Human recombinant tissue factor, platelet-rich plasma, and tetracycilne induce a high-quality human bone graft: a 5-year survey.

PURPOSE: To increase human bone graft regeneration and quality by the use of a mixture containing autologous ground calvarial bone, human recombinant tissue factor (rhTF), platelet-rich plasma (PRP), and tetracycline. MATERIALS AND METHODS: Maxillary sinus floor augmentation was performed on 18 patients by grafting a "bone paste" made of PRP (1.8 x 10(6) platelets/mm3 plasma), about 1 microg rhTF, calvarial bone chips (2 to 5 mm in size), and tetracycline (10 to 30 microg/mL preparation). Five to 6 months after the surgical phase and grafting a bone core was extracted for implant fixation, and the osseous core samples were analyzed microscopically. RESULTS: Histology revealed vascularized connective tissue rich in lamellar bone spicules containing osteocytes and surrounded by osteoblasts. The success rate of grafting was 90.3%. In 6-month postoperative blood samples, no residual coagulating disturbances could be found. DISCUSSION: The combination of calvarial bone chips, rhTF, PRP, and tetracycline results in a paste that is easy to handle, safe for patients, and possesses high bone-regeneration capacity. CONCLUSION: The generalized use in implant dentistry, oral surgery, and orthopedics of such a protocol could facilitate the healing process as well as patient safety and surgeon comfort.

S100A6 overexpression within astrocytes associated with impaired axons from both ALS mouse model and human patients.

Astrogliosis is one of the earliest pathological changes observed in neurodegenerative diseases in general and in amyotrophic lateral sclerosis (ALS) in particular. ALS is characterized by selective degeneration of motoneurons. There are 2 forms of the disease: sporadic ALS (SALS), comprising 90%-95% of cases, and familial ALS (FALS), comprising 5%-10% of cases. FALS is an age-dependent autosomal dominant disorder in which mutations in the homodimeric enzyme Cu/ Zn superoxide dismutase 1 (SOD1) is linked to the disease. The animal model for this disease is a transgenic mouse expressing the mutated human SOD1(G93A) gene. Here we show by immunohistochemistry and double immunofluorescence that astrocytes located near impaired axons of motoneurons that were selectively programmed to die overexpressed S100A6, a Ca2+/Zn2+ binding protein able to translocate into the nucleus. Transgenic mice overexpressing the mutated human SOD1 gene and patients suffering from SALS showed this selective astrocytic S100A6 expression. For instance, the pyramidal tract could be macroscopically detected on S100A6-labeled spinal cord and brainstem sections from SALS patients. Transgenic mice overexpressing the non-mutated SOD1 gene did not overexpress S100A6, although glial fibrillary associated protein astrogliosis was seen. Although these results do not give any clue about the beneficial or detrimental role played by S100A6, its induction may be assumed to appropriately serve some function(s).