Dental Hypotheses
Volume:1 Issue: 2, Apr-Jun 2010

Miller has primarily based his classification of gingival recession defects on two aspects: Extent of gingival recession defects and Extent of hard and soft tissue loss in interdental areas surrounding the gingival recession defects. Based on the above criteria Miller classified the gingival recession defects into four classes and also took prognosis into account. The prognosis decreases from class 1 to class 4 and the treatment options are also limited from class 1 having maximum treatment options and class 4 having minimum options for treatment.The hypothesis: At first glance classification looks comprehensive and simple to use but close screening points out some of the inherent drawbacks associated in this classification system. Since the ultimate goal of any classification system is to facilitate common standardized identification of the condition under consideration, aid in diagnosis and prognosis and thus finalizing an appropriate treatment plan for the condition; the present manuscript is an attempt to emphasize the need to modify Miller’s classification to make it more comprehensive and updated according to the recent concepts. Evaluation of the hypothesis: The hypothesis highlights some inherent drawbacks and necessary changes in Miller’s Classification system and emphasizes the need to update it.

There are more than a half of a billion people in the world who are disabled as a consequence of mental, physical and sensory impairments. The issues related to the care of individuals with disabilities increasingly will impact on the economic and social realities throughout the world as increased numbers of individuals with disabilities continue to survive; in particular, individuals with developmental disabilities and the burgeoning geriatric populations. The question considered is whether dentists are able and willing to provide needed services for patients with disabilities? The issues faced in the United States are used as examples in a commentary which reviews the barriers faced by dentists who would consider providing care to individuals with disabilities. Despite formidable obstacles, the fact is that many do provide needed care to many of these patients. The need is to expand the preparation of future dentists and augment the abilities of current practitioners.

To date, there is no evidence that conventional remineralization techniques using calcium and phosphate ioncontaining media will completely remineralize carious lesions in regions where remnant apatite seed crystallites are absent. Conversely, guided tissue remineralization using biomimetic analogs of dentin matrix proteins is successful in remineralizing thin layers of completely demineralized dentin. The hypothesis: Conventional remineralization strategy depends on epitaxial growth over existing apatite crystallites. If there are no or few crystallites, there will be no remineralization. Guided tissue remineralization uses biomimetic analogs of dentin matrix proteins to introduce sequestered amorphous calcium phosphate nanoprecursors into the internal water compartments of collagen fibrils. Attachment of templating analogs of matrix phosphoproteins to the collagen fibrils further guided the nucleation and growth of apatite crystallites within the fibril. Such a strategy is independent of apatite seed crystallites. Our hypothesis is that 250-300 microns thick artificial carious lesions can be completely remineralized in vitro by guide tissue remineralization but not by conventional remineralization techniques.Evaluation of the hypothesis: Validation of the hypothesis will address the critical barrier to progress in remineralization of cariesaffected dentin and shift existing paradigms by providing a novel method of remineralization based on a nanotechnology-based bottom- up approach. This will also generate important information to support the translation of the proof-of-concept biomimetic strategy into a clinically-relevant delivery system for remineralizing cariesaffected dentin created by micro-organisms in the oral cavity.

Dentin sialoprotein (DSP) is a dentin extracellular matrix protein, a unique marker of dentinogenesis and plays a vital role in odontoblast differentiation and dentin mineralization. Recently, studies have shown that DSP induces differentiation and mineralization of periodontal ligament stem cells and dental papilla mesenchymal cells in vitro and rescues dentin deficiency and increases enamel mineralization in animal models. The hypothesis: DSP as a nature therapeutic agent stimulates dental tissue repair by inducing endogenous dental pulp mesenchymal stem/progenitor cells into odontoblast-like cells to synthesize and to secrete dentin extracellular matrix forming new tertiary dentin as well as to regenerate a functional dentin-pulp complex. As DSP is a nature protein, and clinical procedure for DSP therapy is easy and simple, application of DSP may provide a new avenue for dentists with additional option for the treatment of substantially damaged vital teeth. Evaluation of the hypothesis: Dental caries is the most common dental disease. Deep caries and pulp exposure have been treated by various restorative materials with limited success. One promising approach is dental pulp stem/progenitor-based therapies to regenerate dentin-pulp complex and restore its functions by DSP induction in vivo.

The mechanism of the formation of apical cyst has been elusive. Several theories have long been proposed and discussed speculating how an apical cyst is developed and formed in the jaw bone resulting from endododontic infection. Two popular theories are the nutritional deficiency theory and the abscess theory. The nutritional deficiency theory assumes that the over proliferated epithelial cells will form a ball mass such that the cells in the center of the mass will be deprived of nutrition. The abscess theory postulates that when an abscess cavity is formed in connective tissue, epithelial cells proliferate and line the preexisting cavity because of their inherent tendency to cover exposed connective tissue surfaces. Based on the nature of epithelial cells and the epithelium, nutritional theory is a fairy tale, while abscess theory at best just indicates that abscess may be one of the factors that allows the stratified epithelium to form but not to explain a mechanism that makes the cyst to form. The hypothesis: Apical cyst formation is the result of proliferation of resting epithelial cells, due to inflammation, to a sufficient number such that they are able to form a polarized and stratified epithelial lining against dead tissues or foreign materials. These stratified epithelial lining expands along the dead tissue or foreign materials and eventually wrap around them as a spherical sac, i.e. a cyst. The space in the sac is considered the external environment separating the internal (tissue) environment – the natural function of epithelium. Evaluation of the hypothesis: This theory may be tested by introducing a biodegradable device able to slowly release epithelial cell mitogens in an in vivo environment implanted with epithelial cells next to a foreign object. This will allow the cells to continuously proliferate which may form a cystic sac wrapping around the foreign object.

