Dr. Moez I. Khakiani, Prosthodontist, MIK Dental, Mumbai, India
Vol-15 Issue-03, Feb-Mar 2022
This article is a direct extract from the book by Dr. Moez Khakiani, titled Clinical Fixed Prosthodontics- Master Volume. It is a color atlas suited for clinicians who wish to expand their horizons in advanced prosthodontics. It has over 400, pages, and over 2500 color illustrations distributed over 25 chapters. It is a MUST-HAVE guide for clinical prosthodontics, including chapters like master level occlusion, full mouth rehabilitation, porcelain veneers, table top prostheses, implant dentistry, digital dentistry, etc.
Why don’t you give this book a try?
It is available for preview and purchase on www.mikdental.in, or you could connect on +91 9833400664 for the same.
The term ‘functional anatomy’ emphasizes that each aspect of the human body is specifically designed to fulfil a definite function. As function determines form, any change in functional demand can bring about an alteration in functional anatomy. Accordingly, the unworn dentition is best designed to achieve effortless mastication.
However, when unnatural stresses induced by pathofunction set in, the resultant overstrain within the system can bring about a forced alteration in the occlusal design, typically resulting in wear, fracture or mobility. Such changes have undesirable influences on functional efficiency. This means, the patient is unable to masticate food as efficiently as before. This forces him/her to exert greater forces, increase the number of chewing strokes and even move the mandible beyond its normal functional envelope in order to crush and grind food.
With time, as the patient continues to indulge in non-physiologic movements, the occlusal and incisal form worsens further. Eventually, a cyclic chain of ‘dysfunction related wear’ and ‘wear aggravated dysfunction’ sets in, leaving the patient a dental cripple, necessitating a full mouth reconstruction to restore its lost form.
Fig. 7.1: The vicious cycle of dysfunction
Patients and often clinicians are apprehensive towards undertaking full mouth reconstructions, owing to:
- The innate complexity and irreversible nature of treatment involved,
- The relatively long duration of treatment, and
- The expensive nature of such rehabilitations.
However, full mouth prosthetic treatments can be accomplished with predictable success, provided both, the patient and the clinician are committed towards it. Fortunately, full mouth rehabilitations can be rendered to patients in multiple different forms:
- Definitive reconstruction using porcelain, which is often regarded as the ideal choice,
- Provisional reconstruction using composite resins, which work best as a time and cost effective interim option, and
- Permissive splint therapy, which can be resorted to as a preventive option for patients who cannot afford treatment due to financial, time, age and/or health related issues.
As explained earlier, the entire full mouth rehabilitation segment is discussed in a Q-n-A format. So let us start the introduction chapter by addressing some common questions and then build towards more pertinent topics related to tooth supported full mouth reconstructions.
IS TOOTH WEAR PHYSIOLOGIC?
This may seem too basic, but a mention here is noteworthy for sequencing the thought process.
All teeth undergo some degree of wear and so in a strict sense, wear is physiologic.
Fig. 7.2: Loss of mamelons is an example of physiologic wear under functional load. Image courtesy Dr. Mayur Davda, Mumbai, India.
Anatomically, teeth are designed to resist aggressive wear. Cusp tips for posterior teeth have a dome shaped architecture (regarded as the most resistant geometric design), that allows natural wear to occur without the fear of premature dentin exposure. Additionally, functional surfaces of teeth have a thicker enamel cover, which further protects them from pathologic wear.
However, wear is not just restricted to functional surfaces and can also be seen on proximal areas in the form of widened inter-proximal contacts. This is the result of vertical and bucco-lingual friction between adjacent teeth under the influence of PDL elasticity.
Hence, physiologic wear does not only result in shortening of tooth height, but also causes narrowing of tooth width. Fortunately, nominal loss of enamel does not pose any threat to the stomatognathic system, as two ever present adaptive processes help offset the effects of wear. These are:
- Vertical eruption of teeth to maintain antagonist tooth contact, and
- Mesial drifting of teeth to accommodate for proximal wear.
When analyzing dentitions, a distinction needs to be made between physiologic and pathologic wear on the basis of the patient’s age, symptoms, habit patterns, etc.
- Is associated with gradual loss of convexity (flattening) of cusp tips under the influence of functional masticatory forces.
