually effects, rather than a cause, of joint remodelling (45).

In view of these considerations, the need to play down the importance of having perfect harmony between the position of maximum intercuspation and some, too often arbitrary and “philosophical”, centric relation has been underlined repeatedly in both orthodontic(46) and gnathological settings (22) (Fig.s 7.6a-b).

Indeed, the available large-scale scientific evidence suggests that there actually exists a range of possible centric relations, and not a single position of reference common to all individuals.

Furthermore, no particular spatial position of the condyles in the glenoid fossa has been found to be predictive of TMDs; asymptomatic joints show various combinations of non-extreme glenoid fossa shapes and sizes and condyle positions (47) (Fig. 7.7).

In the light of these observations, therefore, there are no grounds for considering any single condyle position superior to the others.

Similarly, there is absolutely no need for obsessive pursuit of a particular condyle position, often termed myocentric, established in conditions of artificial muscle relaxation (48).

This position is one of the cornerstones of so-called neuromuscular dentistry, one of the many pseudosciences that lie at the border between dentistry and the other medical professions, and whose validity has never been demonstrated (49).

In particular, without dwelling too much on the lack of usefulness of this approach in the management of TMDs – its limits have been widely described in extensive literature reviews and are due above all to the absence of a relationship between the levels of masticatory muscle electromyographic activity and the presence of clinical symptoms (50,51) – the myocentric position can prove to be a misleading reference even in the simple planning stage of an extensive prosthetic rehabilitation.

This affirmation is based on several demonstrations that the muscles are active even in the postural position and that a mandibular rest position, namely the myocentric position, identified by the absence of EMG activity, is associated with an increase in vertical dimension, sometimes in the order of as much as 10 mm (52).

Even though it has also been underlined that the postural position and the EMG rest position are to be considered two distinct entities (53), it is a common clinical observation that rehabilitations based on electromyographic identification of the “therapeutic” position are characterised by an increase in the occlusal vertical dimension compared with the usual one.

The physiopathological significance of this increase, which can nevertheless sometimes be exploited to useful ends, deserves to be discussed in the light of the most recent considerations on the clinical importance of the occlusal vertical dimension.

IS THERE AN IDEAL VERTICAL DIMENSION AND IDEAL OCCLUSION?

For decades, the occlusal vertical dimension (OVD), which may be defined as the distance measured between two points on the face when the teeth are in occlusion (43), has been considered a fundamental parameter in the planning of extensive dental restorations.

Initially a static relation, the OVD is determined by the interaction of an individual’s genetic potential for craniofacial tissue growth with environmental factors and with the dynamic development of neuromuscular function during skeletal growth. Its maintenance is linked, more than anything, to the interaction of the latter two factors during ageing. Interindividual variability of the OVD is attributable mainly to facial morphology, growth and dental morphology (54).

In particular, contrary to what is commonly believed, even the most severe cases of vertical dental wear do not seem to be associated with considerable loss of vertical dimension, thanks to the process of continuous eruption which compensates, albeit sometimes only in part, for the loss of tooth substance (55).

Over the years, many different methods for accurately determining vertical dimension have been proposed, using mathematical calculations involving proportions between measurements of the face (56), phonetic techniques (57), mechanical or electronic instruments (58), and presumed physiological approaches (59), but none has emerged as unequivocally superior to the others; indeed, during pre-prosthetic planning, the established practice is to take the pre-existing vertical dimension as the reference (60).

These considerations notwithstanding, there is little doubt that, in daily clinical practice, increasing the OVD slightly in patients with extremely worn dentition (61) or with masticatory muscle or TMJ pain, in the latter case by means of occlusal splints (62), can sometimes be indicated.

When teeth are very badly worn, as in patients affected by severe forms of nocturnal tooth grinding (Fig. 7.8a), it is very often necessary to increase the OVD for prosthetic reasons, mainly related to the patient’s insufficient interarch space or special aesthetic needs.

This approach can be adopted without hesitation, given that in asymptomatic subjects, who are often the ones that present with bruxism-related tooth wear (63), problems adapting to the new OVD are very unlikely to occur (Fig. 7.8b).

In patients who, instead, do have TMD symptoms, temporarily increasing the OVD by means of occlusal splints worn 24 hours a day can have real benefits, bringing relief of both muscle and joint pain (Fig. 7.9).

