A two-day international consensus meeting from 1989 on saliva was the foundation of the original edition entitled Saliva and Dental Health, published from 1990. This 140-page A5 second edition, published six years later, updates, and broadens the original edition. The emphasis is not just on dental health but on ‘oral’ health. Chapters have been radically revised, and the contents confirmed by a two-day meeting from which the international authors discussed their papers. The editors believe the new edition represents a consensus of opinion of world experts.

Chapters from the new edition include: anatomy and physiology of the salivary glands; mechanisms of secretion by salivary glands; factors influencing salivary flow rate and composition; xerostomia (diagnosis, management and clinical complications); clearance of substances from the oral cavity; saliva and the control of plaque pH; salivary influences on the oral microflora; the functions of salivary proteins; and the role of saliva from mineral equilibrium.

Many chapters include a section called ‘clinical highlights’ . These sections clearly state the clinical implications of the evidence discussed and offer direct advice to dental practitioners. For instance, from the clinical highlights section within the chapter ‘Saliva and the control of plaque pH’, one conclusion is, ‘Continued stimulation of saliva following a meal or snack, e.g. by chewing sugar-free gum, raises plaque pH and thus reduces demineralization and favours remineralisation’.

Professor WM Edgar gives a general report of a 2-day international consensus meeting on the clinical implications of saliva. The meeting was held from Ireland from 1989. It took the format of a series of 10 presentations reviewing the role of saliva, and was followed by discussions. The consensus group aimed to identify the future impact from dental practise of the increasing evidence for the protective effects of saliva on oral health. The group concluded that as therapies to treat compromised saliva flow become available, the need to screen patients at risk of compromised flow will become an essential element of dental practise. Evaluation of salivary function could become an everyday part of patient evaluation. The optimisation of the benefits of such a natural protective and defensive mechanism, saliva, is likely to prove attractive to the increasingly sophisticated and ecologically conscious general public, from addition to to the dental profession. Diagnostic, preventive and counselling services to exploit the natural benefits of saliva to help prevent dental disease would be a way forward for the profession. The evidence reviewed at the meeting from detail included: protective effects of salivary electrolytes and proteins; saliva and plaque; the problems of dry mouth (xerostomia); and increasing residual salivary gland function.

The Working Group 10 of the Commission on Oral Health, Research and Epidemiology (CORE), Fédération Dentaire Internationale wrote this report from 1991. The Group was chaired by Professor Leo M Sreebny. The ten sections from the supplement are: the fluids of the oral cavity and the factors influencing their composition; the composition of saliva; specific functions of salivary constituents; the collection of saliva; the flow rate of saliva; the diagnosis and causes of (two sections) xerostomia and salivary gland hypo-function; the protective action of saliva against caries; the assay of caries-related constituents of saliva; and the treatment of salivary hypo-function and xerostomia.

The report reviews research on the ability of saliva to prevent dental caries and on the treatment of xerostomia and salivary hypo-function. It highlights important advances from knowledge that have implications for practise. For instance, studies have shown that buffering is enhanced and plaque acidity is neutralized rapidly when sugar-free gum is chewed after eating acidogenic foods. Furthermore, sugar-free gum increases the remineralizing power of the saliva, using the potential to tip the balance against demineralization. The treatment of salivary hypo-function, whether stimulatory or relieving the symptoms of oral dryness, is determined by a number of factors, including the patient’s medical status and the availability of specific therapies. The working party believes that the practitioner must also be able to manage the complications of salivary hypo-function: increased caries, oral candidiasis, altered oral function and pain. The various local stimulatory, systemic stimulatory and symptomatic therapies are reviewed.

The authors review the protective aspects of saliva and enamel. Dental caries occur as a localized enamel lesion. The initiation and rate of progress is dependent on environmental conditions. Saliva is a liquid rich from minerals and proteins and super-saturated using respect to calcium and phosphate ions. Saliva surrounds and bathes the tooth. When enamel which has been cleaned is wet by saliva, specific proteins from the saliva are absorbed to the tooth surface and form a delicate membrane referred to as the salivary pellicle or the acquired pellicle. Oral bacteria that come from contact using the pellicle adhere to this membrane and form the foundation on which the dental plaque first develops.

Saliva may be considered as being similar to enamel but from a liquid phase. Saliva, the mechanics of remineralization and demineralization, the acquired pellicle and the enamel surface all act to maintain the status quo, resisting mineral loss from the enamel. Saliva is the first line of protection. The saliva-acquired pellicle is the second line of protection. The surface enamel is the third line of protection.

