Anemia, hematinic deficiencies, and hyperhomocysteinemia in gastric parietal cell antibody-positive and -negative burning mouth syndrome patients.

BACKGROUND/PURPOSE: Our previous study found the serum gastric parietal cell antibody (GPCA) positivity in 12.3% of burning mouth syndrome (BMS) patients. This study assessed whether GPCA-positive BMS (GPCA+BMS) patients had significantly higher frequencies of macrocytosis, anemia, hematinic deficiencies, and hyperhomocysteinemia than healthy control subjects or GPCA-negative BMS (GPCA-BMS) patients. METHODS: The mean corpuscular volume, blood hemoglobin (Hb), and serum iron, vitamin B12, folic acid, homocysteine, and GPCA levels were measured and compared between any two of three groups of 109 GPCA+BMS patients, 775 GPCA-BMS patients, and 442 healthy control subjects. RESULTS: We found that 109 GPCA+BMS patients had significantly higher frequencies of macrocytosis, blood Hb and serum iron and vitamin B12 deficiencies, and hyperhomocysteinemia than 442 healthy control subjects (all P-values < 0.001) and significantly higher frequencies of macrocytosis, blood Hb and serum vitamin B12 deficiencies, and hyperhomocysteinemia than 775 GPCA-BMS patients (all P-values < 0.01). Moreover, 775 GPCA-BMS patients had significantly higher frequencies of macrocytosis, blood Hb and serum iron, vitamin B12, and folic acid deficiencies, and hyperhomocysteinemia than 442 healthy control subjects (all P-values < 0.005). Pernicious anemia (45.5%) and normocytic anemia (24.2%) were the two most common types of anemia in 33 anemic GPCA+BMS patients. Moreover, normocytic anemia (61.3%), thalassemia trait-induced anemia (15.5%), and iron deficiency anemia (14.1%) were the three most common types of anemia in 142 anemic GPCA-BMS patients. CONCLUSION: GPCA+BMS patients have significantly higher frequencies of macrocytosis, blood Hb and serum vitamin B12 deficiencies, and hyperhomocysteinemia than healthy control subjects or GPCA-BMS patients.

Micromolar concentrations of citalopram or escitalopram inhibit glycoprotein VI-mediated and integrin αIIbß3-mediated signaling in human platelets.

Collagen and convulxin induce platelet aggregation through glycoprotein VI (GPVI)-FcRγ-Syk signaling pathway. In addition, fibrinogen induces platelet activation through integrin αIIbß3-FcγRIIa-Syk signaling pathway. We previously reported that high concentrations of selective serotonin reuptake inhibitors (SSRI) reduce platelet aggregation induced by collagen. We further investigated the effects of SSRI on GPVI- and αIIbß3-mediated signaling pathway. Citalopram and escitalopram, two relatively pure SSRI, were used in this study. Both citalopram and escitalopram concentration-dependently inhibited convulxin-induced platelet aggregation, serotonin (5-HT) release and the activation of αIIbß3. 5-HT concentration in washed platelets was unchanged after short-term treatment with citalopram. The additional 5-HT failed to fully rescue the inhibitory effect of citalopram on convulxin-induced aggregation. Convulxin-induced phosphorylation of Syk, LAT, and Akt was inhibited by citalopram and escitalopram. Citalopram inhibited the interaction between FcRγ and Syk, whereas the phosphorylation of FcRγ in response to convulxin remained unaltered. Further, citalopram inhibited the increase of the interaction between serotonin transporter and Syk induced by convulxin. In the presence of Mn2+, escitalopram inhibited the formation of lamellipodia on immobilized fibrinogen. Escitalopram did not influence the binding of fibrinogen to platelets. It inhibited the phosphorylation of Syk and PAK triggered by the adhesion on fibrinogen. Our data demonstrate that micromolar concentrations of citalopram and escitalopram inhibit GPVI- and αIIbß3-mediated platelet functions. The mechanism of the inhibitory effect of citalopram or escitalopram is not the influence on the activation of GPVI or the interaction between fibrinogen and αIIbß3, but the interaction between Syk and its upstream molecules.

Clinical outcomes for primary molars treated by different types of pulpotomy: A retrospective cohort study.