Indeed, contrary to what was believed until a few years ago, i.e., that occlusal splints do not offer biological advantages but are merely a sort of “crutch” and a source of psychological support for patients with TMDs (64), it has recently been hypothesised that the improvement in symptoms obtained using occlusal splints may be due to objective and not just subjective benefits (20).

Indeed, there is some experimental evidence supporting the hypothesis that occlusal splints, by increasing OVDs and modifying the relations between the joint components, can favour a reorganisation of muscle fibre recruitment patterns (65) and a shift in the area of highest loading of the joint (66). These effects, obtained largely simply through occlusal lifting (Fig.s 7.10a-b), can explain a series of frequent clinical observations, for example:

1. Moderate increases in the OVD are well tolerated by the healthy masticatory system and are often even perceived as functional improvements (67);
2. Different types of occlusal splint, often fabricated to achieve different objectives, seem to show comparable success rates in the management of TMD (68);
3. The clinical efficacy of occlusal splints created according to theories with no scientific basis (e.g. neuromuscular orthotic appliances) is similar to that of other types of splint (69).

In view of these considerations, it seems clear that, even in these times of evidence-based medicine, numerous aspects of topics “central” to many branches of dentistry still remain to be clarified, such as, indeed, centric relation and the occlusal vertical dimension.

However, for the moment, the best approach to occlusion seems to be, also in the prosthetic field, that of low-tech, conservative methods that are as simple as possible, as has already been underlined in relation to the management of TMDs (18).

GUIDELINES FOR “TMD-SAFE” PROSTHETIC IMPLANT REHABILITATIONS

Obviously, the earlier remarks about the need to minimise the importance of assessing occlusion in the context of TMD and orofacial pain do not give us licence to ignore or avoid assessing this aspect in the planning and execution of prosthetic or prosthetic implant work (70).

Indeed, even though the stomatognathic system has remarkable capacities of adaptation and accommodation (71), the potential risk of iatrogenically provoked TMD symptoms arising in the wake of extensive rehabilitations nevertheless remains.

The rare cases in which this happens are those in which the position of the condyle and the usual OVD of a healthy individual are not respected and, also, are modified beyond the system’s tolerance threshold.

Any repositioning planned on the basis of some preconceived idea of “normal” relations between the components of the stomatognathic system can, potentially, backfire, especially considering that there exists no way of predicting how the system might react (72).

Therefore, as a general rule, modifications should be carried out only for valid prosthetic reasons, as occurs in orthodontics and orthognathic surgery (73); furthermore, the extent of these modifications should be kept to the minimum and they should be performed over a longer period of time (Fig. 7.11).

On the basis of these considerations, there seem to emerge at least two potential risk situations: 1. Rehabilitations that hinge on a rest position identified by the absence of EMG activity, given the considerable increase in OVD that can sometimes be required in these cases; 2. Full-arch restorations with immediate loading, on account of the fact that these solutions allow the system very little time to adapt to the possible new position, or even no time at all in the case of some protocols in which the definitive prosthesis is delivered directly, without a provisional one. In the first case, there can emerge, for example, paradoxical situations of anterior open bite following rehabilitation of the four quadrants (Fig. 7.12), while in the second, OVD or centric relation errors may not be clearly apparent on a first clinical inspection.

The clinical symptom that characterises these situations is the onset, sometimes immediate and sometimes more delayed, of pain in the temporal area; this may be described by the patient as a feeling of oppressive tension, or it may be detectable by muscle palpation (Fig. 7.13). In such cases, an initial, conservative approach could be to submit the patient to a course of treatment with myorelaxant drugs (74), although in many cases it is necessary to remake the prosthesis.