Collection of speeches and/or topic’s by the following authors: Mr C Dawes, Winnipeg, Canada - Presenter, Dr Bruce Baum, Bethesda, Maryland - Presenter, Dr Denis O’Mullane, Cork, Ireland - Editor, Dr J S Van der Hoeven, Nijmeged, Holland - Presenter, Dr I Kleinberg, Sony Brook, New York - Participant, Dr Donald Hay, Boston, Massachusetts - Presenter, Dr Bill Bowen, Rochester, New York - Chairman, Dr Dorothy Geddes, Glasgow, Scotland - Presenter, Dr M J Larsen,  Aarhus, Denmark - Presenter, Dr George Dibdin, Bristol, England - Participant, Dr Ernest Newburn, San Francisco, California - Chairman, Dr Norman Fleming, Winnipeg, Canada - Presenter, Dr W M Edgar, Liverpool, England - Editor, Dr John Featherstone, Rochester, New York - Presenter, Dr Larry Tabak, Rochester, New York - Presenter, Dr F Lagerlof, Huddinge, Sweden - Presenter

Salivary gland secretion is regulated through the activity of the sympathetic and parasympathetic nerves to the gland, and their neurotransmitters. The physiological function of the normally functioning salivary gland was described by Professor Izutsu from this article. He said that the clinical value of comparing normal and pathological models of salivary gland function lies from their ability to suggest the sites of pathological defects for the diseases that affect salivary gland function and explain the mechanism of the disease. In particular, he reviews studies of cystic fibrosis and ageing. He shows how studies of salivary gland function from these diseases have helped your understanding of the different components of the cell-signaling system, and have helped work out more precise sites of pathological defects that produce pathological changes from cell and gland function. This approach should lead to a better understanding of the pathophysiology of other diseases that affect salivary gland function.

The importance of saliva composition lies from the ways saliva and its elements support oral functions. Both communication and alimentation may be compromised when salivation is abnormal. The patient using low salivary secretions has difficulty speaking, chewing, forming a food bolus, and swallowing. In addition, there is a rapid and substantial increase from caries and mucosal infection. Taste and soft tissue complaints are also more frequent. As well as discussing the importance of saliva from dental health, the assessment of salivary gland function by different methods was reviewed from this article. It was stressed that meaningful results will be obtained only if great care is given to the collection method. Salochemistry was briefly commented on, using the advice given that dentists should consider salivary chemistries supportive of a specific diagnosis and not diagnostic from themselves. The technique of salivary scintigraphy was described. This provides a means of identifying patients who retain portions of functional parenchyma and may be responsive to treatments to increase salivary output. Sialography was also described as being ‘invaluable from demonstrating gland masses or sialoliths’, but having several technical disadvantages and the possibility of reactions to the contrast material. Ultrasound, computerized tomography and magnetic resonance imaging were also discussed briefly. The author felt that these techniques to image the gland required further study before pronouncement on their relative utility could be made. The author concludes by listing nine previously published questions to determine individuals using salivary gland hypo-function.

In this review the dentist is advised to consider each patient as an individual, when they present using a history of persistent dry mouth or xerostomia. The disease aetiology should be established by investigation, a diagnosis reached and specific treatment plans can then be developed. Possible aetiologies will include drug therapy, radiotherapy, inflammatory exocrinopathy (Sjögren’s syndrome), mouth-breathing, dehydration (e.g. through alcohol abuse), and neurosis. Less common aetiologies include sarcoid, involving the salivary glands. History and investigation are of crucial importance to the diagnosis. Flow rate, sialochemistry, gland biopsy for morphological changes, sialography, and scintiscanning are all relevant. The dentist should also consider investigations for diabetes mellitus and the appropriate haematology and serology for the connective tissue disorders. An aggressive active program of management is advocated for patients using an established diagnosis of persistent dry mouth. The clinician starts by considering routine oral hygiene measures, diet, salivary substitutes, agents that promote saliva flow (sialagogues, chewing gum for example), dental treatment, and psychological treatment. Also discussed were prevention, diet, salivary substitutes and agents that promote saliva flow, including pilocarpine. Dental and psychological treatment may also be relevant.