BACKGROUND/PURPOSE: Pulpotomy is the amputation of coronally infected pulp tissue to maintain the vitality and function of the radicular pulp. This study was designed to assess the clinical and radiographic success rates of primary molars treated by pulpotomy using diode laser, sodium hypochlorite, or no medication after a follow-up period of 24 months. METHODS: A retrospective study was conducted by evaluating the success rates of primary molars treated by pulpotomy with diode laser, sodium hypochlorite, or no medication according to the clinical symptoms and signs and radiographic features. RESULTS: There were 145 primary molars included in the study. No significant differences in clinical and radiographic success rates were found among primary molars treated by pulpotomy using diode laser, sodium hypochlorite, or no medication, when the teeth were treated by experienced pedodontists and restored with stainless steel crowns. The 2-year clinical success rates for primary molars treated by pulpotomy using diode laser, sodium hypochlorite, or no medication were all 100%. The 2-year radiographic success rates were 90.9%, 100%, and 87.5% for primary molars treated by pulpotomy using diode laser, sodium hypochlorite, or no medication, respectively. However, when the pulpotomy for primary molars was performed by less-experienced residents, a reduced overall success rate from 94% for attending doctors to 58% for residents was found. CONCLUSION: Operators and final restorations are confounding factors for determining the success rate of primary molars treated by pulpotomy. Pulpotomy with diode laser, sodium hypochlorite, or no medication are all acceptable treatments of choice for coronally infected primary molars.

Shear bond strength and microleakage results for three experimental self-etching primer compositions for pit and fissure sealing.

OBJECTIVES: This in vitro study evaluated the shear bond strength (SBS) and microleakage of three experimental self-etching primers for pit and fissure sealing. MATERIALS AND METHODS: The material used three formulations of an experimental fissure primer (EFP) applied without phosphoric acid etching (EFP-1/EFP-2/EFP-3) and one control group with sealant application after 30 s of acid etching. Four groups of sealants (n = 40 specimens/group) were tested for SBS, and a failure analysis was conducted after 1-day water storage, 3-month water storage, and 5000-fold thermocycling. In addition, microleakage was tested. RESULTS: The SBSs of the EFPs (range 8.2 MPa (standard deviation 4.2) to 15.4 MPa (5.4)) were generally significantly lower than those of conventional fissure sealing (range 15.6 MPa (4.4) to 19.1 MPa (6.2)). The SBS of EFP-3 was better than that of the EFP-1 or EFP-2 formulations. Microleakage was significantly lower in the control group (1.1 %) than in the EFP-1 (3.8 %) and lower than in EFP-3 (7.7 %) group. In the (multiple) linear regression analysis, material and aging significantly influenced SBS. CONCLUSIONS: The SBS of EFP-3 was 15 to 32 % lower than it was for the corresponding controls. CLINICAL RELEVANCE: The SBS is lower, but the main potential benefit of this new approach is a reduced application time in clinical practice.

Which Factors Influence the Shear Bond Strength of Sealant Materials?

PURPOSE: This study investigated the influence of several methodological details on the shear bond strength (SBS) testing of pit and fissure sealants. The following variables were considered: type of enamel surfaces, prismatic vs aprismatic enamel, etching time, and aging and shearing procedures. MATERIALS AND METHODS: The surfaces of 180 healthy human third molars were divided into 4 different sections (mesial, distal, buccal, and oral). After tooth separation, the specimens were randomly allocated to the following groups: 1) enamel preparation: prismatic vs aprismatic; 2) etching: 30 s vs 60 s; 3) aging: 1 day or 3 months vs 5000 thermocycles; 4) shearing: notched-edge method (ISO 29022:2013) vs knife-edge method. After following each protocol, SBS was determined using a universal testing machine, followed by failure mode analysis. Data were analysed using Mann-Whitney U-tests and regression analyses. RESULTS: In the aprismatic enamel group, the longer etching time resulted in slightly, not statistically significantly higher SBS. When aging sealants on aprismatic enamel with different procedures, significantly lower SBS was found for 5000 thermocycles. In the case of aprismatic enamel etched for 60 s and sheared with the notched-edge blade, there was no significant difference between the aging procedures. Failure mode analysis showed adhesive failures to be predominant. Simple linear regression revealed that all of the included factors significantly influenced SBS. In a multiple linear regression model, the variables "aprismatic enamel" and "distal surface" were associated with a higher SBS; "5000 thermocycles" reduced SBS significantly. CONCLUSION: Enamel grinding, aging method, and type of enamel surface significantly influenced the SBS.

