Long-term stimulation of myocardial beta-receptors by isoproterenol is a well-established model of heart damage and failure. This study investigated the potential interactions of isoproterenol administration with the renin-angiotensin-aldosterone system (RAAS) and whether sacubitril/valsartan (ARNI) protection against left ventricular (LV) remodeling and dysfunction was associated with the modulation of the RAAS. Four groups of three-month-old male Wistar rats were treated for six weeks as follows: controls, sacubitril/valsartan (ARNI, 68 mg/kg/day orally), isoproterenol (5 mg/kg the first day and 1 mg for next six days + four weeks recovery), isoproterenol (as above) + ARNI (one week pre-treatment followed by 5 weeks treatment during ISO-treatment and recovery period). Systolic blood pressure (SBP) was markedly reduced only in the first week of both ISO-treated groups. Isoproterenol induced pathological remodeling of the LV, as well as deterioration of its function as determined by echocardiography. Yet, no changes in serum renin-angiotensin-aldosterone levels were observed. ARNI lowered SBP, alleviated LV remodeling, improved LV systolic and diastolic dysfunction and also raised the serum levels of angiotensin (Ang) II, Ang III, Ang IV, Ang 1-5, Ang 1-7 and aldosterone. We conclude that isoproterenol treatment for one week followed by a four-week recovery induced a normal-to-low serum renin-angiotensin-aldosterone model of left ventricular damage. Protection by ARNI against pathological remodeling and LV dysfunction was related to Ang II blockade and upregulation of the alternative pathway of the renin-angiotensin-aldosterone system.

Cardiovascular disorders and the medications used to treat them can affect physiological patterns of behavior. The aim of the present study was to determine whether the dual inhibition of neprilysin and angiotensin II—sacubitril/valsartan (ARNI) can modify anxiety-like behavior in male spontaneously hypertensive rats (SHR). We compared ARNI with two other drugs in the portfolio of heart failure treatment, captopril and ivabradine. Six groups (n = 13) of 12-week-old rats were treated for six weeks: control (Wistar rats), control + ARNI, SHR, SHR + ARNI, SHR + captopril, and SHR + ivabradine. The elevated plus maze test, the open field test, and the light–dark box test were used to determine anxiety-like behavior. SHRs exhibited higher systolic blood pressure (SBP), heart rate (HR), left ventricular weight (LVW), and hydroxyproline concentration (LVHP) but displayed a reduced level of anxiety-like behavior in comparison to controls. ARNI reduced SBP, HR, and LVW but had no significant effect on the level of anxiety in SHR, and similar results were achieved by captopril and ivabradine. Additionally, correlation analysis indicated that anxiety-like behavior in Wistar rats or SHR, either with or without cardiovascular therapy, was independent of SBP, HR, LVW, or LVHP. The level of anxiety-like behavior can, therefore, be considered part of the inherent neurobehavioral traits unrelated to fundamental hemodynamic or structural cardiovascular parameters.

There is ample evidence on the benefit of angiotensin receptor-neprilysin inhibitors (ARNIs) in heart failure, yet data regarding the potential protective action of ARNIs in hypertensive heart disease are sparse. The aim of this study was to show whether an ARNI exerts a protective effect in a model of Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension with a hypertensive heart and to compare this potential benefit with an angiotensin-converting enzyme inhibitor, captopril. Five groups of adult male Wistar rats were studied (14 per group) for four weeks: untreated controls; ARNI (68 mg/kg/day); L-NAME (40 mg/kg/day); L-NAME treated with ARNI; and L-NAME treated with captopril (100 mg/kg/day). L-NAME administration induced hypertension, accompanied by increased left ventricular (LV) weight and fibrotic rebuilding of the LV in terms of increased concentration and content of hydroxyproline in insoluble collagen and in total collagen and with a histological finding of fibrosis. These alterations were associated with a compromised systolic and diastolic LV function. Treatment with either an ARNI or captopril reduced systolic blood pressure (SBP), alleviated LV hypertrophy and fibrosis, and prevented the development of both systolic and diastolic LV dysfunction. Moreover, the serum levels of prolactin and prolactin receptor were reduced significantly by ARNI and slightly by captopril. In conclusion, in L-NAME-induced hypertension, the dual inhibition of neprilysin and AT1 receptors by ARNI reduced SBP and prevented the development of LV hypertrophy, fibrosis, and systolic and diastolic dysfunction. These data suggest that ARNI could provide protection against LV structural remodeling and functional disorders in hypertensive heart disease.

