Stroke is one of the leading causes of disability and death worldwide. Despite intensive medical care, many of the complaints directly threatening the patient’s life marginalize their dental needs after the stroke. Recent studies indicate reduced saliva secretion in stroke patients in addition to the increased incidence of caries and periodontal disease. Since oxidative stress plays a vital role in the pathogenesis of salivary gland hypofunction and neurodegenerative disorders (including stroke), this is the first to evaluate the relationship between salivary gland activity and protein glycoxidation and nitrosative damage. The content of glycation and protein oxidation products and nitrosative stress was assessed in nonstimulated (NWS) and stimulated (SWS) whole saliva of stroke patients with normal salivary secretion and hyposalivation (reduced saliva production). The study included 30 patients in the stroke’s subacute phase and 30 healthy controls matched by age and sex. We have shown that stroke patients with hyposalivation show increased contents of protein glycation (↑Amadori products and ↑advanced glycation end products), glycoxidation (↑dityrosine), and nitration (↑nitrotyrosine) products compared to stroke cases with normal salivary secretion and control group. Interestingly, higher oxidative/nitrosative stress was found in NWS, which strongly correlates with salivary flow rate, total protein content, and salivary amylase activity. Such relationships were not observed in the control group. Summarizing, oxidative and nitrosative stress may be one of the mechanisms responsible for the impairment of saliva secretion in stroke patients. However, extraglandular sources of salivary oxidative stress in stroke patients cannot be excluded. Further studies to assess salivary gland hypofunction in stroke cases are necessary.
Stroke is a severe health problem in the modern world. It is defined as sudden, focal, vascular damage to the central nervous system confirmed by the presence of a stroke focus in neuroimaging studies or persistence of focal symptoms for more than 24 hours [
A key role in stroke pathogenesis is attributed to oxidative stress (OS) [
In our previous study, we showed that in stroke patients, enhanced OS occurs not only in the blood but also in saliva [
Our study is aimed at assessing the relationship between salivary gland function/protein secretion into saliva and protein glycoxidation and nitrosative damage. The content of glycation and protein oxidation products and nitrosative stress was evaluated in NWS and SWS of stroke patients with normal salivary secretion and hyposalivation.
Before the study, it was approved by the Bioethics Committee of the Poznan University of Medical Sciences (resolutions 59/19 and 890/19).
All participants, i.e., stroke patients and healthy controls, were provided with information concerning the research’s purpose, procedures, benefits, and risks. Full written consent was obtained from all patients in accordance with the Declaration of Helsinki for dental examination and sampling of saliva.
The study was performed between June and September 2019 in a health center (Bonifraterskie Centrum Zdrowia) in Piaski–Marysin (Piaski, Poland). The health center hospitalizes patients with various disorders, including those after cerebral stroke, from different country provinces.
The participation of each individual in the study was voluntary. One experienced neurorehabilitation specialist qualified all the individuals for the study according to its criteria.
The study group consisted of stroke patients in the subacute phase who were emerged out of 385 individuals that were subjects in the neurorehabilitation ward following different incidents, such as spinal cord injury, brain injury, vascular brain damage, surgically treated patients with a brain tumor, myelopathy, polyneuropathy, and sclerosis multiplex. It was established that 253 (65.71%) patients were stroke survivors. They were admitted to the neurorehabilitation unit directly from the hospital, in a subacute stroke phase, immediately after the acute phase cessation. Most individuals were able to communicate, cooperate, and understand instructions. A medical doctor assessed each patient, and subsequently, he/she was subjected to comprehensive individual and similar rehabilitation. Moreover, most individuals followed the same diet divided into a baseline diet for most people or a diet for diabetes mellitus patients. All the meals were distributed to the patients at the same time daily and were prepared in this hospital.
Data concerning the condition and general health status of individuals were obtained from patients’ files and contained: age, gender, time since diagnosis of cerebral stroke, medical history, and medication used.
In addition, for measurement of the functional status of the patient, the following scales were utilized:
Addenbrooke’s Cognitive Examination III (ACE III)—to differentiate individuals without and with cognitive impairment [ The Berg Balance Scale (BBS) for determining an individual’s inability or ability to safely balance during a series of predetermined tasks [ The Barthel Index (BI) for measurement of performance in activities of daily living (ADL) [ The functional independence measure (FIM) explores the patient’s physical, psychological, and social functioning [
Finally, 30 (11.86% of stroke survivors; 7.79% of all rehabilitated patients at the health center) fully completed the examination and were considered in the analysis (Table
Characteristics of both groups of stroke patients and controls.