As far as the occlusal design is concerned, there are very few grounds for believing that one particular design is superior to others in preventing the onset of TMD symptoms (22). There are, of course, certain characteristics, such as, for example, the need for bilateral distribution of the posterior contacts, whose importance to dental stability and the patient’s subjective comfort are supported by evidence derived from clinical research. In the absence of such evidence, the most accepted and best rules of clinical practice currently available indicate simply that the dental prosthesis should satisfy the patient’s priorities and expectations as regards his/her dental and facial anatomy (72). The clinical view that certain occlusal schemes (primarily, maximum intercuspation in retruded condyle position; canine guide) are indicated in order to optimise function and prevent the onset of clinical symptoms have never been scientifically demonstrated (75). The literature data, as a whole, seem to suggest that somatosensory information plays an important role in the control of all mandibular movements, and that this information is used by the mandibular motor system to learn new tasks and adapt to occlusal modifications (76). Therefore, thanks to the neuroplasticity of the motor control system, relatively small occlusal modifications are well accomodated without resulting in clinical symptoms or imbalances (77). It is interesting to note that this neuroplasticity provides a basis for explaining the fact that different occlusal schemes (different protrusive guides; different types of antagonistic contacts; different characteristics of contacts in centric occlusion; different CR-MI position relations) are all enthusiastically extolled by their proponents and, in fact, are similarly able to optimise function (Fig. 7.14) (78,79).

In conclusion, a prosthetic implant rehabilitation that optimises function and is “TMD-safe” must reflect a few simple principles, summarised in Box 7.3.

PROSTHETIC IMPLANTS IN PATIENTS WITH TMD

In routine clinical practice, it is not uncommon to be asked to perform prosthetic or prosthetic implant rehabilitations in patients with signs and/or symptoms of TMD.

Since, as explained in the section on occlusion and TMDs, neither the literature nor clinical observations support the hypothesis that an irreversible occlusal treatment can be considered the standard approach to the treatment of TMDs, and given that there exists a high risk of planning errors when defining the usual occlusion of a patient with musculoskeletal pain, it is fundamental to manage the TMD-related symptoms before performing any definitive occlusal intervention (80).

In particular, the presence of TMJ and/or masticatory muscle pain and a limited range of joint movement must be considered absolute contraindications to prosthetic implant treatments and to the definitive modification of a patient’s occlusal schemes.

Instead, the presence of clinical signs, such as “click” sounds that indicate anterior displacement of the articular disc from its normal position in relation to the condyle (Fig. 7.15), do not per se constitute contraindications to occlusal rehabilitations, even though such conditions should be considered to warrant specialist investigation.

Parafunctional subjects, too often generically referred to as “bruxers”, should also be carefully assessed in an attempt to distinguish between grinding and clenching activities.

Indeed these two activities, quite apart from having different aetiopathogenetic substrates (81,82), undoubtedly have different effects on the components of the stomatognathic system (83).

In the case of prosthetic implant rehabilitations, the complications relating to grinding activities concern only technical-mechanical aspects (prosthetic implant materials and components) (84), whereas clenching activities can be associated with the appearance of masticatory muscle and/or TMJ fatigue and pain (85), which can be aggravated in cases in which the rehabilitation considerably modifies the occlusal pattern (86). All these aspects considered, there exist numerous approaches to the management of TMD symptoms.

The key concept to underline is the fact that TMDs must be considered from a medical and not just a purely dental perspective.

In other words, TMDs are not occlusal disorders, but rather musculo-skeletal disorders whose clinical signs and symptoms need to be managed in line with the standards followed for similar disorders in other specialist settings (e.g. in rheumatological, physical medicine and orthopaedic settings) and, in the most severe cases, with support from other specialists for the management of chronic pain (e.g. neurologists, psychiatrists, psychologists) (87).

The treatment of TMDs is based on the use of reversible and conservative therapeutic methods, the most frequently used being physiotherapy, pharmacotherapy, cognitive-behavioural therapy and occlusal splints (17).

Even though only a very small minority of patients require surgical correction, there now also exist temporomandibular joint replacement prostheses, which have given encouraging results (88).

As regards treatments designed to relieve pain in patients with inflammatory-degenerative disorders of the TMJ, or to increase the range of joint motion in patients with acute closed lock of the TMJ, the recent literature supports the efficacy, in the medium- to long-term, of arthrocentesis (or wash out) of the joint, followed by injections of medications such as cortisone or hyaluronic acid (89-91), also performed using an innovative single-needle technique (92) (Fig. 7.16).

Individuals affected by TMDs display hypervigilance to many events and stressors, both local and systemic (93).

This hypervigilance plays a very important role both in the onset and in the maintenance of the symptoms, and it manifests itself as increased sensitivity to stress (94) and as an increased tendency to respond abnormally even to non-nociceptive stimuli (95).

This characteristic explains the results of the study mentioned earlier in which the placement of acute occlusal interferences resulted in the appearance of clinical symptoms in individuals with a history of TMDs, but not in a sample of healthy controls (36).

