Use of calcitonin for the treatment of an odontoid fracture. Case report.

The authors report on the efficacy of nonsurgical treatment of an older patient with a fractured odontoid process. The patient, an 85-year-old woman, had multiple medical problems that put her at an increased surgery-related risk. Therefore, an alternative approach was elected, including immobilization with a Philadelphia collar and the provision of calcitonin nasal spray. Bone union and clinical recovery were achieved within 8 weeks of initiating the nasal calcitonin therapy (12 weeks postinjury). Considering the patient's age, comorbidities, and the severity of the fracture, the recovery period was unusually short. The authors believe that calcitonin played a pivotal role in the healing process of the fractured odontoid bone. There is no question that the fusion in this patient could be unrelated to the medical therapy. This description of one patient, as well as the lack of a large randomized study, precludes any scientific conclusions. Nevertheless, the authors believe that the development of a successful fusion in this high-risk patient should be reported as an observation that merits confirmation and study. The authors also discuss the physiological effects of calcitonin and the research and clinical experience with this hormone in different conditions affecting bone.

Changes of MPO activity and brain water accumulation in traumatic brain injury experiments.

Comparison of brain tissue water content (BWC) data with myeloperoxidase activity assay (MPO) allows for analysis of the complex pathophysiological mechanisms of cerebral edema following catastrophic brain injuries. The neuroprotective effect of an experimental anti inflammatory drug (FL1003, butyrolactone) was tested in a traumatic brain injury (TBI) model using BWC and MPO analysis. We conducted these studies on a mini-pig model of severe TBI that is well characterized in our laboratory. The animals were divided into three animal groups: no injury, no treatment (control), injured and treated with FL1003, and injured, untreated with FL1003. They were maintained with fluids for 24 hours under general anesthesia. We employed the MPO assay to identify the degree of inflammatory cellular response (polymorphonuclear leukocytes, PMNLs) 24 hours following TBI and calculated brain density from the data of the gravimetric (Percoll) column method for BWC on brain samples. Our results demonstrated increased infiltration of PMNLs and a shift of water into the extravascular space in the injured animals. These changes were significantly (P < 0.05) attenuated in the animal group treated with FL1003.

Mechanisms of cerebrovascular dysfunction.

Cerebrovascular dysfunction characterized by the loss of endothelial integrity has been observed following ischemic and traumatic insults to the brain, resulting in the net movement of fluid and solute out of the intravascular space and into the interstitium. Following traumatic brain injury, the development of intracranial hypertension secondary to cerebral edema plays a major role in the high morbidity and mortality in these patients. Although the precise mechanisms responsible for the disruption of the normally tightly regulated cerebrovascular tissue interface remain unclear, there is increasing evidence implicating inflammatory events in this process through the transient opening of tight junctional complexes. This article will examine the interaction of astrocytes, activated neutrophils, and inflammatory mediators in inducing endothelial contraction, thereby physically opening the permeability barrier and allowing the net movement of fluid out of the intravascular space.