Long-term follow-up of anatomic graduated component total knee arthroplasty: a 15- to 20-year survival analysis.

The aims of this study were to determine survival rate, the clinical performance, and radiologic results of an Anatomic Graduated Component (AGC) total knee arthroplasty (TKA). Survival analysis was assessed by analyzing all hospital records of 211 AGC TKAs in 177 patients after 15 to 20 years. The survival rate was 87%, with failure defined as revision for any reason including infection. The main reasons for failure were infection and failure of the metal-backed patellar component. Clinical evaluation of 30 patients (33 TKAs) and questionnaires of 20 patients (23 TKAs) were taken, showing moderate to good results (mean Knee Society Score, 51; mean Western Ontario and McMaster Universities Osteoarthritis index, 82; mean University of California Los Angeles score, 4). Radiologic evaluation of 13 TKAs in 12 patients showed that none was suspect for loosening. Three knees showed significant medial wear but no clinical complaints. In conclusion, this is one of the first studies showing that AGC total knee prosthesis has good results 15 to 20 years after surgery.

Total knee arthroplasty in younger patients: a 13-year follow-up study.

Total knee arthroplasty (TKA) is a well-established treatment at the end stage of a degenerated knee joint. This operative treatment generally relieves pain, improves physical function, and has a high level of patient satisfaction, especially in the elderly. Younger patients, however, are demanding and have a higher level of physical activity compared to elderly patients. One could therefore expect more mechanical problems such as prosthetic loosening and polyethylene wear after long-term follow-up. The goal of this retrospective cohort study was to determine the survival and long-term results of TKA in young patients. Patients who received a TKA at age 60 years or younger for any reason were included. Minimum follow-up was 10 years. Thirty-nine TKAs (Anatomic Graduate Components; Biomet, Warsaw, Indiana) in 31 patients were included. Average patient age was 52.6 years. There were 3 revisions because of infection; in 1 knee the patella was revised because of aseptic loosening. After an average 13-year follow-up, the survival rate was 89.7% and function scores showed a reasonably functioning TKA. There was no difference in survival rate and function scores between patients with rheumatoid arthritis and those with primary or secondary (posttraumatic) osteoarthritis. Our experience with TKA in a younger patient population has been encouraging. The risk of loosening and wear of the implant in our study is low, and this type of TKA also seems to be an effective and safe treatment for younger patients.

Single UVB overexposure stimulates melanocyte proliferation in murine skin, in contrast to fractionated or UVA-1 exposure.

Overexposure to short- and long-wave ultraviolet radiations (UVB, UVA) may contribute to melanoma development through combined genotoxic and mitogenic effects in melanocytes. This study compares the impact of UVA-1 versus UVB, and single versus fractionated exposures on melanocyte proliferation in hairless SKH-2 mice. A single erythemal dose was compared with an equal dose fractionated over 8 d, and dose-dependency was studied. Proliferation (Ki-67 positive-sign) in melanocytes (melanoma antigen recognized by T-cells-1 positive or micropthalmia transcription factor positive) was ascertained in double-labeled skin sections. Single erythemal UVB exposures caused a delayed, dose-dependent increase of melanocyte proliferation. The highest, 17-fold, increase (from 0.05% to 0.8% of melanocytes) occurred 4 d after UVB exposure, without any detectable effect on overall melanocyte numbers. Correspondingly, DNA repair-deficient xeroderma pigmentosum A (Xpa) mice proved exquisitely sensitive to melanocyte proliferation induction by UVB exposure. No discernable effects were measured from fractionated suberythemal UVB exposures, or from any UVA-1 exposure regimen. Hence, melanocyte proliferation appears to be most efficiently induced by a single UVB overexposure. Moreover, the ineffectiveness of UVA-1 radiation and the enhanced sensitivity of Xpa mice point at pyrimidine dimers as causative DNA lesions. Consequently, murine nevi and melanoma are expected to be most effectively induced by intermittent UVB overexposures.