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1.6 Classification of HSCs
1.1 Introduction
In the last 70 years or so, our understanding of dental materials has progressed from the more or less purely pragmatic to a more structure–function design‐based science. This process is not yet complete. That is, despite the currency of ‘evidence‐based dentistry’ – which has its own Wikipedia entry and an eponymous journal – there remains much work to be done to make everyone appreciate the value of the science of those materials. Inadequate teaching and dogmatic schools of thought are also manifest in endodontics to no lesser extent. It is my understanding that this book represents an attempt to begin the essential process of modernization in this field. Accordingly, I shall attempt to provide some foundations for the necessary insight.
Once the vitality of the dental pulp becomes compromised, endodontic intervention is necessary to preserve a functional natural dentition, with natural alveolar (as opposed to ankylosed) bone attachment, and thus the preservation of that very bone. More, perhaps, than in some other areas of dentistry, the materials used in endodontic work have an intimate relationship with tissues. Most obviously, the dentine is subject to exposure to a variety of more or less aggressive irrigants as well as fillers and (putative) sealers, often involving calcium hydroxide. Another possibility is of a strong oxidizing agent in the form of hypochlorite. Whilst the need for microbial elimination is not disputed, it is appropriate to be aware of the implications of such treatments: the chemistry demands that if a reaction is possible, it will occur, whether you like it or not, whether you meant it or not, and whether you are aware of it or not. Of course, apical extrusion of almost all materials can have very unfortunate consequences. Such intimacy is quite undesirable. At the least, a foreign body reaction will be elicited; at the worst, destruction of periapical bone – but the risk of infection is always high, with potentially wider implications.
1.2 The Substrate
Dentine has a complex composite structure whose matrix is largely proteinaceous, but it also has an inorganic component, biological apatite. As such, it is vulnerable to hydrolysis (whether acid‐ or base‐catalysed), even at pH 7 – although this may then be at a very low rate [1]. Since the mechanical properties of a composite structure are dependent on the integrity of the matrix, any such hydrolysis must be considered detrimental. In this light, the frequent finding that root fracture is associated with the use of calcium hydroxide, or materials containing it, is a predictable outcome for inevitable chemistry. The increased risk has to be treated as a necessary sequela of such a treatment, with the unhappy implication that the life of the remaining tooth may be limited (bearing in mind that the loads experienced by such teeth depend on a number of circumstances). Indeed, the use of oxidants such as sodium hypochlorite (which also deliberately has a high pH) must likewise contribute to such deterioration, because all organic material must be subject to oxidation, and indiscriminately. Add to this the penetration and diffusion of fluids and the effect can be seen to be not necessarily local. We therefore need to recognize that all such treatments involve compromise, a trade‐off between immediate benefit and longer‐term failure risk.
Disruption of the dentine matrix has further implications. As is discussed in Chapter 3, many biologically important molecules become bound within it during its development. Should these molecules be released through matrix breakdown, they may become once again biologically active and thus be important in reparative or regenerative processes. Such release through mechanical processes has little implication for that activity. Likewise, demineralization under mild conditions, such as with ethylene diamine tetra‐acetic acid or ‘EDTA’ (what is used in dentistry is actually closer to the trisodium salt, in order to provide enough solubility at around pH 7–8), may be considered in the same context. Such demineralization can be presumed to offer an easier diffusive path through the now much more porous tissue, and so may release these molecules without detriment to them, although perhaps the larger ones – proteins, for example – may emerge more slowly. It is, however, worth considering whether the more aggressive media at high pH cause any destruction of such molecules: proteins of whatever kind are still subject to hydrolysis. Are any of the other important matrix components capable of reaction, and thus damage and inactivation, under those conditions? Naturally, this is not necessarily an all‐or‐nothing kind of event – the kinetics of the reaction determines how much survives. It would follow, though, given that these molecules are believed to be of value in the course of treatment, that finding more benign means of release than the presently documented range of products would be of value for a more reliable effect of full efficacy. It would be wrong to assume, again, that the chemical reaction that destroys the matrix and releases these substances is selective. For example, urea may solubilize (that is, make soluble, as opposed to merely releasing) the matrix protein, but at the risk of unfolding, and therefore inactivating, enzymes of interest. There will probably not be a perfect resolution of this problem, but the means may conceivably be designed or selected for specific targets. It should be apparent that oxidizing agents are liable to destroy any and all biologically active molecules more rapidly than high pH alone. What appear to be needed are assays of the sequestered substances for comparison with release rates and survival in an active form after the various possible treatments.
The use of demineralizing and matrix‐destroying agents has an important implication. If bonding to collagen is intended, it must be left intact. If interaction with the calcium or phosphate of the mineral is contemplated, that must remain available. It is clearly illogical to use a treatment that removes an essential component of a subsequently intended process.
The preceding discussions are essentially of simple chemistry. It is curious then that in the historical focus on sterility and its maintenance in the present context, there has been little consideration of the inevitable effects of some of the agents used. Ignorance of the chemistry is no excuse, and to claim, for example, that a particular effect is not required is a chemical absurdity: as already stressed, if a reaction is possible, it will occur; if a pathway exists, it will be taken. The only debate is about relative rates. Materials science – and no less in endodontics than anywhere else – must recognize the chemistry of systems and design accordingly. The dogma mentioned must be designed out of dentistry. Again, though, compromise is inevitable; perfection is – at best – unlikely. Rational assessment is not optional, it is essential.
1.3 Nomenclatural Hype: ‘Bioactivity’, ‘Bioceramics’
It is clear that substances released unaltered from the dentine matrix must retain their biological function and activity, although whether the balance that originally obtained during development in the many complex interacting pathways is effectively and usefully maintained remains a matter for investigation. Nevertheless, it is proper to argue that this is indeed biological activity – bioactivity, to use the current jargon – because these are natural substances involved in entirely normal biological processes. Unfortunately, the field of dentistry is heavily trampled and muddied by the indiscriminate use of the term in any context where a biological response is elicited. That is, in the absence of those natural biological substances, any action, process, or material that provokes a response of any kind is automatically labelled ‘bioactive’. Such responses fall for now into just two classes: simple chemical and challenge defence.
Simple chemical responses typically involve the provision of a species that perturbs a chemical equilibrium, such as by changing the local pH. To take an ordinary example, adding sufficient calcium ions to a tissue fluid (by dissolution of a component