Clinical characteristics | Control group | Study group | |||||
---|---|---|---|---|---|---|---|
Stroke with NS | Stroke with HP | NS vs. CG | HP vs. CG | NS vs. HP | |||
Sex | Male | 19 (63.33) | 11 (68.75) | 7 (50.00) | ns | ||
Female | 11 (36.67) | 5 (31.25) | 7 (50.00) | ||||
Age in years | ( | ns | |||||
Place of residence | Urban Center | 10 (33.33) | 6 (37.5) | 2 (14.28) | ns | ||
Small town | 9 (30.00) | 4 (25.00) | 7 (50.00) | ||||
Rural area or small village | 11 (36.67) | 6 (37.5) | 5 (35.71) | ||||
Household member(s) | With family member | 18 (60.00) | 11 (68.75) | 10 (71.43) | ns | ||
None | 12 (40.00) | 5 (31.25) | 4 (28.57) | ||||
Education | Primary | 3 (10.00) | 2 (12.5) | 1 (7.14) | ns | ||
Vocational | 12 (40.00) | 5 (31.25) | 7 (50.00) | ||||
Secondary | 7 (23.33) | 3 (18.75) | 4 (28.57) | ||||
University | 8 (26.67) | 6 (37.5) | 2 (14.28) | ||||
Systemic diseases | Hypertension | 21 (70.00) | 13 (81.25) | 9 (64.29) | ns | ||
Diabetes | 8 (26.67) | 4 (25.00) | 4 (28.57) | ||||
Epilepsy | 4 (13.33) | 2 (12.5) | 1 (7.14) | ||||
Arteriosclerosis | 7 (23.33) | 3 (18.75) | 4 (28.57) | ||||
Gout | 1 (3.33) | 1 (6.25) | 1 (7.14) | ||||
Limb thrombosis | 2 (6.67) | 2 (12.5) | 0 (0.00) | ||||
Atrial fibrillation | 3 (10.00) | 1 (6.25) | 3 (21.43) | ||||
Medications | <5 drugs/day | 10 (33.33) | 7 (43.75) | 5 (35.71) | ns | ||
≥5 drugs/day | 20 (66.67) | 9 (56.25) | 9 (64.29) | ||||
Type of stroke | Hemorrhagic | — | 3 (18.75) | 3 (21.43) | ns | ||
Ischemic | — | 13 (81.25) | 10 (71.43) | ||||
Ischemic ⟶ hemorrhagic | — | 0 (0.00) | 1 (7.14) | ||||
Numbers of strokes in the patient’s life | 1 | — | 13 (81.25) | 13 (92.86) | ns | ||
2 | — | 3 (18.75) | 1 (7.14) | ||||
Cognitive and physical functional status | ACE III ( | <0.0001 | <0.0001 | ns | |||
BI ( | <0.0001 | <0.0001 | ns | ||||
FIM ( | <0.0001 | <0.0001 | ns | ||||
BBS ( | <0.0001 | <0.0001 | ns |
Abbreviations: NS: normal salivary secretion; HP: reduced salivary secretion; ns: not significant; n: number of patients; CG: control group; ACE III: Addenbrooke’s Cognitive Examination; BI: Barthel Index; FIM: functional independence measure; BBS: Berg Balance Scale; nd: no data; differences statistically significant at
Patients from the study group (
The inclusion criteria of stroke patients to the study were as follows: confirmed cerebral infarction or cerebral hemorrhage based on CT and magnetic resonance imaging (MRI); recovery from the acute phase of ischemic or hemorrhagic stroke in all brain areas; good general condition; consciousness and giving of written and informed consent for saliva sampling and oral examination; the age of consent (>18 years); first admission to cure stroke unit was more than 5–6 (to 10) hours from the onset of the early neurological symptoms; adequate capacity to follow instructions, i.e., being able to answer questions during the examination, understanding how to perform the procedures and ability to collect a saliva sample.