Thus, even though occlusion is not a key factor in the aetiopathogenesis of TMDs, clinical experience nevertheless shows that patients with a history of TMDs have an extremely delicate stomatognathic equilibrium and can be hypersensitive to occlusal scheme modifications.

This observation provides further justification for minimising the importance of occlusion as a therapeutic target and for advocating simple rehabilitation schemes that do not grossly alter the previous occlusal status, in order to prevent patients from developing occlusal hypervigilance (i.e. from focusing excessively on their occlusion) (96,97).

CONCLUSIONS

The relationship, if one exists, between TMDs and rehabilitations using prosthetic implants does not seem to differ, in any aspect, from the relationship between TMDs and any procedure that intervenes on the dental occlusion. In short, the literature evidence is sufficient to allow a series of conclusions to be drawn:

• TMDs are not occlusal disorders and therefore should not be treated with extensive occlusal rehabilitation interventions.
• Because the stomatognathic system has such a remarkable capacity for accommodation, its adaptability, in most clinical situations, is guaranteed.
• There is no such thing as the ideal articular position or ideal occlusal design, superior to all the others and valid for every single individual; for this reason, it is best to follow the rule “simple is best”, avoiding the use of preconceived and “forced” or artificial rehabilitation protocols.
• Prosthetic implant procedures give rise to clinical symptoms but only if their execution repeatedly and considerably modifies the patient’s usual occlusal scheme.
• The clinical symptoms of individuals with TMDs who require or request rehabilitation with prosthetic implant procedures for prosthetic, aesthetic or functional reasons must be carefully managed using internationally accepted approaches (e.g. occlusal splints, physiotherapy, pharmacotherapy, injections); moreover, definitive rehabilitation can only be undertaken after a symptom-free period.

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CHAPTER 8

BRUXISM AS A RISK FACTOR IN IMPLANT PROSTHETICS

Daniele Manfredini

Visiting professor, Department of Maxillofacial Surgery, University of Padua

 

The American Academy of Sleep Medicine defines bruxism as a stereotyped oral motor disorder characterised by sleep-related grinding and/or clenching of the teeth (1), while the American Academy of Orofacial Pain has extended the definition to the presence of the same characteristics during wakefulness (2). Of all the parafunctional activities of the stomatognathic system, bruxism is considered the most detrimental, causing tooth wear and representing a potential risk factor for the appearance of signs and symptoms of temporomandibular disorders (TMD) (3). Even though bruxism has major clinical consequences, a discussion on its role in the different branches of dentistry must first seek to clarify certain complex aspects of its aetiology.

Indeed, the aetiology of bruxism is undoubtedly an extremely complex and controversial topic. Most authors agree that it is a disorder of central origin, as shown by many literature reviews which reveal a tendency to attach less importance to the role of peripheral (e.g. occlusal) factors, and more to central ones (e.g. arousal responses, stress, anxiety, temperamental traits) (4-9). Only a small proportion of the most recent studies (around 10%) explore the role of morphological factors in the aetiology of bruxism, while a slightly higher proportion (around 20%) focus on the role of psychosocial factors. The vast majority of studies (around 70%), however, consider the role of potential aetiological factors classifiable as pathophysiological (10). These percentages confirm the trends commonly observed in the research setting, where attention is turning away from the role of occlusion and increasing importance is being attached to biomedical and biopsychosocial models. Psychosocial factors can play a role in the aetiopathogenesis of bruxism, to varying degrees in different forms of grinding or clenching occurring in the different stages of the sleep-wake cycle (11-13) (Box 8.1), while occlusal interferences have not been found to show a significant association with the presence of bruxism (14) (Table 8.1); at most, the placement of acute occlusal interferences can constitute a stimulus capable of triggering parafunctional activity in subjects with occlusal hypervigilance (15) (Fig. 8.1).

 

 

Over the years, in efforts to synthesise knowledge of this topic, various aetiological theories have been proposed.

At present, the most plausible explanation of the aetiopathogenesis of bruxism hypothesises the existence of a multifactorial model in which psychosocial and pathophysiological factors interact with peripheral morphological stimuli (16-18).

