Extacorporeal shock wave therapy unsuccessful for chronic medial epicondylitis

Medial epicondylitis is a chronic noninflammatory condition resulting from mechanical injury. Despite many treatment options, including rest, medications, physiotherapy and operative interventions, the results are too often poor; thus new treatment options are sought. We treated 4 men with chronic epicondylitis (5 affected joints) with extracorporeal shock wave therapy after failed attempts of other treatments. The patients’ complaints were graded with the Nirschl scoring system prior to and six months after therapy. The treatment consisted of three sessions, at 20-day intervals, of 3000 pulses of ultrasonic shock waves from a Piezolith 3000 unit (energy dosage was gradually increased to reach step 10 equaling 0.9 mJ/mm²). At the 6-month follow-up, no patient was pain free. Three cases had slightly lower Nirschl scores than prior to the procedure but the patients rated this difference as insignificant; two cases were unchanged. No complications were observed but all patients rated the procedure as very unpleasant. The well recognized biologic effects of ultrasonographic waves (heat generation, oscillations, cavitation, etc.) that result in functional and structural changes of cellular membranes with sonochemical reactions (acceleration of normal metabolism, oxygenation and reduction in water solutions, polymer degradation, etc.), even if present in our cases, did not result in a noticeable decrease of symptoms, even though we used high energy and more impulses per session. Significant variations in methodology make inconclusive the results of numerous reports on the use of extracorporeal shock waves in epicondylar degenerative problems, although ineffectiveness of such therapy is the conclusion of a review by Haake and colleagues.     

Enamel loss associated with orthodontic adhesive removal on teeth with white spot lesions: an in vitro study.

Teeth with white spot lesions (WSL) might be more prone to enamel loss during bracket debonding. This in vitro study compared enamel loss from teeth with (n = 14) and without (n = 14) WSL after polishing with low-speed finishing burs or disks (Sof-Lex, 3M ESPE, St Paul, Minn). Debonded surfaces were analyzed with a contact stylus profilometer, and digitized data were compared with baseline readings by using AnSur NT software (Regents, University of Minnesota, Minneapolis, Minn). Specimen surfaces were also examined with a scanning electron microscope. Two-way analysis of variance was performed to analyze the data. In teeth without WSL, the volume losses were 0.16 mm(3) for the bur group and 0.10 mm(3) for the disk group; the mean maximum depths were 47.7 microm for the bur group and 54.3 microm for the disk group. In teeth with WSL, the volume losses were 0.06 and 0.17 mm(3), and the mean maximum depths were 35.1 and 48.7 microm for the bur and disk groups, respectively. There were no significant differences in enamel loss between the 2 groups of teeth without WSL (P =.12). However, in teeth with WSL, the burs removed less enamel than the disks (P = 0.006). Scanning electron microscope examination showed that any damage on the enamel surface was usually located in the cervical third of the teeth. On most specimens, even though tooth surfaces appeared resin-free to the naked eye, there were remnants of it. The differences between groups were so small that they might be clinically insignificant.     

The 6-min walking distance: long-term follow up in patients with COPD.

The 6-min walking distance (6MWD) test is used in clinical practice and research into patients with chronic obstructive pulmonary disease (COPD). However, little is known about natural long-term change in this parameter. The 6MWD was measured at baseline and then annually for 5 yrs in 294 patients with COPD and its annual rate of decline was determined. Forced expiratory volume in one second (FEV1) was also measured and the relationship between changes in both markers was explored. At baseline, the median 6MWD was 380 m (range 160-600 m). It declined by 19% (16 m.yr(-1)) over the 5 yrs compared with baseline in patients with American Thoracic Society/European Respiratory Society stage III COPD (FEV1 30-50% predicted) and by 26% (15 m.yr(-1)) in patients with stage IV COPD (FEV1 <30% pred). Over the 5-yr follow-up, the proportion of patients with a minimal clinically significant decline of 54 m increased with the severity of the disease. It was 24% in stage II, 45% in stage III, and 63% in stage IV disease. In contrast, the rate of decline of FEV1 was greater in patients with milder airflow obstruction and lesser in patients with lower absolute FEV1 values. In conclusion, the 6-min walking distance test provides increasingly useful information as the severity of chronic obstructive pulmonary disease increases.     

Cardiovascular and metabolic effects of CPAP in obese males with OSA.

Obstructive sleep apnoea is associated with increased blood pressure and other features of the metabolic syndrome. The aim of the present study was to determine the relative effectiveness of continuous positive airway pressure (CPAP) in modifying these outcomes. A randomised placebo-controlled blinded crossover trial comparing cardiovascular and metabolic outcomes after 6 weeks of therapeutic and sham CPAP was performed in 34 CPAP-na?ve patients (mean+/-SD body mass and respiratory disturbance indices were 36.1+/-7.6 and 39.7+/-13.8, respectively). Mean waking systolic and diastolic blood pressure fell by 6.7 and 4.9 mmHg, respectively, when compared with sham CPAP. No change was observed in glucose, lipids, insulin resistance or the proportion of patients with metabolic syndrome. In CPAP-compliant patients the fall in blood pressure was greater and the baroreceptor sensitivity improved significantly but no metabolic variable changed. In obese Caucasians with untreated obstructive sleep apnoea, continuous positive airways pressure can improve baroreceptor responsiveness and reduce waking blood pressure within 6 weeks, but this treatment period was insufficient to modify insulin resistance or change the metabolic profile. The mechanisms underlying this difference in the time course of blood pressure and metabolic response to continuous positive airway pressure in obstructive sleep apnoea requires further exploration.