The exclusion criteria of subjects from the research were as follows: unconfirmed cerebral infarction or cerebral hemorrhage with CT and magnetic resonance imaging (MRI); stroke recurrence during subacute phase; poor general condition; unconsciousness and inability to give informed consent for saliva sampling and oral check-up; insufficient cooperation due to cognitive/language deficits; incapability to collect saliva sample; patients under the age of 18; legal guardianship; ischemic stroke treated with thrombectomy or thrombolysis; patients with psychiatric or cognitive disorders; lung disease (chronic obstructive pulmonary disease) or cardiovascular disease (angina or uncontrolled hypertension); autoimmune disease (rheumatoid arthritis, systemic lupus erythematosus); heart failure resting oxygen saturation
The control group contained 30 individuals similar to the study group regarding gender and age, comorbidities, dentition and periodontium status, and oral hygiene (Table
The sampling of saliva was carried out in the health center during summer time, i.e., between June and September, to keep similar weather conditions outside.
The research material was total mixed nonstimulated saliva (NWS) and stimulated saliva (SWS), and both types of these oral bioliquid samples were collected via spitting. The saliva was collected between 7 : 30 a.m. and 9 : 00 a.m. from patients who had restrained from intensive physical activity for the preceding twelve hours. Subjects were instructed not to intake any liquid and/or solid food other than clean water at least two hours before sampling of saliva. The individuals were also indicated not to perform any oral hygiene practices (i.e., teeth brushing, gum chewing, and mouth rinsing). Because all patients were in the subacute phase of stroke, they had to take medicines approximately eight hours before saliva sampling, but the time from the last dose of any medication was minimally two hours. The controls had not taken any medication eight hours before saliva sampling [
The dental examination was carried out in a separate room, shortly after saliva sampling. According to the World Health Organization criteria, the dentition was evaluated in artificial lighting, using a plane mouth mirror and a dental probe [
All reagents (unless otherwise stated) were purchased from Sigma-Aldrich Nümbrecht, Germany, and Sigma-Aldrich Saint Louis, MO, USA. Salivary glycoxidation and nitrosative stress assays were performed in duplicate samples. The absorbance/fluorescence was measured using Infinite M200 PRO Multimode Microplate Reader (Tecan Group Ltd., Männedorf, Switzerland). The results were standardized to 1 mg of total protein (TP).
TP content was analyzed using a commercial kit (Thermo Scientific PIERCE BCA Protein Assay; Rockford, IL, USA), according to the manufacturer’s instructions. The salivary amylase activity was determined colorimetrically using 3,5-dinitrosalicylic acid (POCH, Gliwice, Poland) as a substrate reaction [
The formation of salivary Amadori products was determined using nitro blue tetrazolium (NBT) assay [
The content of salivary advanced glycation end products (AGE) was analyzed fluorimetrically at 350/440 nm [
The concentration of salivary protein carbonyls (PC) was determined colorimetrically based on the reaction with 2,4-dinitrophenylhydrazine (2,4-DNPH) [
The concentration of total thiols was determined using Ellman’s reagent [
The fluorescence assessment of salivary glycoxidative damage was also done. For this purpose, dityrosine, kynurenine, N-formylkynurenine, and tryptophan contents were measured fluorimetrically. The characteristic fluorescence at 330/415, 365/480, 325/434, and 295/340 nm, respectively, was measured in 96-well black-bottom microplates [
The concentration of salivary nitric oxide (NO) was determined colorimetrically using sulfanilamide and N-(1-naphthyl)-ethylenediamine dihydrochloride [
The salivary peroxynitrite concentration was determined colorimetrically based on peroxynitrite-mediated nitration resulting in nitrophenol formation [
The concentration of salivary nitrotyrosine was determined using ELISA commercial kit (Immundiagnostik AG; Bensheim, Germany), according to the manufacturer’s instructions.
GraphPad Prism 8.3.0 (GraphPad Software, Inc. La Jolla, USA) and Microsoft Excel 16.16.22 for macOS were used for statistical analysis. The distribution of results was assessed using the Shapiro–Wilk test, while homogeneity of variance using Levene’s test. ANOVA analysis of variance and Tukey’s HSD post hoc test were used for comparison of quantitative variables. ANOVA Kruskal–Wallis test and Dunn’s post hoc test were used if the results’ distribution was not normal. Multiplicity adjusted
The number of patients was calculated
Sixteen stroke patients with normal salivary secretion, aged between 34 and 67 years, and fourteen individuals after stroke with hyposalivation, aged from 52 to 84 years, were recruited to the research. All subjects were in the subacute phase of cerebral stroke. The procedures, including oral examination and saliva sampling, were performed between 45 and 50 days following the stroke incident (on average 46.78 days;
Both groups of stroke patients presented the highest caries prevalence that amounted to 100.00%, which means none of the patients had
Dental characteristics of both groups of stroke patients and controls.