In short, one or more factors (stress, anxiety, genetics, neurochemical factors, arousal response, deficits in dopaminergic transmission, factors linked to the quality of sleep, oral and dental anatomy) may, in different ways and to different degrees, contribute to increasing the frequency, duration and intensity of normal masticatory muscle activity during sleep, in accordance with the “bruxism generator model” (19).

While this hypothesis fits perfectly into a context of a multifactorial aetiology of bruxism, there nevertheless remain many aspects to be clarified as regards the weight of the various factors in the different forms.

Indeed, study of the aetiology of bruxism is complicated by the existence of diagnostic framing difficulties that have always constituted an obstacle to research in this field.

At the current state of knowledge, it seems fairly apparent that the pathogenesis of sleep bruxism is different from that of bruxism during wakefulness (12), but it is difficult to distinguish between the two conditions clinically (20).

Similarly, there is a need for a clearer distinction between objectively diagnosed bruxism and subjective, patient-reported bruxism, as the latter is liable to be over-diagnosed as a result of preconceived ideas, on the part of either the patient or the examining physician (21).

Currently, polysomnographic recording (PSG) is considered the gold standard for the diagnosis of sleep bruxism, but the use of this technique is limited by the high costs involved and the shortage of adequately equipped sleep laboratories (22).

For this reason, a number of diagnostic hypotheses based on electromyographic recording of masticatory muscle activity during sleep have recently been advanced (23,24), even though it will not be possible to collect data of real clinical value until we have portable EMG devices able to record the nocturnal activity of various muscle groups, and not just that of the masseter muscles (25).

Therefore, at present, the clinical approach to the diagnosis of bruxism, albeit incomplete and lacking the ability to distinguish between the different forms of the disorder, continues to be the simplest assessment and data collection method available, and the most widespread.

THE CLINICAL DIAGNOSIS OF BRUXISM

The literature proposes various methods of diagnosing bruxism (Box 8.2).

However, given that, for the reasons already given, both prolonged (hours-long) electromyography of the masseter muscles and PSG are unsuitable for routine use, clinical assessment, combined with the use of questionnaires, remains the best of the diagnostic options currently available to the clinician for identifying bruxers.

Because questionnaires, even though many different types have been proposed, generally do not provide sufficient diagnostic accuracy, their use without integrated objective approaches is not recommended (20).

The many different questionnaires constructed in order to detect bruxist activity are all based on a series of common questions (e.g. Does your partner say that you tend to grind your teeth loudly at night? Do you have a sensation of pain and/or tenderness in your jaw muscles on awakening? Do you ever wake up at night aware that you are clenching your teeth? Do you ever have tooth or gum pain on awakening? During the day, do you tend to contract your jaw muscles, clenching your teeth? Do you ever grind your teeth during the daytime?); the limitation of such instruments, however, is the subjective nature of the responses, and thus of the “diagnosis”.

Furthermore, the few studies that have attempted to quantify the diagnostic validity of questionnaires as a means of diagnosing bruxism, while producing generally encouraging results, lack methodological rigour, failing to include “control” assessments conducted using reference standards (e.g. PSG, EMG) (27,28).

These questions, also commonly used during clinical history-taking, are based on a few preconceptions that become sources of bias in the clinical and research settings.

For example, many of the questions are based on the assumptions that bruxist activity produces muscle pain/tenderness and/or manifests itself through sounds caused by tooth-grinding.

The literature has shown that neither of these assumptions is necessarily true and thus that their use as the basis for the formulation of diagnostic criteria will result in a low positive predictive value.

Indeed, the association between bruxism and muscle, tooth or gum pain is much more complex than was believed in the past, given that the proportion of bruxers who develop pain is smaller than that of bruxers who do not (3,29,30).

Similarly, individuals whose nocturnal tooth-grinding is so loud that they wake themselves or their bed partner usually account for only a small proportion of the complex category of subjects with “bruxism behaviour”, given that at least 80% of episodes of bruxism do not produce noise, i.e. are clenching activities (19).

For years, the use of self-report diagnostic instruments based on the above questions fed the belief that bruxism is associated with muscle pain (31).

In actual fact, the results of many literature studies that describe a strong association between bruxism and myofascial pain were probably influenced by the fact that the presence of muscle pain was considered a potential diagnostic criterion for bruxism (32).

