Effects of habitual knuckle cracking on metacarpal cartilage thickness and grip strength.

Joint cracking involves a manipulation of the finger joints resulting in an audible crack. This study aimed to determine whether habitual knuckle cracking (KC) leads to an alteration in grip strength and metacarpal head (MH) cartilage thickness. Thirty-five habitual knuckle crackers (cracking their joints ≥5times/day) (20 M, 15 F, aged 19-27 years) and 35 age-, gender-, and body mass index-matched non-crackers were enrolled in the study. MH cartilage thickness was measured with ultrasound and grip strength was measured with an analog Jamar hand dynamometer. Grip strength was similar between groups (P>0.05). Habitual knuckle crackers had thicker MH cartilage in the dominant and non-dominant hands than those of the controls (P=0.038 and P=0.005, respectively). There was no correlation between MH cartilage thickness and grip strength in both groups (P>0.05). While habitual KC does not affect handgrip strength, it appears to be associated with increased MH cartilage thickness.

Sclerostin and Dkk-1 in patients with ankylosing spondylitis.

OBJECTIVE: To determine the serum Dickkopf-related protein 1 (Dkk-1) and sclerostin levels, and their relationship to structural damage and disease activity in patients with ankylosing spondylitis (AS), as well as to compare the serum Dkk-1 and sclerostin levels in patients receiving and not receiving anti-TNF-a treatment. MATERIALS AND METHOds: This cross-sectional study included 44 AS patients and 41 healthy age- and gender- -matched controls. Demographic data, disease activity parameters, and Bath Ankylosing Spondylitis Radiologic Index (BASRI) scores were recorded. Serum Dkk-1 and sclerostin levels were measured using commercially available ELISA. RESULTS: Serum Dkk-1 levels were lower (P > 0.05) and sclerostin levels were significantly lower (P < 0.05) in the AS patients than in the controls. Dkk-1 and sclerostin levels were similar in the patients that did and didn't receive anti-TNF-a treatment, and in the patients with active and inactive disease (P > 0.05). There wasn't a correlation between serum Dkk-1 or sclerostin levels, and disease activity indices (P > 0.05). BASRI scores did not correlate with serum Dkk-1 or sclerostin levels (P > 0.05). DISCUSSIOn: Sclerostin expression is impaired in AS, but this is not the case for Dkk-1. The lack of an association between Dkk-1 or sclerostin levels, and anti-TNF-a treatment, disease activity indices, and radiological damage might indicate that neither the Dkk-1 nor sclerostin level induce inflammation and radiological damage in AS patients. Pathologic bone formation in AS might be due to molecular dysfunction of sclerostin and Dkk-1 at the cellular level.

Diffuse osteosclerosis in a patient with prostate cancer.

A 61-year-old man was referred to our outpatient clinic because of severe bilateral upper leg pain for 1 year. On admission, the patient had anemia and a high serum alkaline phosphatase level. Lumbar and femoral neck T-scores were +10.5 and +9.6, respectively. His radius 33 % T-score was -2.8. Plain radiographs of the patient's pelvis, spine, and long bones revealed osteosclerosis. The patient had previously undergone a prostate biopsy, which showed prostate adenocarcinoma (Gleason score 3 + 4). The patient's total and free prostate-specific antigen were very high. According to previous records, the patient did not have anemia, and his serum alkaline phosphatase (ALP) level was normal. An abdominal radiograph taken 2 years earlier revealed a normal spine and pelvic bone. Bone scintigraphy yielded nontypical findings for prostate cancer metastasis. Computed tomography of the patient's thorax and abdomen showed heterogeneous sclerotic areas in all bones consistent with prostate cancer metastasis. A bone marrow biopsy disclosed disseminated carcinomatosis of bone marrow in association with prostate cancer. Clinicians should be aware of the possibility of prostate malignancy as a cause of high bone mineral density (BMD), even in the absence of typical localized findings on plain radiographs.

The relationship between anti-cyclic citrullinated peptide and bone mineral density and radiographic damage in patients with rheumatoid arthritis.

