An interhemispheric subdural abscess (author's transl)]

A subdural abscess which is cinfined to the interhemispheric space alone, which does not extend over the convexity is rare. This is a specific form and is a complication of a common intracranial subdural abscess. It is of great practical importance to determins this uncommon location, and cerebral angiography is most useful. Multiple trephinations or craniotomy for exploration and evacuation must be performed near the midline. A 20 year old female was in a comatose state on admission. There was a flaccid paralysis of the right lower extremity and a dilated left pupil. Examination of the eyegrounds showed bilateral choked discs. Left cerebral angiography revealed the proximal pericallosal artery to be shifted to the right side and the callosomarginae artery was displaced from the midline parallel to the distal pericallosal artery. Although 20 ml of pus was evacuated through the parietal burr hole, which was located a bout 2.5 cm from the midline, she died. At autopsy, a subsural abscess was found in the interhemispheric space. It extended from the frontal pole to the occipital and had a thick membrane which adhered firmly to the falx medially. We could find no other subdural nor intracerebral pus collections. The left cerebral hemisphere was edematous. The superior sagittal sinus had a thick wall and was almost occluded. This dural sinus thrombophlebitis may have developed into the interhemispheric subdural abscess. It is emphasized that this uncommon location for subdural abscess poses a specific problem in clinical practice.     

Osteopontin is required for mechanical stress-dependent signals to bone marrow cells

Mechanical stress to bone plays a crucial role in the maintenance of bone homeostasis. It causes the deformation of bone matrix and generates strain force, which could initiate the mechano-transduction pathway. The presence of osteopontin (OPN), which is one of the abundant proteins in bone matrix, is required for the effects of mechanical stress on bone, as we have reported that OPN-null (OPN-/-) mice showed resistance to unloading-induced bone loss. However, cellular mechanisms underlying the phenomenon have not been completely elucidated. To obtain further insight into the role of OPN in mediating mechanical stress effect on bone, we examined in vitro mineralization and osteoclast-like cell formation in bone marrow cells obtained from hind limb bones of OPN-/- mice after tail suspension. The levels of mineralized nodule formation of bone marrow cells derived from the femora subjected to unloading were decreased compared with that from loaded control in wild-type mice. However, these were not decreased in cells from OPN-/- mice after tail suspension compared with that from loaded OPN-/- mice. Moreover, while spreading of osteoclast-like cells derived from bone marrow cells of the femora subjected to unloading was enhanced compared with that from loaded control in wild-type mice, this enhancement of spreading of these cells derived from the femora subjected to unloading was not recognized compared with those from loaded control in OPN-/- mice. These data provided cellular bases for the effect of the OPN deficiency on in vitro reduced mineralized nodule formation by osteoblasts and on enhancement of osteoclast spreading in vitro induced by the absence of mechanical stress. These in vitro results correlate well with the resistance to unloading-induced bone loss in OPN-/- mice in vivo, suggesting that OPN has an important role in the effects of unloading-induced alterations of differentiation of bone marrow into osteoblasts and osteoclasts.     

Osteopontin deficiency protects joints against destruction in anti-type II collagen antibody-induced arthritis in mice

Rheumatoid arthritis is one of the most critical diseases that impair the quality of life of patients, but its pathogenesis has not yet been fully understood. Osteopontin (OPN) is an extracellular matrix protein containing Arg-Gly-Asp (RGD) sequence, which interacts with alpha(v)beta3 integrins, promotes cell attachment, and cell migration and is expressed in both synovial cells and chondrocytes in rheumatoid arthritis; however, its functional relationship to arthritis has not been known. Therefore, we investigated the roles of OPN in the pathogenesis of inflammatory process in a rheumatoid arthritis model induced by a mixture of anti-type II collagen mAbs and lipopolysaccharide (mAbs/LPS). mAbs/LPS injection induced OPN expression in synovia as well as cartilage, and this expression was associated with joint swelling, destruction of the surface structures of the joint based on scanning electron microscopy, and loss of toluidine blue-positive proteoglycan content in the articular cartilage in wild-type mice. In contrast, OPN deficiency prevented the mice from such surface destruction, loss of proteoglycan in the articular joint cartilage, and swelling of the joints even when the mice were subjected to mAbs/LPS injection. Furthermore, mAbs/LPS injection in wild-type mice enhanced the levels of CD31-positive vessels in synovia and terminal deoxynucleotidyltransferase-mediated UTP end labeling-positive chondrocytes in the articular cartilage, whereas such angiogenesis as well as chondrocyte apoptosis was suppressed significantly in OPN-deficient mice. These results indicated that OPN plays a critical role in the destruction of joint cartilage in the rheumatoid arthritis model in mice via promotion of angiogenesis and induction of chondrocyte apoptosis.