Dental characteristics | Control group | Study group ( | ||||
---|---|---|---|---|---|---|
Stroke with NS | Stroke with HP | NS vs. CG | HP vs. CG | NS vs. HP | ||
DMFT ( | ns | ns | ns | |||
GI (in stroke patients with HP six completely edentulous patients were excluded from calculations, i.e., | ns | ns | ns | |||
PlI (in stroke patients with HP six completely edentulous patients were excluded from calculations, i.e., | ns | ns | ns |
Abbreviations: NS: normal salivary secretion; HP: reduced salivary secretion; ns: not significant; n: number of patients; CG: control group; DMFT index: a sum of decayed teeth (DT), teeth missing due to carious process (MT), and teeth filled because of caries (FT); GI: Gingival Index; PlI: Plaque Index.
Both PlI and GI were higher in stroke patients with normal salivary secretion than in those with hyposalivation.
NWS’s salivary flow was significantly higher in patients with stroke and normal salivary secretion than controls, while significantly lower in patients with stroke and hyposalivation. NWS’s total protein content was considerably lower in patients with stroke and decreased salivary secretion than controls and stroke patients with normal salivation. The salivary amylase activity in NWS was significantly lower in both groups of stroke patients than controls and patients with stroke with hyposalivation compared to normal salivary output (Figure
Salivary gland function in stroke patients and healthy controls. NS: stroke patients with normal salivary secretion; HP: stroke patients with reduced salivary secretion; NWS: nonstimulated whole saliva; SWS: stimulated whole saliva; TP: total protein concentration; ns: not significant. Differences statistically significant at
The stimulated salivary flow was significantly lower in patients with stroke and decreased salivary secretion than controls and patients with normal salivary function. Similarly, total protein content and salivary amylase activity in SWS were significantly lower in patients with stroke and decreased salivary secretion than controls and stroke patients with normal salivary function (Figure
The content of Amadori products was significantly higher in NWS for patients with stroke and reduced salivary secretion compared to patients with normal salivary flow and control. In SWS, Amadori products were significantly higher in the stroke HP group compared to the control (Figure
Protein glycation products in stroke patients and healthy controls. AGE: advanced glycation end products; NS: stroke patients with normal salivary secretion; HP: stroke patients with reduced salivary secretion; NWS: nonstimulated whole saliva; SWS: stimulated whole saliva; ns: not significant. Differences statistically significant at
In both nonstimulated and stimulated saliva in patients with stroke and reduced salivary secretion, the AGE content was significantly higher than patients with normal salivary flow and control (Figure
PC concentration was significantly higher in NWS of stroke patients with hyposalivation than controls, while in SWS, it did not differ between all groups (Figure
Protein oxidative damage in stroke patients and healthy controls. PC: protein carbonyls; NS: normal salivary secretion; HP: reduced salivary secretion; NWS: nonstimulated whole saliva; SWS: stimulated whole saliva; ns: not significant. Differences statistically significant at
In both NWS and SWS, the total thiols concentration was significantly lower in both groups of stroke patients than in control (Figure
The fluorescence of oxidatively-modified amino acids was shown in Figure
Glycoxidation products in stroke patients and healthy controls. NS: stroke patients with normal salivary secretion; HP: stroke patients with reduced salivary secretion; NWS: nonstimulated whole saliva; SWS: stimulated whole saliva; ns: not significant. Differences statistically significant at
Dityrosine fluorescence was significantly higher in the NWS of patients with stroke and hyposalivation compared to other groups. In SWS, we did not show any statistical differences between the groups.
The fluorescence of kynurenine and N-formylkynurenine was significantly higher in NWS of stroke patients with hyposalivation than other groups. We found no significant differences in SWS.
Fluorescence of tryptophan was significantly lower in NWS and SWS of stroke patients with hyposalivation than controls and in NWS compared to stroke patients with normal salivary secretion.
Salivary nitrosative stress was presented in Figure
Nitrosative stress in stroke patients and healthy controls. NO: nitric oxide; NS: stroke patients with normal salivary secretion; HP: stroke patients with reduced salivary secretion; NWS: nonstimulated whole saliva; SWS: stimulated whole saliva; ns: not significant. Differences statistically significant at
NO concentration was significantly lower in the group of stroke patients with hyposalivation compared to other groups. However, no differences in NO concentration in SWS were found.