Increased placenta growth factor mRNA level is significantly associated with progression, recurrence and poor prognosis of oral squamous cell carcinoma.

BACKGROUND/PURPOSE: Expression of placenta growth factor (PlGF) mRNA is shown to correlate with the progression and prognosis of several human cancers. In this study, we assessed whether the PlGF mRNA level in oral squamous cell carcinoma (OSCC) tissue could be used to predict the progression and prognosis of OSCCs in Taiwan. METHODS: This study used quantitative real-time reverse transcription-polymerase chain reaction (quantitative RT-PCR) to detect the PlGF mRNA levels in 63 paired OSCC and adjacent normal-looking oral mucosa (non-OSCC) tissues. Threshold cycle (CT) was defined as the PCR cycle number needed to generate a pre-determined amount of DNA (threshold). For a chosen threshold, a smaller starting copy number of mRNA results in a higher CT value. In this study, the relative expression level of tissue PlGF mRNA in each OSCC patients was expressed as -ΔCT = -(OSCC CT - non-OSCC CT). Thus, the higher the -ΔCT, the greater the copy number of PlGF mRNA in tissues. RESULTS: We found that the higher mean PlGF mRNA -ΔCT value was significantly associated with OSCCs with larger tumor size (p = 0.03), positive lymph node metastasis (p = 0.003), more advanced clinical stages (p = 0.013) or the presence of loco-regional recurrence (p = 0.039). Positive lymph node metastasis (p = 0.019) and PlGF mRNA -ΔCT value >2 (p = 0.016) were identified as two independent unfavorable prognosis factors by multivariate analyses with Cox regression model. Moreover, Kaplan-Meier curve showed that OSCC patients with a PlGF mRNA -ΔCT value >2 had a significantly poorer recurrence-free survival than those with a PlGF mRNA -ΔCT value ≤2 (log-rank test, p = 0.017). CONCLUSION: The OSCC tissue PlGF mRNA level can be used to predict the progression and prognosis of OSCCs in Taiwan.

Efficacy of oral nystatin treatment for patients with oral mucosal dysesthesia but without objective oral mucosal manifestations and necessity of Candida culture test before oral nystatin treatment.

Background/purpose: Previous studies have shown that some of the patients with oral mucosal dysesthesia but without objective oral mucosal manifestations (so-called oral dysesthesia patients in this study) may have good responses to oral nystatin treatment. This study evaluated the efficacy of oral nystatin treatment for oral dysesthesia patients and the necessity of Candida culture test before oral nystatin treatment. Materials and methods: The 147 oral dysesthesia patients were divided into 3 groups: Candida culture (+) group (n = 29), Candida culture (-) group (n = 34), and without Candida culture test group (n = 84), and treated with oral nystatin. The pain improvement was evaluated by the reduction of numeric pain rating scale (NRS) and global perceived effects (GPE). We defined the GPE score ≥4 points as a great improvement. Results: We found that 44.8% of 29 patients in the Candida culture (+) group, 47.1% of 34 patients in the Candida culture (-) group, and 47.6% of 84 patients in the without Candida culture test group showed a significant reduction in the NRS score and achieved a great improvement after oral nystatin treatment for 1-4 weeks. Moreover, 72.4% of our 29 patients with Candida culture test achieved a great improvement within one week, and all the 29 patients achieved a great improvement within 4 weeks of oral nystatin treatment. Conclusion: A portion of our oral dysesthesia patients are infected by Candida and it is beneficial to our patients to use oral nystatin treatment before the Candida culture test.

Expression of vascular endothelial growth factor is significantly associated with progression and prognosis of oral squamous cell carcinomas in Taiwan.