This study investigated whether sacubitril/valsartan or valsartan are able to prevent left ventricular (LV) fibrotic remodelling and dysfunction in two experimental models of pre-hypertension induced by continuous light (24 hours/day) exposure or by chronic lactacystin treatment, and how this potential protection interferes with the renin-angiotensin-aldosterone system (RAAS). Nine groups of three-month-old male Wistar rats were treated for six weeks as follows: untreated controls (C), sacubitril/valsartan (ARNI), valsartan (Val), continuous light (24), continuous light plus sacubitril/valsartan (24+ARNI) or valsartan (24+Val), lactacystin (Lact), lactacystin plus sacubitil/valsartan (Lact+ARNI) or plus valsartan (Lact+Val). Both the 24 and Lact groups developed a mild but significant systolic blood pressure (SBP) increase, LV hypertrophy and fibrosis, as well as LV systolic and diastolic dysfunction. Yet, no changes in serum renin-angiotensin were observed either in the 24 or Lact groups, though aldosterone was increased in the Lact group compared to the controls. In both models, sacubitril/valsartan and valsartan reduced elevated SBP, LV hypertrophy and fibrosis and attenuated LV systolic and diastolic dysfunction. Sacubitril/valsartan and valsartan increased the serum levels of angiotensin (Ang) II, Ang III, Ang IV, Ang 1–5, Ang 1–7 in the 24 and Lact groups and reduced aldosterone in the Lact group. We conclude that both continuous light exposure and lactacystin treatment induced normal-to-low serum renin-angiotensin models of pre-hypertension, whereas aldosterone was increased in lactacystin-induced pre-hypertension. The protection by ARNI or valsartan in the hypertensive heart in either model was related to the Ang II blockade and the protective Ang 1–7, while in lactacystin-induced pre-hypertension this protection seems to be additionally related to the reduced aldosterone level.

Obstructive sleep apnea syndrome (OSAS) is a frequently underdiagnosed sleep disorder marked by recurrent episodes of apnea and/or hypopnea during sleep, primarily resulting from the partial or complete collapse of the upper airway. OSAS significantly affects patients’ health and quality of life. Additionally, it is a recognized risk factor for inducing microsleep episodes during daily activities, particularly in occupations such as professional driving, where sustained attention is critical. The aim of our study was to identify an effective screening test for use in outpatient settings, capable of distinguishing patients with a severe form of OSAS. Patients who test positive with this screening tool would subsequently be prioritized for polysomnographic evaluation in a sleep laboratory. A total of 64 patients who underwent polysomnography (PSG) or polygraphy (PG) examination at our clinic were subsequently examined by USG of the tongue with measurements of tongue base thickness (TBT) and the distance between lingual arteries (DLA) during wakefulness and in a relaxed tongue position. The measurements of TBT and DLA were subsequently correlated with the apnea–hypopnea index (AHI) obtained from PSG or PG. In our cohort of patients diagnosed with severe OSAS, a TBT threshold of ≥65 mm served as an effective cutoff value. A TBT value of ≥65 mm reached an AUC value of 78.1%, sensitivity of 74.4%, specificity of 61.9%, positive predictive value of 80%, negative predictive value of 54.2% and overall accuracy of 70.3%. A DLA value of ≥30 mm in our sample of patients with severe OSAS showed an AUC of 76.5%, sensitivity of 69.8%, specificity of 71.1%, positive predictive value of 83.3%, negative predictive value of 53.6%, and overall accuracy of 70.3%. Tongue USG markers, particularly TBT and DLA measurements during wakefulness and in a relaxed tongue position, show potential as effective screening tools for identifying severe OSAS in European populations. These markers demonstrate improved accuracy over traditional screening questionnaires by reducing the likelihood of false-negative results. Patients with a positive screening should preferably be referred for polysomnography. In this way, patients with a serious illness could receive adequate therapy sooner.

