Nowadays more attention is paid to the quality of life during and after cancer treatment, and fatigue is an important factor influencing this. Still little is known about the development of fatigue before, during and after cancer treatment and its contributing factors. We analyzed the level of fatigue, pain, anxiety and activity before and after the treatment of benign or low-grade malignant bone and soft tissue tumours in 43 patients. All patients were treated with surgery only. The mean age of the patients was 40 years (range 20 to 67 years). Fatigue severity was measured with the CIS-fatigue questionnaire, where a score of 35 or higher reflects severe fatigue. The VAS score was used to measure pain (0=no pain, 10=severe pain), and the Dutch version of the Spielberger State-Trait Anxiety Inventory to measure state anxiety. Physical activity was measured with an actometer, worn at the ankle for two weeks. All measurements were done before the tumor surgery and twelve months later. Severe fatigue was seen in 35% of the patients before they had tumor surgery. After 12 months 32% of the patients still was severely fatigued. The mean VAS pain score was 2,3 before treatment and 2,2 after 12 months. The anxiety score lowered from 38,1 before treatment to 33,2 one year later. Actometer scores increased from 57,7 before treatment to 69,9 after 12 months. Fatigue severity correlated with pain and anxiety both before and 12 months after treatment, but not with actometer scores. In this study we see that severe fatigue is present in 35% of tumor patients before they are treated, and this percentage remains high (32%) until one year after surgery. Since severe fatigue correlated with more anxiety and pain, these symptoms can help us understand and treat severe fatigue in tumor patients better.
Data were prospectively collected from the tumour register and patient records. Functional scores of the affected limbs were assessed according to the Musculo-Skeletal Tumour Society scoring system.
The minimal follow up was two years, and the average follow up 50 months (range 24–119 months). At follow up three recurrences had occurred in patients treated for enchondroma. One residual tumour was diagnosed in a patient with chondrosarcoma grade Ib. All patients were treated again with curettage and cryosurgery and disease free at the latest follow-up. Of the 37 complications the most common were a fracture at the surgical site (18), fracture of osteosynthesis (6), 3 wound infection (3), delayed soft tissue healing (3), and transient nerve palsy (3). Functional MSTS scores increased in time to an average of 28 points (94%) at two year follow up. No significant difference in scores were found regarding to localisation of the lesion, age or gender. A significant discrepancy in functional scores was observed between patients who did suffer from one or more complications and patients who did not.
Type I and II collagen-based scaffolds, with and without attached chondroitine sulphate (CS), were implanted without additional chondrocytes into full-thickness defects in the trochlea of young adult rabbits. We hypothesise that the chemical composition of the matrix will have a direct effect on the speed of repopulation and the phenotypic expression of the subchondral repair cells. Evaluation of the repair process was performed with routine histology and with two quantitative histological grading systems, four and twelve weeks after implantation. Four weeks after implantation, type I collagenous scaffolds were completely filled with a cartilage-like repair tissue. By contrast, type II collagenous scaffolds showed a superficial zone of cartilaginous tissue, and in many defects chondrocyte-like cells at the interface of the implant material with the subchondral bone. In collagen type II filled lesions larger areas of the scaffolds were completely devoid of repair tissue. Control defects showed a repair reaction that was very similar to that observed in defects filled with a type I scaffold. After 12 weeks, the subchondral defect was largely replaced by bone and the differences between the scaffolds were less pronounced. The quantitative blind score of the sections confirmed that the scores of the control defect and of the collagen type I based scaffolds were slightly higher as compared to the type II based scaffolds. Irrespective of the type of scaffold, there was a trend that the scaffolds with CS scored slightly higher than those without CS. We conclude that different types of scaffold induce different repair reactions. Collagen types I based scaffolds seem superior to guide progenitor cells from a subchondral origin into the defect. Repair cells in collagen type II based scaffolds seem to assume a chondrocyte-like phenotype, which could have a negative effect on the mobility of the repair cells.