Many associateship employment contracts in U.S. general dental practice, probably about 85% based on our review of over 100 contracts in the past decade, are silent about a key issue in associateships--namely, compensating associates for supervising dental hygiene production. Not addressing this issue raises ethical questions as well as concerns about professional liability regarding the supervision of dental hygiene. The associate and owner need to include in an employment agreement what compensation will be given to the associate for supervising dental hygiene production. Compensating associates for supervising dental hygiene production will certainly have a financial impact on the practice. However, directly addressing the issue will allow the owner to manage the financial impact on the practice while also providing a more mutually beneficial employment experience. The associate and owner-dentist need to discuss thoroughly and openly what compensation options are available, if any, to the associate for supervising dental hygiene production. In turn, these should be incorporated in an employment agreement. Five specific compensation strategies are suggested for managing this issue, ranging from production credit for periodic examinations fees and/or radiographs, to compensation for a set amount for each hygiene patient supervised, to profit-sharing based on a pro-rated basis of supervised hygiene production. Successful associateship arrangements, including those intended to lead to future practice buy-in or buy-outs, depend in large part of meeting mutual expectations of both parties. Compensating associates for supervising dental hygiene production is a seldom discussed but vitally important issue to manage.

There will almost always be gaps between cylindrical or screw shaped prefabricated implant surface and funnel-shaped tooth socket when an implant is placed immediately after tooth extraction. Hence expensive and difficult bone grafting is required. A custom fabricated implant will be a pragmatic solution for this limitation. The hypothesis: First step following extraction of a tooth is data capture or scanning via a 3D scan method e.g. coordinate measuring machine or non-contact laser scanners such as triangulation range finder. Second step is reconstruction or modeling via editable CAD (computer-aided design) model, allowing us to add retentive holes and correction of implant angle. Third step is fabrication via CAM (computer aided manufacturing) followed by plasma cleaning process. Fourth step is insertion of the CAD/CAM custom fabricated one-stage implant in the fresh tooth socket. Optimal time for this step is 24-48 hours after extraction. The custom fabricated implant should not load 3-4 months. Usage of chlorhexidine mouth-rinse or chewing gum twice daily for 2 weeks and, in some cases oral antibiotic is recommended. Evaluation of the hypothesis: Contemporary dental implant system faced with several clinical and anatomical limitations such is low sinuses or nerve bundles. Complex and expensive surgical procedures such as nerve repositioning and sinus lift are frequently required. With custom fabricated implant we can overcome several of these limitations because insertion of custom fabricated implant will perform before alveolar bone recession.

Blinding is one of the key design features of randomized clinical trials (RCTs). Studies not involving blinding could yield biased estimates of the effect of treatment. A meta-analysis found that doubleblind RCTs found 14% lower treatment effect on average than similar RCTs not described as double-blind. During past years many researchers have emphasized the need for more research in the area of blinding. For example, sub-item 11b of the 2007 CONSORT statement suggested the need for an assessment of blinding. We have been waiting for a revision and extension of this item, which would encourage people to collect and report more data and share lessons learned. Yet, disappointingly, it was eliminated from CONSORT 2010. As stated by the CONSORT authors, the rationale for this elimination was interpretational and measurement difficulties. Since the claim of internal validity for RCTs with a control arm rests on the assumption of appropriate blinding, we cannot afford to lose the CONSORT’s incentive for improvement and change. It seems contrary to an evidence-based approach to avoid obtaining data because we have to struggle with interpretation and measurement, which is a common and natural problem in various scientific fields. The philosophy of “let us give up because it is difficult to do or interpret” may not be well justified in professional scientific communities, especially when some reasonable statistical methods and clinical guidelines are available or can be developed.

Bell’s palsy is a sudden unilateral paralysis of the facial nerve. Postoperative Bell’s palsy following surgery is rare. It occurs in less than 1% of operations. The hypothesis: We premise that the main cause of immediate postoperative Bell's palsy is latent herpes viruses (herpes simplex virus type 1 and herpes zoster virus), which are reactivated from cranial nerve ganglia. Inflammation of the nerve initially results in a reversible neurapraxia, but ultimately Wallerian degeneration ensues. The palsy is often sudden in onset and evolves rapidly, with maximal facial weakness developing within two days. Associated symptoms often seen in idiopathic Bell’s palsy are tearing problems, hyperacusis and altered taste.Evaluation of the hypothesis: Facial paralysis presenting postoperatively is distressing and poses a diagnostic challenge. A complete interruption of the facial nerve at the stylomastoid foramen paralyzes all the muscles of facial expression. Taste sensation may be lost unilaterally and hyeracusis may be present. Idiopathic Bell’s palsy is due to inflammation of the facial nerve in the facial canal. Bell’s palsy may also occur from lesions that invade the temporal bone (carotid body, cholesteatoma, dermoid cyst, acoustic neuromas). Although traumatic Bell’s palsy cannot be ruled out, it seems logic to postulate that the main cause of immediate postoperative Bell's palsy is latent herpes viruses.