- It results in some wear facets which are minimal in surface coverage and produce no symptoms.
- It never results in pre-mature dentin exposure and deterioration of the dentition.
- It requires no corrective treatment.
- Literature suggests that wear is acceptable if it occurs at the rate of < 1 mm/century. No wonder, teeth outlast the body.
Fig. 7.3: Teeth showing minimal loss of enamel, which is physiologic for a 67 year old individual
- Is associated with substantial loss of enamel and pre-mature exposure of dentin under the influence of dysfunctional or parafunctional forces.
- Tooth loss is associated with sensitivity and/or pain.
- Wear can progress so rapidly that secondary dentin formation fails to keep pace with it and in extreme cases can lead to pulpal exposure (most commonly seen with lower incisors).
- Corrective intervention is essential to prevent further breakdown and restore the altered form and function.
Fig. 7.4: Loss of complete occlusal anatomy and exposure of dentin leaving the tooth susceptible to premature breakdown in this 43 year old patient.
Tooth wear associated with coarse food habits was regarded as the most common cause of tooth loss amongst the prehistoric population.
Fig. 7.5: Mandible of prehistoric men showing severe tooth wear from coarse dietary habits.
Although such abrasive food habits are no longer present, new risk factors have emerged. The modern lifestyle, with its associated increase in consumption of refined foods, acidic colas, increased stress levels, greater prevalence of systemic illness, compromised sleep cycles, etc. have once again resulted in a steady rise in the incidence of pathologic or accelerated tooth wear.
Thus prior to treating wear, it is important to first gain insight into what possibly caused the current level of destruction, such that necessary management strategies can be formulated to overcome the aetiology. Hence, an understanding of the different causes of tooth loss is in order.
WHAT ARE THE BASIC MECHANISMS FOR TOOTH SURFACE DEFORMATION?
Deformation, loss or wasting of tooth material results from three basic mechanisms:
Stress, that produces micro fractures, cracks and abfractions,
Friction, that produces wear, and
Corrosion, which produces chemical degradation.
Although stress related occlusal overload is considered the more dominant factor for tooth loss, most surface deformations are cumulative in aetiology, as causative mechanisms often overlap and accelerate the breakdown process.
Tooth material loss in dental terminology is referred to as:
Attrition, where wasting of tooth surface is caused by tooth-totooth friction, e.g. empty mouth pathofunction.
Fig. 7.6: Attrited dentition caused by dysfunctional mandibular movements
Abrasion, where deformation of tooth surface is caused by tooth-to- exogenous agent friction, e.g. tobacco chewing, faulty brushing, improper use of floss, toothpicks, pencils, pins or any foreign object. Wear patterns caused by abrasion can sometimes be extremely confusing, ranging from shallow saucers to deep V shaped defects.
Fig. 7.7: Gross abrasion defects seen in a chronic tobacco chewer with verzealous brushing
Erosion, where loss of tooth surface is caused by chemical action, resulting in cupping or cratering defects.
Erosion can be of two sub-types:
Endogenous erosion, where the chemical agent comes from within the body, e.g. Bulimia nervosa, Gastroesophageal reflux disease, etc. Besides, gingival crevicular fluid also has an acidic pH and can be a cause for erosive loss in patients with cervical lesions.
Fig. 7.8: Erosion on upper anterior teeth caused by frequent vomiting. Note the characteristic loss of enamel along the palatal face on anterior teeth.
Exogenous erosion, where the chemical agent comes from outside the body. Any food or liquid with a pH of less than 5.5 can demineralize teeth, e.g. carbonated drinks, vitamin C tablets, acidic drugs, etc.
Fig. 7.9: Labial erosion on central incisors is characteristic of an exogenous source. This patient had a habit of cola consumption on a daily basis for over 10 years.
Abfraction, where tooth surface breakdown is caused by tensile stresses from bending of teeth under non-axial forces. Such flexure of teeth produces microfractures and structural loss along the cervical area. With time, acid penetrates these microcracks and chips of enamel break away, leaving wedge-shaped lesions with sharp internal line angles.
Fig. 7.10: Multiple abfractions caused by a pathologic occlusion.
HOW TO DIFFERENTIATE BETWEEN ATTRITION, ABRASION AND EROSION CLINICALLY?
