Dental care professionals' awareness of oral dryness and its clinical management: a questionnaire-based study.

BACKGROUND: Despite the high prevalence of oral dryness and awareness of its complications, there is limited research on the clinical management of patients with oral dryness in general dental care. PURPOSE: To (1) describe and compare awareness among dental care professionals regarding saliva functions, potential causes and complications of oral dryness, and patient management (2) Investigate if the length of professional experience influences these aspects. METHODS: A digital self-administrated survey was sent to 2668 dental care professionals working in the general dental care, Public Dental Service, in Sweden. Twelve dental care professionals reviewed the questionnaire prior to its distribution. The questionnaire comprised 32 questions about patient management, awareness of saliva functions, causes and complications of oral dryness, and self-assessment queries. RESULTS: The response rate was 18.6% (241 dentists and 257 dental hygienists). Older adults (65+) were asked more often about dry mouth (93.0%) compared to those aged 18-23 years (50.0%) and those under 18 years (24.9%). Dental hygienists encountered individuals with oral dryness more frequently (61.1%) than dentists (48.5%) (p < 0.01), and more often asked individuals in the age groups 18-23 years (p = 0.003), 24-40 years (p = 0.045), and 41-65 years (p = 0.031) about dry mouth. A higher proportion of dental hygienists (88.3%) than dentists (51.0%) had measured salivary secretion rate, (p < 0.001) and more often suggested preventive dental care 3-4 times a year, (42.5% vs. 30.5%) (p < 0.007). Dentists had a higher awareness of saliva functions, while dental hygienists had a higher awareness about causes and complications of oral dryness. Higher proportions of dentists and dental hygienists with over 10 years of professional experience had measured salivary secretion rate (69.1% vs. 95.7%) compared to their counterparts with less than 10 years of professional experience (35.9% vs. 79.5%) (p < 0.001 for both). CONCLUSION: Compared to dentists, dental hygienists were more attentive to patients with oral dryness as they encountered these individuals more often, asked more age-groups, suggested frequent preventive measures, and had higher awareness of the causes and complications of oral dryness. Length of professional experience could improve both the management of patients with oral dryness and awareness of its causes, particularly for dental hygienists.

Melatonin-evoked in vivo secretion of protein and amylase from the parotid gland of the anaesthetised rat.

The intravenous infusion of melatonin (5 and 25 mg/kg over 10 min) evoked a dose-dependent output of protein and amylase but no overt fluid secretion from the parotid gland of the pentobarbitone-anaesthetised rat, as revealed by increased concentrations of protein and amylase activity in a subsequent wash-out flow of saliva in response to an intravenous bolus injection of methacholine (5 microg/kg) 10 min later. The secretory responses to melatonin occurred in the presence of alpha- and beta-adrenoceptor antagonists. They were not affected by the cholecystokinin A-receptor antagonist, lorglumide, and they were reproduced in eviscerated animals acutely subjected to postganglionic sympathetic and parasympathetic denervation of the gland. The responses to melatonin were partially dependent on nitric oxide generation, through the activity of nitric oxide synthase of the neuronal type. Immunoblotting showed both melatonin receptors of type 1 and type 2 to be expressed in parotid gland tissue. The relative specific melatonin 2-receptor antagonist luzindole prevented the expected secretory effects of melatonin. The results favour a direct action by melatonin on melatonin receptors of parotid secretory cells and suggest a potential physiological role for melatonin in the regulation of salivary glandular activities.

Pentagastrin-induced nitric oxide-dependent protein secretion from the parotid gland of the anaesthetized rat.

Infusion of pentagastrin (20 microg kg(-1) h(-1), i.v.) for 10 min evokes protein output but no overt fluid secretion from the parotid gland of the rat, as revealed by increased protein concentration in a subsequent wash-out flow of saliva in response to a bolus injection of methacholine (5 microg kg(-1), i.v.) 10 min later. Using this experimental set-up, the contribution of nitric oxide (NO) generation to the protein and amylase response evoked by pentagastrin was investigated. Neither the neuronal type NO synthase inhibitor N(omega)-propyl-L-arginine (N-PLA; 30 mg kg(-1), i.v.) nor the non-selective NO synthase inhibitor L-NAME (30 mg kg(-1), i.v.) as such affected the methacholine-evoked volume response or the outputs of protein and amylase. However, when preceeded by the pentagastrin infusion, the expected increases in concentrations of protein (145%) and amylase activity (127%) of the methacholine-evoked response (compared to a pre-infusion methacholine response) were reduced to 68 and 74%, respectively, in the presence of N-PLA, and to 70 and 63%, respectively, in the presence of L-NAME. Thus, NO generation resulting from the activity of the neuronal type NO synthase, most probably of parenchymal origin, plays an important role in the pentagastrin-induced protein and amylase secretion of the rat parotid gland.

Lipopolysaccharide induced-in vivo increases in beta-defensins of the rat parotid gland.

Antimicrobial beta-defensins are thought to protect epithelial surfaces. Their mobilization in response to inflammation was studied in the rat parotid gland using an ELISA assay. Bacterial lipopolysaccharide (LPS), injected into the parotid duct on one side, induced a marked local inflammatory response in the parotid gland as judged by several fold increases in myeloperoxidase activity and, in histological sections, infiltration of neutrophils. Three hours after the injection, beta-defensin 1 and 3 were increased (by 41% and 15%, respectively, P<0.01) as compared to the contralateral gland. Though still elevated 6h after the injection, the percentage figures for beta-defensin 1 were, at this time, somewhat lower (30%) compared to the situation at 3h, while those for defensin 3 were significantly higher 65% (P<0.01); neither at the early nor at the late time of observation were any changes in the level of beta-defensin 2 observed. The beta-defensins under study were not detected in submandibular and sublingual glands, neither were they detected in the inflamed submandibular gland, showing also here several fold increases in myeloperoxidase activity and, in addition, the presence of inflammatory cells, following ductal injection of LPS towards the gland.

Cholecystokinin- and gastrin-induced protein and amylase secretion from the parotid gland of the anaesthetized rat.

I.V. infusion of pentagastrin (20 microg/kg/h) or cholecystokinin (CCK)-8 (1 microg/kg/h) for 10 min caused secretion of salivary proteins from the parotid gland in the anaesthetized rat without any accompanying overt fluid secretion. This "occult" response was revealed by a subsequent wash-out injection of methacholine (5 microg/kg, I.V.) 10 min after the end of the infusion period (aiming at avoiding synergistic interactions). While the fluid response to methacholine was unaffected by the preceding infusion of pentagastrin and CCK-8, the output of protein increased by 147% (pentagastrin) and 74% (CCK-8) and that of amylase by 45% (CCK-8) compared to the responses to methacholine upon saline infusion. Those increases were abolished by the CCK-A receptor blocker (lorglumide), but not by the CCK-B receptor blocker (itriglumide). Evisceration, combined sympathetic and parasympathetic denervation of the glands and assay under adrenoceptor blockade excluded contribution from the gastro-intestinal tract, central or ganglionic mechanisms and circulating catecholamines to the increase in protein/amylase. Furthermore, Western blot demonstrated CCK receptors for both A and B subtypes in normal and chronically denervated glands. In the submandibular gland, both pentagastrin and CCK-8 evoked a trace secretion of saliva but, under the present experimental set-up, no statistically significant increase in protein output. Thus, in addition to the autonomic nervous system, gastrointestinal hormones may, in some types of glands, be involved in the secretion of salivary gland proteins.