BACKGROUND/PURPOSE: Expression of vascular endothelial growth factor (VEGF) correlates with progression and prognosis of several human cancers. The main purposes of this study were to assess expression of VEGF in specimens of oral squamous cell carcinoma (OSCC) and to evaluate the possible influence of VEGF on the progression and prognosis of OSCC in Taiwan. METHODS: An immunohistochemical technique was used to examine the expression of VEGF in 100 specimens of OSCC, 66 specimens of oral epithelial dysplasia, and 36 specimens of normal oral mucosa. RESULTS: We found that the mean labeling indices (Lis) of VEGF increased significantly from normal oral mucosa (13 ± 6%), through mild (22 ± 8%), moderate (24 ± 13%), and severe oral epithelial dysplasia (32 ± 14%), to OSCC samples (50 ± 18%, p < 0.001). The higher mean VEGF LI was significantly related to OSCC with positive lymph node metastasis (p = 0.022) and with more advanced clinical stages (p = 0.046). In addition, positive lymph node metastasis (p = 0.008) and VEGF LI > 40% (p = 0.046) were identified as independent unfavorable prognosis factors for OSCC patients by multivariate analysis with the Cox regression model. Moreover, the Kaplan-Meier curve showed that OSCC patients with a VEGF LI > 40% had a significantly poorer cumulative survival than those with a VEGF LI ≤ 40% (log-rank test, p = 0.016). CONCLUSION: We conclude that VEGF may be a biomarker for prediction of the progression and prognosis of OSCC in Taiwan.

Differential toxicities of intraneurally injected mercuric chloride for sympathetic and somatic motor fibers: an ultrastructural study.

BACKGROUND/PURPOSE: Mercury is a well-known neurotoxin but the susceptibility of autonomic nerves to mercury poisoning in vivo has seldom been studied. Our previous studies have shown that the hypoglossal nerve in hamsters contains somatic motor and postganglionic sympathetic fibers. The aim of this study was to investigate the ultrastructural changes in the nervous system following intraneural injection of mercuric chloride into the hypoglossal nerve in hamsters. METHODS: Six adult hamsters were used in this study. After anesthesia, the digastric muscle on the right side was removed and the trunk of the hypoglossal nerve was exposed. Two microliters of mercuric chloride aqueous solution was injected into the main trunk of the hypoglossal nerve at the bifurcation. The contralateral hypoglossal nerve was kept intact and used as the normal control. Animals were allowed to survive for 1 or 3 days and were prepared for ammonium sulfide histochemistry and electron microscopy. RESULTS: Three days after injection of mercuric chloride solution, almost all unmyelinated sympathetic fibers in the hypoglossal nerve trunk were lost, whereas myelinated somatic axons were spared. Although mercury deposition in the myelin sheaths of neuronal processes was observed in the hypoglossal nucleus, the neuronal somas were intact. By contrast, degenerated neuronal processes and mercury deposition in neuronal somas were frequently found in the superior cervical ganglia. CONCLUSION: This study demonstrated an undue susceptibility of sympathetic fibers to mercury intoxication. The mechanisms that underlie the selective reaction of sympathetic fibers to mercury warrant further investigation.

Anemia, hematinic deficiencies, and gastric parietal cell antibody positivity in burning mouth syndrome patients with or without hyperhomocysteinemia.

BACKGROUND/PURPOSE: Our previous study found that 170 of 884 burning mouth syndrome (BMS) patients have hyperhomocysteinemia. This study assessed whether these 170 BMS patients with hyperhomocysteinemia had significantly higher frequencies of anemia, hematinic deficiencies, and serum gastric parietal cell antibody (GPCA) positivity than 714 BMS patients without hyperhomocysteinemia or 442 healthy control subjects. MATERIALS AND METHODS: The blood hemoglobin (Hb) and serum iron, vitamin B12, folic acid, homocysteine, and GPCA levels in 170 BMS patients with hyperhomocysteinemia, 714 BMS patients without hyperhomocysteinemia, and 442 healthy control subjects were measured and compared. RESULTS: We found that 170 BMS patients with hyperhomocysteinemia had significantly higher frequencies of macrocytosis, blood Hb and serum iron, vitamin B12, and folic acid deficiencies, and serum GPCA positivity than 442 healthy control subjects (all P-values < 0.001) or 714 BMS patients without hyperhomocysteinemia (all P-values < 0.05). Anemia was found in 77 of 170 BMS patients with hyperhomocysteinemia and in 98 of 714 BMS patients without hyperhomocysteinemia. Normocytic anemia (47 cases) and pernicious anemia (15 cases) were the two most common types of anemia in 170 BMS patients with hyperhomocysteinemia. Moreover, normocytic anemia (48 cases), iron deficiency anemia (21 cases), and thalassemia trait-induced anemia (21 cases) were the three most common types of anemia in 714 BMS patients without hyperhomocysteinemia. CONCLUSION: BMS patients with hyperhomocysteinemia had significantly higher frequencies of macrocytosis, anemia, serum iron, vitamin B12, and folic acid deficiencies, and serum GPCA positivity than healthy control subjects or BMS patients without hyperhomocysteinemia.