The peroxynitrite content was significantly higher in NWS of both stroke groups compared to the control. In SWS, the ONOO- content was considerably higher in patients with stroke and hyposalivation than stroke patients with normal salivary secretion and controls.
Nitrotyrosine concentration was significantly higher in patients with stroke and hyposalivation than patients with normal salivary secretion and control but did not differ considerably in SWS.
In general, the content of glycoxidation products and nitrosative stress biomarkers was significantly higher in NWS compared to SWS in both control and stroke patients. However, total thiols were statistically higher in stimulated saliva compared to NWS. Interestingly, in stroke patients, Amadori products’ concentration was significantly higher in NWS than SWS, and such changes were not observed in control (Table
Comparison between NWS and SWS in healthy controls and stroke patients.
Parameter | Control | Stroke NS | Stroke HP | ||||||
---|---|---|---|---|---|---|---|---|---|
NWS | SWS | NWS | SWS | NWS | SWS | ||||
Amadori products ( | 0.16 | 0.01 | <0.0001 | ||||||
AGE (AFU/mg protein) | 0.004 | 0.88 | 0.47 | ||||||
PC (nmol/mg protein) | 0.13 | 0.06 | 0.04 | ||||||
Thiol groups ( | <0.0001 | 0.0002 | 0.0002 | ||||||
Dityrosine (AFU/mg protein) | <0.0001 | 0.03 | <0.0001 | ||||||
Kynurenine (AFU/mg protein) | 0.093 | 0.56 | 0.39 | ||||||
N-formylkynurenine (AFU/mg protein) | 0.001 | 0.002 | 0.002 | ||||||
Tryptophan (AFU/mg protein) | 0.55 | 0.002 | 0.39 | ||||||
NO (ng/mg protein) | 0.004 | 0.005 | 0.89 | ||||||
Peroxynitrite (nmol/mg protein) | <0.0001 | <0.0001 | <0.0001 | ||||||
Nitrotyrosine (pmol/mg protein) | <0.0001 | 0.18 | 0.002 |
Abbreviations: NS: normal salivary secretion; HP: reduced salivary secretion; NWS: nonstimulated whole saliva; SWS: stimulated whole saliva; AGE: advanced glycation end products; PC: protein carbonyls; NO: nitric oxide.
In stroke patients, the content of glycoxidation products (Amadori products, AGE, PC, dityrosine, kynurenine, and N-formylkynurenine) in NWS correlated remarkably negatively with salivary flow rate, as did the concentration of selected nitrosative stress biomarkers (NO and nitrotyrosine). However, the content of total thiols correlated positively with the NWS flow. Such changes were not observed in SWS of stroke patients (except for dityrosine and N-formylkynurenine) as well as in NWS and SWS of healthy subjects (Table
Correlations between clinical parameters, redox biomarkers, and salivary flow rate in healthy controls and stroke patients.
Parameter | Control | Stroke | ||||||
---|---|---|---|---|---|---|---|---|
NWS flow | SWS flow | NWS flow | SWS flow | NWS flow | SWS flow | NWS flow | SWS flow | |
Amadori products | 0.197 | -0.169 | 0.297 | 0.372 | -0.875 | 0.084 | <0.0001 | 0.658 |
AGE | 0.255 | 0.03 | 0.174 | 0.873 | -0.768 | -0.283 | <0.0001 | 0.13 |
PC | 0.055 | -0.394 | 0.772 | 0.031 | -0.451 | -0.268 | 0.012 | 0.153 |
Thiol groups | 0.014 | 0.161 | 0.943 | 0.395 | 0.533 | 0.369 | 0.002 | 0.045 |
Dityrosine | -0.269 | 0.044 | 0.15 | 0.816 | -0.706 | -0.401 | <0.0001 | 0.028 |
Kynurenine | 0.096 | 0.353 | 0.613 | 0.055 | -0.392 | 0.207 | 0.032 | 0.272 |
N-formylkynurenine | 0.178 | -0.167 | 0.348 | 0.378 | -0.585 | -0.484 | 0.001 | 0.007 |
Tryptophan | 0.03 | -0.102 | 0.876 | 0.592 | 0.291 | 0.155 | 0.119 | 0.414 |
NO | -0.344 | -0.047 | 0.063 | 0.806 | 0.665 | 0.004 | <0.0001 | 0.985 |
Peroxynitrite | -0.133 | 0.222 | 0.484 | 0.238 | -0.102 | 0.025 | 0.592 | 0.898 |
Nitrotyrosine | 0.028 | -0.013 | 0.884 | 0.945 | -0.682 | 0.072 | <0.0001 | 0.706 |
Abbreviations: NS: normal salivary secretion; HP: reduced salivary secretion; NWS: nonstimulated whole saliva; SWS: stimulated whole saliva; AGE: advanced glycation end products; PC: protein carbonyls; NO: nitric oxide.
