Elderly men and women with protein deficiencies have low levels of circulating IGF-I, and it is likely this contributes to reduced bone formation and increased bone resorption. We hypothesized that calcitropic hormones are involved in this effect and are affected by dietary protein. We therefore investigated the influence of a low-protein diet on the PTH-1,25-dihydroxyvitamin D3 [1,25(OH)2D3] axis and IGF-I in rats, using pamidronate to block resorption that normally contributes to mineral homeostasis. We fed 6-month-old Sprague Dawley female rats isocaloric diets containing 2.5% or 15% casein for 2 wk. Pamidronate was then administered sc (0.6 mg/kg/) for 5 d. Blood samples were collected at different time points. Serum 1,25(OH)2D3, IGF-I, PTH, calcium, and phosphorus were determined in all rats; vertebral bone strength and histomorphometric analysis were performed in rats subject to the longest low-protein diets. We found 2 wk of low protein increased PTH levels, decreased 1,25(OH)2D3, calcium, and IGF-I, suggesting that increased PTH compensates for low-protein-induced decreases in 1,25(OH)2D3. Pamidronate augmented the increased PTH after 8 wk of low protein and prevented the 1,25(OH)2D3 decrease. IGF-I remained low. Protein malnutrition induced decreases in relative bone volume and trabecular thickness, which was prevented by pamidronate. Maximal load was reduced by protein restriction, but rescued by pamidronate. In summary, the low protein diet resulted in hyperparathyroidism, a reduction in circulating levels of IGF-I, and reduced 1,25(OH)2D3 despite hyperparathyroidism. Blocking resorption resulted in further increases in PTH and improved microarchitecture and biomechanical properties, irrespective of vitamin D status or protein intake.

We studied a cohort of 26 diabetic patients with chronic ulceration under the first metatarsal head treated by a modified Jones extensor hallucis longus and a flexor hallucis longus transfer. If the first metatarsal was still plantar flexed following these two transfers, a peroneus longus to the peroneus brevis tendon transfer was also performed. Finally, if ankle dorsiflexion was < 5° with the knee extended, a Strayer-type gastrocnemius recession was performed.The mean duration of chronic ulceration despite a minimum of six months’ conservative care was 16.2 months (6 to 31). A total of 23 of the 26 patients were available for follow-up at a mean of 39.6 months (12 to 61) after surgery. All except one achieved complete ulcer healing at a mean of 4.4 weeks (2 to 8) after surgery, and there was no recurrence of ulceration under the first metatarsal.We believe that tendon balancing using modified Jones extensor hallucis longus and flexor hallucis longus transfers, associated in selected cases with a peroneus longus to brevis transfer and/or Strayer procedure, can promote rapid and sustained healing of chronic diabetic ulcers under the first metatarsal head.

Nowadays, Kingella kingae (K. kingae) is considered as the main bacterial cause of osteoarticular infections (OAI) in children aged less than 48 months. Next to classical acute hematogenous osteomyelitis and septic arthritis, invasive K. kingae infections can also give rise to atypical osteoarticular infections, such as cellulitis, pyomyositis, bursitis, or tendon sheath infections. Clinically, K. kingae OAI are usually characterized by a mild clinical presentation and by a modest biologic inflammatory response to infection. Most of the time, children with skeletal system infections due to K. kingae would not require invasive surgical procedures, except maybe for excluding pyogenic germs’ implication. In addition, K. kingae’s OAI respond well even to short antibiotics treatments, and, therefore, the management of these infections requires only short hospitalization, and most of the patients can then be treated safely as outpatients.

Rapid bone defect filling with normal bone is a challenge in orthopaedics and dentistry. Strontium ranelate (SrRan) has been shown to in vitro decrease bone resorption and increase bone formation, and represents a potential agent with the capacity to accelerate bone defect filling. In this study, bone tibial defects of 2.5 mm in diameter were created in 6-month-old female rats orally fed SrRan (625 mg/kg/d; 5/7 days) or vehicle for 4, 8, or 12 weeks (10 rats per group per time point) from the time of surgery. Tibias were removed. Micro-architecture was determined by micro-computed tomography (µCT) and material level properties by nanoindentation analysis.µCT analysis showed that SrRan administration significantly improved microarchitecture of trabecular bone growing into the defect after 8 and 12 weeks of treatment compared to vehicle. SrRan treatment also accelerated the growth of cortical bone over the defect, but with different kinetics compared to trabecular bone, as the effects were already significant after 4 weeks. Nanoindentation analysis demonstrated that SrRan treatment significantly increased material level properties of both trabecular bone and cortical bone filling the defect compared to vehicle. SrRan accelerates the filling of bone defect by improving cortical and trabecular bone microarchitecture both quantitatively and qualitatively.