Anemia, hematinic deficiencies, hyperhomocysteinemia, and gastric parietal cell antibody positivity in burning mouth syndrome patients with vitamin B12 deficiency.

BACKGROUND/PURPOSE: Our previous study found that 42 of 884 burning mouth syndrome (BMS) patients have vitamin B12 deficiency. This study assessed whether the vitamin B12-deficient BMS (B12D/BMS) patients had significantly higher frequencies of anemia, hematinic deficiencies, hyperhomocysteinemia, and serum gastric parietal cell antibody (GPCA) positivity than healthy control subjects and evaluated whether all B12D/BMS patients had pernicious anemia (PA). MATERIALS AND METHODS: The blood hemoglobin (Hb) and serum iron, vitamin B12, folic acid, homocysteine, and GPCA levels in 42 B12D/BMS patients and 442 healthy control subjects were measured and compared. RESULTS: We found that 42 B12D/BMS patients had significantly lower mean blood Hb and serum iron and vitamin B12 levels as well as significantly higher mean corpuscular volume (MCV) and mean serum homocysteine level than healthy control subjects (all P-values < 0.05). Moreover, 42 B12D/BMS patients had significantly higher frequencies of macrocytosis (52.4%), blood Hb (61.9%) and serum iron (26.2%) and vitamin B12 (100.0%) deficiencies, hyperhomocysteinemia (83.3%), and serum GPCA positivity (42.9%) than 442 healthy control subjects (all P-values < 0.001). Moreover, of 26 anemic B12D/BMS patients, 15 (57.7%) had PA, 5 (19.2%) had macrocytic anemia other than PA, 4 (15.4%) had normocytic anemia, and 2 (7.7%) had thalassemia trait-induced anemia. CONCLUSION: B12D/BMS patients have significantly higher frequencies of macrocytosis, blood Hb and serum iron and vitamin B12 deficiencies, hyperhomocysteinemia, and serum GPCA positivity than healthy control subjects. Although PA is the most common type of anemia in our B12D/BMS patients, only 15 (35.7%) of 42 B12D/BMS patients have PA.

Anemia, hematinic deficiencies, hyperhomocysteinemia, and gastric parietal cell antibody positivity in burning mouth syndrome patients with iron deficiency.

BACKGROUND/PURPOSE: Our previous study found that 143 of 884 burning mouth syndrome (BMS) patients have iron deficiency (ID). This study assessed whether all BMS patients with ID (so-called ID/BMS patients) had iron deficiency anemia (IDA) and evaluated whether the ID/BMS patients had significantly higher frequencies of anemia, hematinic deficiencies, hyperhomocysteinemia, and serum gastric parietal cell antibody (GPCA) positivity than healthy control subjects. MATERIALS AND METHODS: The blood hemoglobin (Hb) and serum iron, vitamin B12, folic acid, homocysteine, and GPCA levels in 143 ID/BMS patients and 442 healthy control subjects were measured and compared. RESULTS: We found that 143 ID/BMS patients had significantly lower mean blood Hb and serum iron, vitamin B12, folic acid levels as well as significantly higher mean serum homocysteine level than healthy control subjects (all P-values < 0.01). Moreover, 143 ID/BMS patients had significantly higher frequencies of blood Hb (55.9%) and serum iron (100.0%), vitamin B12 (7.7%), and folic acid (2.1%) deficiencies, hyperhomocysteinemia (27.3%), and serum GPCA positivity (12.6%) than 442 healthy control subjects (all P-values < 0.001). Furthermore, of 80 anemic ID/BMS patients, 5 (6.3%) had pernicious anemia, 5 (6.3%) had macrocytic anemia other than pernicious anemia, 42 (52.5%) had normocytic anemia, 21 (26.3%) had IDA, and 7 (8.8%) had thalassemia trait-induced anemia. CONCLUSION: ID/BMS patients had significantly higher frequencies of blood Hb and serum iron, vitamin B12, and folic acid deficiencies, hyperhomocysteinemia, and serum GPCA positivity than healthy control subjects. Normocytic anemia is the most common type of anemia in ID/BMS patients.

Shear bond strength and microleakage of a new self-etch adhesive pit and fissure sealant.