We did not show any significant correlations between salivary redox biomarkers and clinical parameters (data not shown).
Saliva secretion is a reflex process. The reflex arch consists of afferent signals from sensory receptors in the oral cavity and is transmitted to the salivary nuclei in the medulla oblongata [
The direct analysis of the formation of oxygen and nitrogen free radicals is practically impossible. Therefore, for the assessment of OS/nitrosative stress, the products of free radical interactions with cell components are most often used. They are much more durable than free radicals and provide information on the consequences of oxidative/nitrosative damage to the body [
We have shown increased oxidation and glycation of proteins in stroke patients with hyposalivation and enhanced nitrosative damage compared to stroke cases with normal salivary secretion and control groups. Interestingly, we found higher oxidative/nitrosative stress in nonstimulated saliva, which strongly correlates with salivary flow rate, total protein content, and salivary amylase activity. Notably, such relationships were not observed in the control groups.
Glycation is a slow physiological process that intensifies in many diseases [
The increase in salivary secretion in stroke patients with normosalivation (compared to control) may be surprising. However, this may suggest salivary secretion disorders at the level of extraganglionic parasympathetic and sympathetic nerves/salivary nuclei rather than at the salivary gland level [
Nitric oxide (NO) plays an essential role in the initiation of saliva secretion [
Saliva is produced in an amount of about 500-1000 ml per day. Without stimulation, the largest volume of saliva is produced by the submandibular glands. These salivary glands are mixed glands containing follicular cells, which secrete mucous and mucin-rich saliva. However, during stimulation, saliva is secreted mainly by the parotid salivary glands [
Nevertheless, salivary oxidative/nitrosative stress may not only be the origin of the salivary glands. In fact, many compounds pass from plasma to saliva through passive/facilitated diffusion and active transport or are also the gingival fluid filtrate [
Many experimental and clinical studies have confirmed the contribution of OS/nitrosative stress in stroke pathology [
It must be emphasized that the present research has some strengths. Firstly, the participants were adequately chosen from a stroke patient population and divided into two subgroups, i.e., normal and reduced salivary secretion. Secondly, two saliva samples from each individual, i.e., stimulated and unstimulated, were collected. Thirdly, saliva sampling was performed under the same conditions during the same season, and storage, handling, processing, and analysis methods were uniform. Finally, most subjects used the same diet, except for the individuals who had diabetes mellitus. Unfortunately, this study also has some limitations. We assessed only selected biomarkers of oxidative/nitrosative stress, and therefore, we could not fully characterize the redox homeostasis of stroke individuals. In addition, the redox status was determined only in saliva. Thus, in subsequent researches, it would be advisable to evaluate the saliva–blood interconnection of redox biomarkers and their diagnostic utility in much more numerous groups of subjects and including more biomarkers. Moreover, samples of saliva were collected from stroke individuals in the shortest possible time, i.e., in the disease’s early subacute phase. The gathering of material directly after the stroke and receiving informed and written consent from all individuals was impossible because of patients’ lesser or greater cognitive and physical deficits. Moreover, we could not exclude the influence of comorbidities on the assessed redox biomarkers. Finally, the impact of pharmacotherapy on the composition and secretion of saliva could not be eliminated.
In stroke patients, the function of salivary glands (mainly submandibular glands) is disturbed, and salivary protein glycoxidation/nitration is increased. Oxidative and nitrosative stress may be one of the mechanisms responsible for the impairment of saliva secretion in stroke patients. In these patients, antioxidant supplementation may be considered. However, extraglandular sources of salivary oxidative stress in stroke patients cannot be excluded. Further studies to assess salivary gland hypofunction in stroke cases are necessary.
The article contains complete data used to support the findings of this study.
The authors declare no conflict of interest.
This work was supported by grants from the Medical University of Bialystok, Poland (grant numbers: SUB/1/DN/20/002/1209 and SUB/1/DN/20/002/3330). Dr. Mateusz Maciejczyk was supported by the Foundation for Polish Science (FNP).