This study investigated whether chronic isoproterenol administration could induce kidney alterations and whether ivabradine, a heart rate (HR)-reducing substance exerting cardiovascular protection, is able to attenuate potential kidney damage. Twenty-eight Wistar rats were divided into non-diseased controls, rats treated with ivabradine, rats treated with isoproterenol, and rats treated with isoproterenol plus ivabradine. Six weeks of isoproterenol administration was associated with decreased systolic blood pressure (SBP) (by 25%) and glomerular, tubulointerstitial and vascular/perivascular fibrosis due to enhanced type I collagen volume (7-, 8-, and 4-fold, respectively). Ivabradine reduced HR (by 15%), partly prevented SBP decline (by 10%) and site-specifically mitigated kidney fibrosis by decreasing type I collagen volume in all three sites investigated (by 69, 58, and 67%, respectively) and the ratio of type I collagen-to-type III collagen in glomerular and vascular/perivascular sites (by 79 and 73%, respectively). We conclude that ivabradine exerts protection against kidney remodelling in isoproterenol-induced kidney damage.

This study investigated whether sacubitril/valsartan and ivabradine are able to prevent left ventricular (LV) fibrotic remodelling and dysfunction in a rat experimental model of spontaneous hypertension (spontaneously hypertensive rats, SHRs) and whether this potential protection is associated with RAAS alterations. Five groups of three-month-old male Wistar rats and SHRs were treated for six weeks as follows: untreated Wistar controls, Wistar plus sacubitril/valsartan, SHR, SHR plus sacubitril/valsartan, and SHR plus ivabradine. The SHRs developed a systolic blood pressure (SBP) increase, LV hypertrophy and fibrosis, and LV systolic and diastolic dysfunction. However, no changes in serum RAAS were observed in SHRs compared with the controls. Elevated SBP in SHRs was decreased by sacubitril/valsartan but not by ivabradine, and only sacubitril/valsartan attenuated LV hypertrophy. Both sacubitril/valsartan and ivabradine reduced LV collagen content and attenuated LV systolic and diastolic dysfunction. Sacubitril/valsartan increased the serum levels of angiotensin (Ang) II, Ang III, Ang IV, Ang 1-5, Ang 1-7, and aldosterone, while ivabradine did not affect the RAAS. We conclude that the SHR is a normal-to-low serum RAAS model of experimental hypertension. While the protection of the hypertensive heart in SHRs by sacubitril/valsartan may be related to an Ang II blockade and the protective Ang 1-7, the benefits of ivabradine were not associated with RAAS modulation.

OBJECTIVE:The objective of this study was to evaluate the influence of lip sucking on dentofacial development in a pair of 6.5-year-old monozygotic twins.BACKGROUND:Lip sucking, which causes an imbalance in splanchnocraniums soft tissues pressures, can influence the hard tissues development, and contribute to orthodontic anomalies.METHODS:Analysis of lateral cephalometric X-rays was performed by 9 orthodontists. Data were compared using the Mann-Whitney and Kruskal-Wallis tests. Statistical significance was defined as p<0.05.RESULTS:SNA, A-NPog, and Cond-A values suggested an anterior shift of the maxilla. The 1u to SN, 1u to A-Pog, 1u to A-Pog angle, and 1u-Avert values indicated an upper incisor protrusion. While the 1l to A-Pog, 1l to A-Pog angle and 1l to Go-Me values showed a retrusion of the lower incisors, the NL-NSL implied a hard palate rotation counterclockwise. The SNA-Me indicated that the mandible of the lip-sucking patient was in a more inferior position.CONCLUSION:Lip sucking can influence the skeletal development of maxilla, the position of upper and lower incisors and the position of mandible. Skeletal development of mandible seems to be unaffected (Tab. 3, Fig. 1, Ref. 26).

Lactacystin is a specific proteasome inhibitor that blocks the hydrolysis of intracellular proteins by ubiquitin/proteasome system inhibition. The administration of lactacystin to rats induced hypertension and remodeling of the left ventricle and aorta. This study tested whether lactacystin induces structural and fibrotic rebuilding of the kidneys and whether melatonin and captopril can prevent these potential changes. Six weeks of lactacystin administration to rats increased their average systolic blood pressure (SBP). In the kidneys, lactacystin reduced glomerular density, increased the glomerular tuft area, and enhanced hydroxyproline concentrations. It also elevated the intraglomerular proportion including the amounts of collagen (Col) I and Col III. Lactacystin also raised the tubulointerstitial amounts of Col I and the sum of Col I and Col III with no effect on vascular/perivascular collagen. Six weeks of captopril treatment reduced SBP, while melatonin had no effect. Both melatonin and captopril increased glomerular density, reduced the glomerular tuft area, and lowered the hydroxyproline concentration in the kidneys. Both drugs reduced the proportion and total amounts of intraglomerular and tubulointerstitial Col I and Col III. We conclude that chronic lactacystin treatment stimulated structural and fibrotic remodeling of the kidneys, and melatonin and captopril partly prevented these alterations. Considering the effect of lactacystin on both the heart and kidneys, chronic treatment with this drug may be a prospective model of cardiorenal damage suitable for testing pharmacological drugs as protective agents.

