A two-day international consensus meeting in 1989 on saliva was the foundation of the original edition entitled Saliva and Dental Health, published in 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 in which the international authors discussed their papers. The editors believe the new edition represents a consensus of opinion of world experts.

Chapters in 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 in 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, in 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 demineralisation and favours remineralisation’.

The Working Group 10 of the Commission on Oral Health, Research and Epidemiology (CORE), Fédération Dentaire Internationale wrote this report in 1991. The Group was chaired by Professor Leo M Sreebny. The ten sections in 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 hypofunction; the protective action of saliva against caries; the assay of caries-related constituents of saliva; and the treatment of salivary hypofunction and xerostomia.

The report reviews research on the ability of saliva to prevent dental caries and on the treatment of xerostomia and salivary hypofunction. It highlights important advances in knowledge that have implications for practice. 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 remineralising power of the saliva, with the potential to tip the balance against demineralisation. The treatment of salivary hypofunction, 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 hypofunction: increased caries, oral candidiasis, altered oral function and pain. The various local stimulatory, systemic stimulatory and symptomatic therapies are reviewed.

Professor WM Edgar gives a general report of a 2-day international consensus meeting on the clinical implications of saliva. The meeting was held in Ireland in 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 in dental practice 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 practice. 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, as well as 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 in 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 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 in minerals and proteins and supersaturated with 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 in contact with 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 in 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.

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 in this article. He said that the clinical value of comparing normal and pathological models of salivary gland function lies in 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 in these diseases have helped our 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 in 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 in the ways saliva and its elements support oral functions. Both communication and alimentation may be compromised when salivation is abnormal. The patient with low salivary secretions has difficulty speaking, chewing, forming a food bolus, and swallowing. In addition, there is a rapid and substantial increase in caries and mucosal infection. Taste and soft tissue complaints are also more frequent. As well as discussing the importance of saliva in dental health, the assessment of salivary gland function by different methods was reviewed in 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, with the advice given that dentists should consider salivary chemistries supportive of a specific diagnosis and not diagnostic in 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 in 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 with salivary gland hypofunction.

The source and supply of saliva in health, and its composition when ‘resting’ or ‘stimulated’ is reviewed in 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 in many physiology textbooks.) About 50-60% of the daily output is derived from basal saliva.

Saliva flow in disease is also reviewed in this article. Saliva is an indicator of whole mouth dryness and diseases and conditions associated with 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 hypofunction. The factors that affect salivary flow were discussed in healthy individuals: ageing, circadian rhythm circannual rhythm, body position, light, smoking, olfactory stimulation and previous gustatory stimulation.

Reductions in saliva flow are usually caused by salivary gland hypofunction 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.

In this review the dentist is advised to consider each patient as an individual, when they present with 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 with 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 in various forms has resulted in a profound change in the pattern of caries. Targeted groups are now: high-risk children; adults with multiple restorations; and older populations with gingival recession and increased susceptibility to root caries. People with xerostomia experience a heightened prevalence of decay and an abnormal distribution of lesions. Their clinical plight dramatically demonstrates the importance of saliva in 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 remineralisation. People who are naturally resistant to caries (regardless of fluorides and diet) have enhanced salivary protective mechanisms that include increased ability to produce base in plaque, a more effective means of bacterial aggregation and decreased pellicle permeability.

Professor Sreebny presents a summation of a symposium that consisted of presentations from five broad topics on the benefits of saliva: Impact of Saliva on Dental Caries, by Irwin D Mandel. Salivary Flow in Health and Disease by Leo M Sreebny; Physiological Aspects of Salivary Gland Function by Kenneth T Izutsu; Saliva Composition and its Importance in Dental Health by Philip C Fox; and Management of Patients with Xerostomia by Martin M Ferguson.

He prefaces this with an argument that saliva has been neglected. He asserts, 'saliva is a neglected secretion and xerostomia is a neglected symptom'. He argues that, because 'there is no money in it,' for the general practitioner, and because many dentists believe that symptoms associated with salivary gland dysfunction are trivial, the area has been neglected. Professor Sreebny says, 'Forgotten is the significant effect of saliva on the health of the oral tissues and on the quality of life'. He then demonstrates the benefits of saliva in his summary of the other speakers talks.

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

The evidence that acid pH has a major role in 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 with the calcium of apatite, but is more likely to be a result from a lowering of the saturation of the plaque with calcium phosphate by complexing calcium already in a soluble form in the plaque. The presence of substances in plaque able to form soluble complexes with calcium cannot be denied; and if they work slowly during the time when the plaque is neutral, their combined effect might be compared with 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.