Although a combination of aetiologies are usually involved, it is possible in most cases to identify the major causative factor. The pattern of tooth loss can help differentiate between the three primary causes of tooth deformation.
The rule is, if worn surfaces can be contacted during centric closure or along any excursive movements, the cause is tooth-to-tooth friction, i.e. attrition.
Fig. 7.11: Note the attrited surfaces match each other (like a hand-in-glove) during translatory movement.
On the other hand, if worn surfaces cannot be contacted by opposing teeth, the cause is either abrasive wear or erosive breakdown. While abrasion produces smooth wear patterns, erosion typically results in cupping or cratering type defects with sharp unsupported enamel edges, which can help differentiate between the two. However, the final diagnosis should always be correlated with patient history.
Fig. 7.12: Active erosion evident from the cupping defect on lower incisors.
While a clean shiny surface producing symptoms of hypersensitivity or pain points to an active stage of breakdown, the presence of stains along worn surfaces with a past history of discomfort suggests of an inactive or arrested phase of deterioration.
WHAT IS THE DIFFERENCE BETWEEN DYSFUNCTION AND PARAFUNCTION?
Occlusal dysfunction relates to attrition that is ‘triggered by interferences’. It is seen in patients with a definite CR-MIP discrepancy that produces occlusal wear. Fortunately, dysfunction related cases can be predictably managed via reconstructions that address the cause. Long term prognosis is good, as long as the condyles remain in CR and the occlusion stays mutually protected.
On the other hand, parafunction (true clenching or bruxism) is a far more serious condition, as attrition is caused by pathologic grinding that is ‘triggered by the brain’. These patients indulge in non-functional mandibular movements that levy excessive stress and strain on the system. Unfortunately, parafunction related wear cannot be predictably managed via reconstructions, as such patients continue to clench or brux on their porcelain prostheses, thereby increasing the risk of premature failure.
Parafunction induced bruxism presents one of the most difficult challenges in reconstructive dentistry, under the pretext, ‘what cannot be cured has to be endured’. Hence, an extended maintenance phase and ‘life-long night-time’ wear of a protective splint is mandatory for these patients.
HOW CAN DYSFUNCTION AND PARAFUNCTION BE DIFFERENTIATED CLINICALLY?
Clinical differentiation between dysfunction and parafunction is very important, as this has a direct impact on treatment strategies, post treatment care and overall case prognosis. Knowing the risks in advance can help us prepare better for possible prosthetic failures, and design a contingency plan for anticipated consequences.
The only certain way of differentiating between dysfunction and parafunction is via use of an acrylic splint or anterior deprogrammer worn by the patient over an extended period of time.
Patients who have dysfunction stop clenching or grinding on the appliance, as the aetiology i.e. occlusal interferences get temporarily eliminated. On the other hand, patients with parafunction continue to clench or brux on the splint, resulting in scratch marks or wear facets. Such a visual finding helps establish the role of higher centers of the brain as an aetiological factor towards the pathologic breakdown.
Some facts about parafunction
- Parafunction involves movements of the mandible that have no functional bearing,
- Most parafunctional habits are sub-conscious, spasmodic and involuntary in nature,
- They are often rhythmic and repetitive,
- Although most parafunction happens during sleep, it is not restricted to a specific diurnal pattern and can happen during wakeful hours as well,
- There is no ‘curative’ treatment to permanently eliminate parafunction,
- Patients with parafunction, continue to clench and brux even after full mouth reconstructions. The assumption that correction of the bite would reverse such bruxism does not hold true,
- However, harmonizing static occlusal contacts with centrically positioned condyles does help reduce the overload within the system, as it eliminates the trigger for incoordinated lateral pterygoid contraction,
- Similarly, strategic disclusion of posterior teeth eliminates potential overload in eccentric positions, as it reduces muscular activity during translation,
- Post-treatment maintenance with strategies that reduce the deleterious effects of forces are an essential part of managing patients with centrally mediated parafunction. Details of such modalities are listed in chapter 19, on page 436
- Parafunctional habits are not limited to bruxism or clenching, but also include nail biting, lip biting, tongue thrusting, etc.
Also refer to section titled, ‘What is the most challenging wear related case to restore prosthetically?’ on page 333 for further details on parafunction, its manifestations and implications on management.