Anxiety disorders are the most common mental diseases. Anxiety and the associated physical symptoms may disturb social and occupational life and increase the risk of somatic diseases. The pathophysiology of anxiety development is complex and involves alterations in stress hormone production, neurosignaling pathways or free radical production. The various manifestations of anxiety, its complex pathophysiological background and the side effects of available treatments underlie the quest for constantly seeking therapies for these conditions. Melatonin, an indolamine produced in the pineal gland and released into the blood on a nightly basis, has been demonstrated to exert anxiolytic action in animal experiments and different clinical conditions. This hormone influences a number of physiological actions either via specific melatonin receptors or by receptor-independent pleiotropic effects. The underlying pathomechanism of melatonin’s benefit in anxiety may reside in its sympatholytic action, interaction with the renin–angiotensin and glucocorticoid systems, modulation of interneuronal signaling and its extraordinary antioxidant and radical scavenging nature. Of importance, the concentration of this indolamine is significantly higher in cerebrospinal fluid than in the blood. Thus, ensuring sufficient melatonin production by reducing light pollution, which suppresses melatonin levels, may represent an endogenous neuroprotective and anxiolytic treatment. Since melatonin is freely available, economically undemanding and has limited side effects, it may be considered an additional or alternative treatment for various conditions associated with anxiety.

Background: Cognitive screening by pharmacists may help to identify seniors with metabolic syndrome (MetS)-related cognitive impairment. We aimed to evaluate the implementation of an easy-to-use cognitive screening into the pharmaceutical care of seniors and to test whether cognitive decline is associated with suspected MetS (sMetS).Methods: Questionnaires were completed by 323 randomly selected elderly patients receiving pharmaceutical care in community pharmacies or in senior care centres in Slovakia. The presence of sMetS was estimated according to criteria of the International Diabetes Federation. Cognitive performance was evaluated by the Montreal Cognitive Assessment (MoCA) test and its short form (s-MoCA). In these tests, the cut-offs for impaired cognitive status were <= 24, and <= 12, respectively.Results: 56% of participants scored below the screening cut-off MoCA threshold. Cognitive impairment was significantly more frequent in sMetS+ subjects (71%) vs. sMetS- (52%; p < 0.05). MoCA scores were significantly lower in sMetS+ (mean +/- SD = 20.0 +/- 5.9 points) vs. sMetS- (22.2 +/- 5.4 points; p < 0.05). sMetS components type 2 diabetes mellitus, hypertension and obesity, but not dyslipidaemia, had an influence on lower cognitive performance.Conclusions: We unveiled a significant relationship of cognitive dysfunction to sMetS in elderly patients. A quick and simple cognitive assessment could be a helpful extension of pharmaceutical care.

Computer-aided design/computer-aided manufacturing (CAD-CAM) sa pri výrobe zubných náhrad využíva čoraz častejšie. To predstavuje novú éru v snímateľnej protetike. CAD/CAM systémy pre digitálne zubné náhrady sa vyvíjajú s prísľubom eliminácie problémov a chýb tradične vyrábaných zubných náhrad. Cieľom tohto článku je predstaviť postup výroby digitálnej zubnej náhrady krok za krokom a zhrnúť jej vlastnosti v porovnaní so zubnou náhradou vyrábanou konvenčne.

Tomáš Baka1*, Peter Stanko1*, Fedor Šimko1, 2, 3 1Ústav patologickej fyziológie, Lekárska fakulta, Univerzita Komenského v Bratislave 2III. interná klinika, Lekárska fakulta a Univerzitná nemocnica, Univerzita Komenského v Bratislave 3Ústav experimentálnej endokrinológie, Biomedicínske centrum, Slovenská akadémia vied v Bratislave *Tomáš Baka a Peter Stanko prispeli k tejto práci rovnakou mierou, a preto zdieľajú prvoautorstvo.