This study aimed to evaluate the shear bond strength (SBS) and microleakage of a new self-etch adhesive-based fissure sealant (EG) on aprismatic enamel in comparison to conventional fissure sealing with 30 s acid etching (CG). The fissures were sealed according to the manufacturer's instructions. Each group was divided into 3 subgroups: 1-day water storage, 3-month water storage, and 5,000× thermocycling. After measuring SBS using the Ultradent method, failure mode was analyzed. In additional 16 teeth, microleakage was tested using dye penetration method. Pairwise comparisons were analyzed using Mann-Whitney U-Test. Multiple linear regression was performed to assess the factors influencing on SBS. EG had significantly lower mean SBS (4.1 MPa±2.1) than the CG (17.6 MPa±6.4). CG (1.1%) performed significantly better than the EG (12.8%) in microleakage analysis. The tested EG yielded significantly inferior results and its clinical use should be decided after weighing its pros and cons.

Selective serotonin reuptake inhibitors reduce P2Y12 receptor-mediated amplification of platelet aggregation.

Selective serotonin reuptake inhibitors (SSRIs) have been reported to reduce platelet aggregation induced by ADP. ADP induces platelet aggregation through two purinergic receptors P2Y1 and P2Y12. We characterized the inhibitory properties of SSRIs on ADP-induced platelet aggregation and investigated the effects of SSRIs on the signaling pathways downstream of P2Y1 and P2Y12 receptors. Specific antagonists were used to evaluate which purinergic receptor-mediated aggregation was influenced by SSRIs. The primary phase of ADP-induced aggregation was not inhibited by citalopram. Citalopram failed to influence ADP-induced platelet shape change, intracellular calcium mobilization and the early phosphorylation of PKCα. Differently, citalopram inhibited the secondary phase of ADP-induced platelet aggregation in a concentration-dependent manner. Other SSRIs, including fluoxetine and sertraline, exhibited the same anti-platelet effects. Under P2Y1 blockade, citalopram inhibited platelet aggregation and integrin αIIbß3 activation in response to ADP, indicating that citalopram inhibited P2Y12-mediated aggregation. Citalopram concentration-dependently inhibited the phosphorylation of Akt, GSK3ß, p38 MAPK and Syk induced by ADP, but showed no effect on the decrease of cAMP and VASP phosphorylation. With integrin αIIbß3 blockade, however, the phosphorylation of Akt triggered by ADP was unaltered by the addition of citalopram. Taken together, under the stimulation of ADP, SSRIs inhibit the amplification of platelet aggregation secondary to the activation of P2Y12 receptor, and subsequently reduce the activation of the downstream molecules of the outside-in signaling pathways.

A selective serotonin reuptake inhibitor, citalopram, inhibits collagen-induced platelet aggregation and activation.

Clinical depression is a significant risk factor for cardiovascular diseases and confers an increased risk of mortality. Increased platelet reactivity may predispose depressed patients to cardiovascular diseases. The antidepressants selective serotonin reuptake inhibitors (SSRIs) have been found to have cardioprotective effects probably via the attenuation of platelet activation independently in addition to treatment of depression itself. However, the characters of the inhibitory effect of SSRIs on platelets remain largely unknown. Here we show that an SSRI, citalopram, specifically inhibited collagen-induced platelet aggregation. Citalopram, however, revealed only little inhibitory effect on platelet aggregation induced by thrombin, U46619, and ionomycin, and failed to inhibit reversible platelet aggregation induced by adenosine diphosphate with fibrinogen. Collagen-induced of αIIbß3 integrin activation in platelets under a static condition was not influenced by citalopram. Citalopram inhibited convulxin-induced platelet aggregation and αIIbß3 integrin activation. In the experiments with fibrinogen-induced aggregation in elastase-treated platelets, citalopram inhibited only collagen-induced αIIbß3 activation but not the binding activities between activated αIIbß3 integrin and fibrinogen. Moreover, citalopram inhibited α-granule and dense granule secretion from platelets in response to collagen, as determined by a reduced expression of P-selectin and adenosine triphosphate release, respectively. In addition, collagen-induced thromboxane A2 release in platelets was attenuated by citalopram pretreatment. These findings might specify the mechanisms of inhibitory effects of citalopram on collagen mediated platelet activation and aggregation, and further support the cardioprotective effect of SSRIs.