Indeed, experimental attempts to reproduce bruxism-induced muscle pain have failed to confirm the existence of an unequivocal cause-effect relationship between prolonged bruxist activity and myofascial pain (33,34), to the point that the time is now ripe for a careful review of the literature on this topic (3).

Clinicians’ convictions constitute a further potential source of bias in the clinical-anamnestic assessment of bruxism: when a clinician believes a patient to be a bruxer, the likelihood of that same patient replying affirmatively to the above questions has been found to be increased, regardless of how the questions are presented: in the form of a self-report questionnaire or during history-taking (35).

In view of all these considerations, it is clearly fundamental that any information furnished by patients be supplemented with the results of objective examinations able to detect the presence of bruxist activities.

Tooth wear has always been considered the clinical hallmark of bruxism (36).

In truth, tooth wear, which is linked to functional activities (e.g. mastication) and parafunctional activities (e.g. bruxism, nail-biting, chewing of objects), is due to a combination of phenomena – abrasion, erosion and friction – which are conditioned by jaw movement patterns (e.g. laterotrusion and protrusion guides) and external factors, such as diet (e.g. consumption of soft or acid drinks) and concomitant disorders (e.g. gastric reflux, eating behaviour disorders) (37).

The literature proposes numerous systems for quantifying and objectively evaluating tooth wear, as well as assessment schemes aiming to identify the wear facets associated with different jaw movements (Fig. 8.2).

The most widely used classification systems, apart from the seminal one by Murphy (38), which, being shown to be reliable, has stood the test of time (39), include the ones proposed by Johansson et al., who, in a series of studies, produced a scale of tooth wear severity, separately considering the different surfaces of the anterior teeth and the occlusal/incisal surface (40,41), by Ekfeldt et al., who attempted to introduce an individual tooth wear index, independent of the number of missing teeth (42), and by Seligman and Pullinger, who described different patterns of tooth wear associated with different jaw movements (43) (Box 8.3).

 

Despite the existence of criteria for evaluating tooth wear objectively, in daily clinical practice it is very difficult to discriminate between the different possible causes and, above all, to differentiate between functional and parafunctional wear (Fig.s 8.3-8.5).

 

 

Moreover, another criticism often levelled at tooth wear-based bruxism assessment systems is the impossibility of determining whether the bruxism itself is still present, in other words, of establishing whether the signs of wear are due to previous or ongoing parafunctional activity.

In some cases, other clinical signs indicating bruxist activities may be present; in particular, there may be evidence of tongue scalloping (Fig. 8.6) or of marked masseter muscle hypertrophy (Fig. 8.7).

 

In the first case, the presence, usually bilateral, of the characteristic indentations on the tongue may be due to a “conscious” parafunctional habit on the part of the patient, who may report a tendency to chew his tongue, rather in the way some people tend to chew objects, or bite their lips or nails. Tongue scalloping is certainly a sign to be noted in a patient’s clinical records and its aetiopathogenesis should be determined through patient interview (44). As regards masseter muscle hypertrophy, the literature contains descriptions of interesting cases in which the increased muscle volume, sometimes also seen in the temporal muscles, was considered to be related to bruxism (45,46).

From a strictly pathogenetic point of view, masseter muscle hypertrophy can be considered a consequence of static clenching, which is characterised by isometric muscle activity that, if protracted for long periods of time (e.g. for many hours a day, in some cases for years), can have a training-type effect and thus result in increased muscle volume. It is also worth underlining that the effects of clenching may potentially differ according to the individual’s facial morphology, since it has been found that the subjects who develop muscle hypertrophy tend to have a brachycephalic facial type (25).

In accordance with the typical clinical observations of those involved in the management of bruxers (observations supported by an ever-increasing body of scientific evidence), occlusal splints are currently the best assessment instrument clinicians have for diagnosing the presence of parafunctional habits.

The assessment itself, which in research settings can also involve measuring the intensity and direction of forces transmitted to a splint during a parafunctional activity (47,48), consists of observation of the wear facets that appear on the splint itself in the weeks following its application (49). In most cases, splint wear, when present, is aspecific and does not make it possible to distinguish between clenching and grinding activities, even though the wear pattern can sometimes be so peculiar as to leave little doubt as to the type of mandibular movement involved (Fig. 8.8).