OBJECTIVES: We aimed to investigate the relationship between anti-cyclic citrullinated peptide (anti-CCP) levels and bone mineral density (BMD), bone turnover, and radiographic damage in patients with rheumatoid arthritis (RA). METHODS: Eighty patients (68 females, 12 males, mean age 46.50+/-14.59 years) with RA were included in the study. Anti-CCP antibodies were measured by enzyme-linked immunosorbent assay (ELISA). Bone turnover was studied by analysing serum levels of C-terminal telopeptide of type I collagen (sCTX, ng/mL), using an enzyme immunoassay. BMD was measured by dual-energy X-ray absorptiometry (DXA). Disease activity was assessed according to the Disease Activity Score that includes 28 joint counts (DAS28). Functional capacity was assessed by the Health Assessment Questionnaire (HAQ). RESULTS: Anti-CCP-positive patients were defined as group 1 and anti-CCP-negative patients as group 2. The mean disease duration was 7.53+/-6.27 years in group 1 and 6.25+/-6.51 years in group 2. Anti-CCP had a limited negative correlation with lumbar BMD (r = -0.220, p = 0.050) and a negative correlation with femoral BMD (r = -0.242, p = 0.031). There was no statistically significant correlation between anti-CCP and sCTX values (r = 0.117, p = 0.301). Sharp scores were significantly higher in anti-CCP-positive than anti-CCP-negative patients (p = 0.012), and anti-CCP levels were significantly correlated with Sharp scores (r = 0.240, p = 0.032). CONCLUSIONS: We found that RA patients with higher levels of anti-CCP antibody had lower lumbar and femoral BMD. Anti-CCP levels were also associated with radiographic damage. Therefore, we suggest that anti-CCP may be a determinant of bone loss in patients with RA.

Botulinum toxin A in the treatment of spasticity - An open label study.

PURPOSE: To assess the efficacy of botulinum toxin type A in spasticity in upper-motor neuron syndromes. METHODS: Twenty-three patients with spasticity resulted from stroke-related hemiplegia, transverse myelitis and multiple sclerosis took part in the study. Following the history and physical examinations of the patients, injections of botulinum toxin-A were applied. The dose ranged from 80 to 400 mouse unit (MU) depending on the size of the muscle injected. In all patients, spasticity, spasms and pain were measured using the Ashworth Scale, Spasm Frequency Score, and Visual Analogue Scale prior to the therapy, at the 1st week, 1st month and 3rd month of the therapy. RESULTS: In all patients, botulinum toxin type A led to a significant decrease in spasticity, spasms and pain after the 1st week, 1st and 3 rd months of the treatment when compared to the baseline values (p<0.001). No significant side effects or complications were observed. CONCLUSION: Our results have demonstrated that botulinum toxin type A is effective in the management of patients with spasticity due to stroke-related hemiplegia, transverse myelitis and multiple sclerosis, without major adverse effects.

Lung perfusion in hemorrhagic shock of rats: the effects of resuscitation with whole blood, saline or Hes 6%.

This study was undertaken to determine the effects of various resuscitation regimens on lung perfusion following resuscitation from hemorrhagic shock. Fourty male Sprague-Dawley rats (250-300 g) were used. The rats were divided randomly into four groups (n = 10 for each) and were sedated with intramuscular ketamine (100 mg/kg). We measured blood pressure, rectal temperature and lung perfusion using radioscintigraphy with a technetium colloid indicator. The systolic blood pressure was decreased 75% by removing blood via v. jugularis in the first three groups and group 4 was accepted as the control group, and blood volume was not diminished. Then the first three groups were resuscitated with autologous blood containing 125 units heparine/ml in group 1, saline in group 2, and hydroxyethyl starch (HES) 6% in group 3. After the correction of hypovolemia, all animals were injected 100 Bg (0.1 cc) technetium 99 m macroaggregated albumin (99mTc MAA) via penil vein. After injection of 99mTc MAA, 3 minutes fixed images were detected by a y camera in posterior position at 15 minutes and 5 hours. 99mTc MAA "wash out" rate in lung was determined quantitatively at 5 hours. Compared to a control group, lung perfusion was decreased significantly in groups resuscitated with saline, and HES 6% while perfusion was restored with autologous blood. We conclude that heparinized autologous blood saved lung capillary circulation in hemorrhagic shock in rats.