Calcific Deposits (calcific + deposit)

Distribution by Scientific Domains


Selected Abstracts


Prognostic factors in nonoperative therapy for chronic symptomatic calcific tendinitis of the shoulder

ARTHRITIS & RHEUMATISM, Issue 10 2009
P. Ogon
Objective To define prognostic factors in chronically symptomatic patients with calcific tendinitis of the shoulder. Methods We evaluated 420 patients (488 shoulders) in the context of a prospective cohort study. Epidemiologic data were assessed. The radiographic and sonographic appearance of the calcific deposits was classified. The mean period of nonoperative therapy was 4.4 years (range 0.5,13.7 years). After referral to our institution, standardized nonoperative therapy was continued for a minimum of 3 months. Failure of nonoperative therapy was defined as the persistence of symptomatic calcific tendinitis of the shoulder after a minimum of 6 months. Prognostic factors (determined at P < 0.05 by chi-square test) were analyzed by logistic regression. Results Of the 420 patients, 269 (64%) were women, 151 (36%) were men. The mean age of the patients was 51.3 years (range 28,84 years). Occurrence of calcific tendinitis of the shoulder was unilateral in 84% and bilateral in 16%. Gärtner type I calcific deposits were found in 37%, type II in 32%, and type III in 31%. Failure of nonoperative therapy was observed in 114 patients (27%). Negative prognostic factors were bilateral occurrence of calcific tendinitis of the shoulder, localization to the anterior portion of the acromion, medial (subacromial) extension, and high volume of the calcific deposit. Positive prognostic factors were a Gärtner type III deposit and a lack of sonographic sound extinction of the calcific deposit. Conclusion Our findings demonstrate the existence of prognostic factors in the nonoperative treatment of chronic symptomatic calcific tendinitis of the shoulder. Guidelines for optimal treatment can be implemented according to these factors to avoid a long-term symptomatic disease course. [source]


Fibroblast growth factor (FGF)-23 and fetuin-A in calcified carotid atheroma

HISTOPATHOLOGY, Issue 6 2010
Mathias Voigt
Voigt M, Fischer D-C, Rimpau M, Schareck W & Haffner D (2010) Histopathology56, 775,788 Fibroblast growth factor (FGF)-23 and fetuin-A in calcified carotid atheroma Aims:, Human atheroma calcification occurs secondary to repetitive injury/remodelling of the vessel wall and might be initiated by adherence of mineral-loaded fetuin-A whether or not professional matrix mineralizing cells are present. The aim was to investigate the contribution of fibroblast growth factor (FGF)-23 to ectopic mineralization. Methods and results:, Serial sections of formalin-fixed paraffin-embedded human carotid atheroma (n = 54) were investigated with respect to (i) size and distribution of calcific deposits, (ii) indicators of chondrogenic/osteogenic transformation, and (iii) expression of fetuin-A and FGF-23. All specimens were calcified and SOX-9, collagen type II, cathepsin-K, fetuin-A and FGF-23 expression was seen in 46, 53, 53, 54 and 48 specimens, respectively. The intracellular detection of FGF-23 (45/48) indicates local synthesis. Whereas fetuin-A expression was seen also within areas of vascular smooth muscle actin-positive cells adjacent to calcific deposits, FGF-23 expression was apparently restricted to the mineralization-prone areas. Both local expression and FGF-23 serum concentrations were significantly associated with the degree of atheroma calcification. Conclusions:, Besides the induction of bone islets and subsequent mineral deposition, severe remodelling of the vessel wall is sufficient to create a mineralizable fetuin-A-attracting microenvironment. FGF-23 might contribute to the formation of proper mineral, i.e. control local phosphate concentration. [source]


Prognostic factors in nonoperative therapy for chronic symptomatic calcific tendinitis of the shoulder

ARTHRITIS & RHEUMATISM, Issue 10 2009
P. Ogon
Objective To define prognostic factors in chronically symptomatic patients with calcific tendinitis of the shoulder. Methods We evaluated 420 patients (488 shoulders) in the context of a prospective cohort study. Epidemiologic data were assessed. The radiographic and sonographic appearance of the calcific deposits was classified. The mean period of nonoperative therapy was 4.4 years (range 0.5,13.7 years). After referral to our institution, standardized nonoperative therapy was continued for a minimum of 3 months. Failure of nonoperative therapy was defined as the persistence of symptomatic calcific tendinitis of the shoulder after a minimum of 6 months. Prognostic factors (determined at P < 0.05 by chi-square test) were analyzed by logistic regression. Results Of the 420 patients, 269 (64%) were women, 151 (36%) were men. The mean age of the patients was 51.3 years (range 28,84 years). Occurrence of calcific tendinitis of the shoulder was unilateral in 84% and bilateral in 16%. Gärtner type I calcific deposits were found in 37%, type II in 32%, and type III in 31%. Failure of nonoperative therapy was observed in 114 patients (27%). Negative prognostic factors were bilateral occurrence of calcific tendinitis of the shoulder, localization to the anterior portion of the acromion, medial (subacromial) extension, and high volume of the calcific deposit. Positive prognostic factors were a Gärtner type III deposit and a lack of sonographic sound extinction of the calcific deposit. Conclusion Our findings demonstrate the existence of prognostic factors in the nonoperative treatment of chronic symptomatic calcific tendinitis of the shoulder. Guidelines for optimal treatment can be implemented according to these factors to avoid a long-term symptomatic disease course. [source]