Histopathological evaluation of canine stifle joint synovial membrane collected at the time of repair of cranial cruciate ligament rupture.

Synovial membranes from 54 dogs were collected at the time of surgery to stabilize the stifle joint following rupture of the cranial cruciate ligament. Histological evaluation revealed lymphoplasmacytic synovitis with the formation of distinct, nodular aggregates in 36 synovial membranes. The remainder had evidence of chronic synovitis with variable numbers of diffuse, mononuclear cells. The presence of a potentially immune-mediated synovitis in the majority of cases suggests the need for further study.

Development of chronic mandibular osteomyelitis in a miniswine model.

Previous attempts to develop a reproducible model of chronic mandibular osteomyelitis have met with limited success. In this study, osteomyelitis was produced in the mandibles of eight adult Yucatan miniswine by the intramedullary application of sodium morrhuate, Staphylococcus aureus, and either polymethylmethacrylate bone cement or bone wax. At 8 weeks' postinfection, the mandibles were surgically debrided and specimens were obtained for culture. Although all of the animals developed clinical evidence of osteomyelitis that was supported by positive cultures, the original organism (S aureus) was recovered only from those animals where bone wax had been used to seal the cortical defects. This animal model may be useful for evaluating newer treatment modalities for chronic osteomyelitis.

Mechanisms of malignant ascites production.

The accumulation of malignant ascites is determined primarily by the obstruction of diaphragmatic lymphatics with tumor inhibiting the outflow of peritoneal fluid. An abnormal increase in peritoneal fluid production has been shown to contribute to ascites formation by a marked neovascularization of the parietal peritoneum. Cell-free malignant ascitic fluid obtained from rats with intra-abdominal Walker 256 carcinoma when infused into the peritoneal cavities of normal animals causes an increase in edema formation and an increase in the permeability of protein from normal omental vessels. Protamine sulfate, a known inhibitor of angiogenesis when infused into the peritoneal cavity along with cell free malignant ascitic fluid, significantly reduces the leak of protein from the intravascular space when compared to ascites alone. Persistent permeability changes continue to exist even after the inhibition of vessel proliferation. These results indicate that angiogenesis is responsible for a major portion of the increase in permeability caused by malignant ascitic fluids. Other tumor-induced factors may be present which alter vascular permeability by other mechanisms which remain to be elucidated.

Malignant ascites. Clinical and experimental observations.

Malignant ascites formation is a grave prognostic sign, but palliative efforts seem justified in some patients. Lack of knowledge concerning the natural history of this process hinders the choice of therapeutic options. Over 5 years, 107 patients with untreated malignant ascites were reviewed to define their survival. Pancreas (20), ovary (18), and colon (18) were the most frequent tumors, with 52% of patients presenting with ascites at the time of the initial cancer diagnosis. Cytology evaluation of the ascitic fluid was positive for tumor cells in 57% of cases and a high protein content was noted in 65%. Mean survival of the entire series was only 20 weeks from the time of diagnosis of ascites, with tumors of ovarian and lymphatic origin having better mean survivals of 32 and 58 weeks, respectively. Patients with high ascitic protein levels fared better than those with low levels. In an effort to explain this correlation of elevated protein levels and a favorable survival rate, a hypothesis was proposed that certain tumors secrete a factor, which alters vascular permeability and causes fluid accumulation in the absence of lymphatic obstruction. In an experimental rat model of malignant ascites, the intraperitoneal infusion of cell-free malignant ascitic fluid caused an increase in edema formation and a significant increase in capillary permeability to protein in the omentum. This demonstrated change in the leak of protein explains the formation of ascites by some tumors in the absence of tumor obstruction of the draining lymphatics of the peritoneal cavity and suggests another important mechanism in the genesis of malignant ascites.