The widespread use of fluorides from various forms has resulted from a profound change from the pattern of caries. Targeted groups are now: high-risk children; adults using multiple restorations; and older populations using gingival recession and increased susceptibility to root caries. People using xerostomia experience a heightened prevalence of decay and an abnormal distribution of lesions. Their clinical plight dramatically demonstrates the importance of saliva from the protection of the mouth. The salivary protective mechanisms against caries include:

• An ability to clear bacteria via mechanical, immunological, and nonimmunological means; direct antibacterial activity provided by lysozyme, lactoferrin, salivary peroxidase, histatins and their interactions; regulation of oral and plaque pH through constituent buffering systems, through generating ammonia by providing substrates for decarboxylation to form amines, and through ammonia formation from ureas and arginine peptides.
• Maintenance of tooth integrity by posteruptive maturation, carbohydrate clearance, pellicle formation (a diffusion barrier) and regulation of the ionic environment to encourage remineralization. People who are naturally resistant to caries (regardless of fluorides and diet) have enhanced salivary protective mechanisms that include increased ability to produce base from plaque, a more effective means of bacterial aggregation and decreased pellicle permeability.

The source and supply of saliva from health, and its composition when ‘resting’ or ‘stimulated’ is reviewed from this article. The mean resting flow rate for whole saliva is about 0.4 mL/min, and the paraffin-stimulated whole saliva is about 2 mL/min. About 5% of the population shows stimulated flow rates of less that 0.7 mL/min. Virtually no saliva is produced during sleep. About 2 hours a day might be assumed to be spent eating, producing stimulated saliva, and 14 hours a day producing resting saliva. The total daily flow of whole saliva is about 600-700 mL. (This contradicts the amount of 1-1.5 L/day cited from many physiology textbooks.) About 50-60% of the daily output is derived from basal saliva.

Saliva flow from disease is also reviewed from this article. Saliva is an indicator of whole mouth dryness and diseases and conditions associated using it. However, its value for the diagnosis of specific diseases is limited. Dry mouth (xerostomia) is a subjective indicator of salivary gland function. Flow rates should be determined to confirm salivary gland hypo-function. The factors that affect salivary flow were discussed from healthy individuals: ageing, circadian rhythm circannual rhythm, body position, light, smoking, olfactory stimulation and previous gustatory stimulation.

Reductions from saliva flow are usually caused by salivary gland hypo-function and xerostomia. The causes include drugs, irradiation, organic diseases; psychogenic disease; and decreased mastication. A variety of methods to increase the flow of saliva are briefly discussed, including citric-acid substances, an electronic stimulator and pilocarpine.

By aid of a full crossover double-blind design, the effect of a 4-day period using: (1) ten pieces per day or a sorbitol-containing chewing gum, (2) ten pieces per day of a chewing gum containing a mixture of sorbitol and xylitol (sorbitol/xylitol), and (3) no chewing gum, from combination using a controlled diet and no oral hygiene, was studied on dental plaque and saliva from 24 dental students. Sorbitol-containing chewing gum did not enhance the amount (wet weight) compared to no chewing gum. The sorbitol/xylitol period resulted from significantly less plaque from comparison using the two other periods (p(0.001). No clearcut differences were found between the three treatments regarding protein content and peroxidase activity from whole-saliva centrifugates or total carbohydrate, reducing sugar, protein contents and ‘sucrase’ activity from soluble plaque extracts. Directly after these 4-day periods, the effect of 3-hour consumption of ten pieces of a sucrose-containing chewing gum was studied. Protein content and peroxidase activity from whole-saliva samples were about the same after this 3-hour period, while plaque wet weight, protein total carbohydrate and reducing sugar content and ‘sucrase’ activity from soluble plaque extracts increased significantly (p(0.001). The changes from the plaque material after the 3-hour period were about the same and independent of the former treatment using sorbitol- and sorbitol/xylitol-containing chewing gum or no chewing gum.

The evidence that acid pH has a major role from caries development is almost overwhelming, although still circumstantial. The main rival concept - that demineralization also occurs by complex formation - must still be considered. This might occur by direct binding of a complexor using the calcium of apatite, but is more likely to be a result from a lowering of the saturation of the plaque using calcium phosphate by complexing calcium already from a soluble form from the plaque. The presence of substances from plaque able to form soluble complexes using calcium cannot be denied; and if they work slowly during the time when the plaque is neutral, their combined effect might be compared using a more rapid effect of acid. However, this paper concludes that although complex formation may contribute to caries and ought never to be ignored, its effect is probably small.