In short, diagnosing the presence and severity of bruxism continues to be a highly complex clinical problem, and the clinical classifications proposed to date inevitably reflect the limitations of what is still an exclusively clinical-anamnestic approach. At the same time, the paucity of data so far gathered in research settings suggests that electronic methods for achieving standardised measurement of bruxism will not be available on a large scale in the near future. This is despite the existence of a practical need in many dental specialties, primarily implant prosthetics, to quantify the intensity and direction of parafunctional activities.

BRUXISM AND IMPLANTOLOGY

In many specialist texts, bruxism is referred to as a risk factor capable of jeopardising the successful outcome of a rehabilitation based on prosthetic implants (50).

Few studies in the literature seek to clarify the relationship between bruxism and implants: indeed, the only experimental study conducted concludes that a prosthetic implant rehabilitation does not increase the severity of bruxism (51); indeed, all the suggestions advanced in this field seem to be based on expert opinion rather than on scientific evidence (52).

The caution that is urged when using prosthetic implants in bruxers is due to the common fear that bruxism can cause overloading and may lead to implant failure.

This aspect is, therefore, worth considering in more depth, also in the light of the ways in which the bone-dental implant interface differs from the bone-natural tooth one.

Since the periodontal ligament has a certain amount of give, it allows the tooth a degree of mobility within the tooth socket, quantified as 25-100 μm in the apical-coronal and 56-108 μm in the vestibular-lingual direction (50)

In normally-supported dentition, occlusal overloading due to the introduction of a premature occlusal contact leads to compressive trauma in the area subjected to greatest pressure.

This causes thickening of the periodontal ligament and increased tooth mobility, without loss of attachment in the apical direction.

Whereas in normal conditions this process is completely reversible, in the presence of periodontal disease it can lead to irreversible loss of bone support around the teeth (53).

Compared with natural teeth, implants are fixed much more rigidly to bone tissue, having a maximum mobility of 3-5 μm in the apical-coronal and 10-50 μm in the vestibular-lingual direction; for this reason, unlike the tooth-periodontium interface, they lack the ability to adapt reversibly to different loading conditions (54).

During normal functional loading, bone homeostasis is maintained through a continuous process of bone resorption and apposition of new bone.

Literature descriptions of peri-implant tissue responses to occlusal overloading are not unequivocal, and the most plausible hypothesis so far advanced to explain the possible progressive loss of bone at cervical level in response to excessive overloading is that of fatigue micro-damage resulting in bone resorption (55).

It is suggested that when microtissue damage exceeds the capacity for repair there is an irreversible loss of bone support.

Most of these data derive from studies on animal models of occlusal interference, which also allow us to formulate several considerations relating to bruxism-induced overloading (56).

Animal studies suggest that dynamic overloading, as occurs during tooth-grinding for example, leads to angular bone loss (56).

The eccentric horizontal forces that characterise occlusal loading during tooth-grinding could thus be considered a risk factor for biological implant failure (57).

This affirmation is based on the best evidence currently available, provided by studies of masticatory load distribution in different types of prosthetic implant rehabilitation, which suggest that the maximum forces applied to implants during functional loading can reach bending moments of 90Nmm in the vestibular-lingual direction and even 170Nmm in the opposite direction (58).

Consequently, the forces developed during unconscious activities, like sleep bruxism, and moreover in individuals, such as those with implants, who have reduced proprioception (59), reach levels of intensity so great as to constitute a real risk factor, also – perhaps mainly – because of biomechanical complications (52).

However, these suppositions notwithstanding, the current evidence for a cause-effect relationship between bruxism and implant failure is not high-level evidence.

There exist few prospective studies in which bruxism has been evaluated as a risk factor in implanted patients monitored over long periods of time, and the majority of studies examined in the most reliable literature review currently available were retrospective studies with various sources of bias and confounders (57).

In what is, to date, the longest prospective study to include bruxism among the factors evaluated – it lasted 15 years –, clenching was not found to be related either to loss of bone support or to problems with dental implant superstructures (60).

Instead, other studies, including one by the authors of the previous trial, have produced contrasting results, reporting for example, a greater frequency of biomechanical complications (60% vs 20% at five years) and implant failures (41% vs 12% at one year) in bruxers compared with non-bruxers (61-63).

Therefore, the literature provides conflicting data on the relationship between bruxism and implant failures, a situation that is not improved even by attempts to apply the criteria deemed necessary to demonstrate a cause-effect relationship (Box 8.4).