Despite advances in heart failure (HF) pharmacotherapy over the last three decades, the residual mortality with HF remains high.The antipode to the drug-induced inhibition of vasoconstrictive and proliferative substances could be an increase of vasodilative and antiproliferative humoral substances, including the natriuretic peptides (NPs).NPs are secreted by the distended myocardium and stimulate diuresis and vasodilation, exert antiproliferative effects, and inhibit both the sympathetic and renin-angiotensin systems (RAS).The proteolytic enzyme neprilysin cleaves NPs and thus limits their effects.However, this non-specific protease degrades a variety of other proteins, including angiotensin II (Ang II).Therefore, neprilysin inhibition increases the level of both NPs and Ang II.Sacubitril/valsartan, a representative of the new drug class: angiotensin receptor-neprilysin inhibitors (ARNi), contains one molecule of Ang II type 1 receptor blocker (valsartan) and one molecule of neprilysin inhibitor (sacubitril).The interaction of these substances, ensuing potential increase of NPs without RAS activation, brings an additive morbidity and mortality benefit in the management of HF with reduced ejection fraction (HFrEF), as compared to RAS inhibition alone.Yet, the hope for ARNi's benefit in HF with preserved ejection fraction (HFpEF) remains is unmet.Preliminary studies suggest a potential benefit by ARNi in hypertensive heart disease, kidney protection and post-myocardial infarction cardiac remodelling.Tab. 1, Ref. 50, on-line full text (Free, PDF) www.cardiologyletters.sk

Hypertension-induced renal injury is characterized by structural kidney alterations and function deterioration. Therapeutics for kidney protection are limited, thus novel renoprotectives in hypertension are being continuously sought out. Ivabradine, an inhibitor of the If current in the sinoatrial node reducing heart rate (HR), was shown to be of benefit in various cardiovascular pathologies. Yet, data regarding potential renoprotection by ivabradine in hypertension are sparse. Thirty-six adult male Wistar rats were divided into non-diseased controls and rats with NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension to assess ivabradine's site-specific effect on kidney fibrosis. After 4 weeks of treatment, L-NAME increased the average systolic blood pressure (SBP) (by 27%), decreased glomerular density (by 28%) and increased glomerular tuft area (by 44%). Moreover, L-NAME induced glomerular, tubulointerstitial, and vascular/perivascular fibrosis by enhancing type I collagen volume (16-, 19- and 25-fold, respectively). L-NAME also increased the glomerular type IV collagen volume and the tubular injury score (3- and 8-fold, respectively). Ivabradine decreased average SBP and HR (by 8 and 12%, respectively), increased glomerular density (by 57%) and reduced glomerular tuft area (by 30%). Importantly, ivabradine decreased type I collagen volume at all three of the investigated sites (by 33, 38, and 72%, respectively) and enhanced vascular/perivascular type III collagen volume (by 67%). Furthermore, ivabradine decreased the glomerular type IV collagen volume and the tubular injury score (by 63 and 34%, respectively). We conclude that ivabradine attenuated the alterations of glomerular density and tuft area and modified renal fibrosis in a site-specific manner in L-NAME-hypertension. It is suggested that ivabradine may be renoprotective in hypertensive kidney disease.

This study investigated the effect of lisinopril (angiotensin-converting enzyme inhibitor) on potential behavioural alterations in spontaneously hypertensive rats (SHR). Three groups of 15-17-week-old rats were investigated for 2 weeks: Wistar control group, SHR group and SHR+lisinopril group. Systolic blood pressure (SBP) was normal in Wistar rats, SHR expressed hypertension and lisinopril normalized the SBP. We observed increased time spent in and increased frequency of entries to the central area of the open field in SHR, while lisinopril induced a trend to reduce the time spent in the central area of the open field and reduced the frequency of entries there. There was a positive correlation between SBP and reduced anxiety-like behaviour in normotensive rats; no correlations in the SHR or SHR+lisinopril groups were observed. We conclude that lisinopril normalized the increase in SBP and partly reversed the alterations of anxiety-like behaviour in SHR.

Cieľ štúdie: Použiť metódu mystery shopping pri vzdelávaní študentov farmácie s cieľom sledovať, ako sa odporúčania o správnej dispenzácii a poradenstve realizujú vo verejných lekárňach na Slovensku. Použité metódy: 54 študentov Farmaceutickej fakulty Univerzity Komenského v Bratislave bolo edukovaných počas vzdelávacieho projektu o dispenzácii a poradenstve o OTC lieku a súčasne na úlohu mystery shopperov. Pre zvolenú tému poradenstva (prechladnutie, nádcha) sa vypracovali dva scenáre (priama požiadavka lieku a požiadavka na liečbu podľa symptómov ochorenia). Sledovali sme 3 kategórie poradenskej činnosti (identifikácia pacienta, dispenzačné informácie a komunikácia). Položky týchto kategórií sme hodnotili skórovaním (áno/nie), v prípade komunikácie to bola 5-stupňová Likertova škála (1 – výborná; 5 – nedostatočná) a opísali ich deskriptívnymi ukazovateľmi. Celkové skóre poradenstva sme vyjadrili ako váženú priemernú percentuálnu úspešnosť uvedených troch oblastí a ich váh (0–100 %). Pri analýze prediktorov úspešnosti poradenstva sme použili participačný model (p < 0,005). Všetky údaje sme získali anonymným spôsobom. Výsledky: Mystery shopping vykonali študenti v 270 lekárňach v 42 slovenských mestách. Celkové skóre poradenstva všetkých lekární dosiahlo úspešnosť 39,0 ± 22,4 %; identifikácia pacienta 30,6 ± 28,7 %; dispenzačné informácie 39,8 ± 25,1 % a komunikácia 74,3 ± 11,5 %. Pri takmer polovici návštev expedienti identifikovali pacienta a symptómy ochorenia. Z dispenzačných informácií sa až v 70 % návštev podali informácie o dávkovaní a o cene lieku. Bezpečnosti liečby sa nevenovala dostatočná pozornosť. Pozitívne sa vyhodnotila zrozumiteľnosť rozhovoru a očný kontakt. Spôsob poradenstva (p = 0,008), trvanie poradenstva (p = 0,022), expedient a vek expedienta (obidve s p < 0,001) boli signifikantnými prediktormi úspešnosti poradenstva. Záver: Práca poukazuje na možnosť použitia metódy mystery shopping ako inovácie pri vzdelávaní študentov farmácie a ako objektívneho spôsobu sledovania dispenzačnej a poradenskej činnosti vo verejných lekárňach. Kľúčové slová: študent, farmácia, vzdelávanie, dispenzácia a poradenstvo, mystery shopping.

Stem cells derived from human dental pulp tissue (DP-MSC) differ from the other mesenchymal stem cells prepared from bone marrow or adipose tissue due to their embryonic origin from the neural crest and are of special interest because of their neurotropic character. Furthermore, the therapeutic potential of DP-MSCs is realized through paracrine action of extracellularly released components, for which exosomes play an important role. In this review, we intend to explore the properties of these cells with an emphasis on exosomes. The therapeutic applicability of these cells and exosomes in dental practice, neurodegenerative diseases, and many other difficultly treatable diseases, like myocardial infarction, focal cerebral ischemia, acute lung or brain injury, acute respiratory distress syndrome, acute inflammation, and several others is concisely covered. The use of cellular exosomes as an important diagnostic marker and indicator of targeted cancer therapies is also discussed, while the importance of stem cells from human exfoliated deciduous teeth as a source of evolutionally young cells for future regenerative therapies is stressed. We conclude that exosomes derived from these cells are potent therapeutic tools for regenerative medicine in the near future as clinical administration of DP-MSC-conditioned medium and/or exosomes is safer and more practical than stem cells.

Purpose. The goal of this paper is to find out the correlation, and evaluate the accuracy of labial minor salivary gland biopsy as a diagnostic tool in the multidisciplinary management of patients with Sjögren’s syndrome. Patients and Methods. Thirty seven patients referred to our outpatient office between January 2016 and December 2017 from a rheumatologist for biopsy examination, as part of the complex diagnostic plan for suspected Sjögren syndrome were included in the current study. Each specimen was examined histomorphometrically by the pathologist to calculate the focus score describing the degree of salivary gland inflammatory infiltration. Results. From the total number of patients, 25 presented with an established Sjögren syndrome diagnosis by fulfilling the revised American-European criteria. From those 15 had a positive lip biopsy. The rest 10 patients from the total group who were diagnosed with Sjögren syndrome based on the same criteria had a negative lip biopsy. Conclusion. The labial minor salivary gland biopsy is a valuable diagnostic tool to establish the diagnosis of Sjögren syndrome. However, a positive biopsy result must always be correlated with all the other diagnostic criteria to prove the exact diagnosis.