Occlusal forces cause stress which morphologically affects the supporting tissues of implants. The aim of this study was to examine the effects of occlusal forces on the distribution of neurofilament protein (NFP)-positive nerve fibers in the tissue of peri-implant bone. The bilateral 2nd, 3rd and 4th mandibular premolars and the 1st molars were extracted from three mongrel dogs. After 4 months of healing, 4 screw-type implants were inserted in the oral cavity. Three months after insertion, the implants on the molar site were loaded by occlusal forces, while those on the premolar site were unloaded. After a further 3 months, the dogs were sacrificed, and specimens were prepared for immunohistochemical NFP-positive staining by the labeled-streptavidin-biotin method. Many NFP-positive nerve fibers were found in the tissues of the loaded site when compared with the unloaded site. These fibers were localized in both the bone marrow space and in the peri-implant fibrous tissue. They had two types of nerve endings: simple free nerve endings, and nerve endings with tree-like ramifications. The present results suggest that loading by occlusal force causes an increase in the number of NFP-positive nerve fibers, many of which have free nerve endings in the peri-implant tissue. The possible role of these NFP-positive nerve fibers is discussed.

No abstract

No abstract

Chronic pulmonary thromboembolism is known to be associated with poor prognosis with conservative medical treatment. Pulmonary thromboendarterectomy for chronic pulmonary thromboembolic disease is a potentially lifesaving procedure that prevents right-sided cardiac failure as a result of secondary pulmonary hypertension caused by pulmonary thromboembolism. We report a rare case of systemic lupus erythematosus with antiphospholipid syndrome in a patient who presented with pulmonary hypertension secondary to chronic proximal multiple pulmonary thromboembolism. To our knowledge, this is the first case report of chronic pulmonary thromboembolism complicated by systemic lupus erythematosus with antiphospholipid syndrome. Thromboendarterectomy was performed with satisfactory results.

We report a 67-year-old man who developed pulmonary hypertension as an initial clinical manifestation of occult gallbladder adenocarcinoma. He had a 6-week history of persistent dry cough followed by progressive dyspnea on exertion. Physical examination and chest roentgenogram revealed signs of precapillary pulmonary hypertension. He died of shock 1 h after pulmonary angiography, which failed to show any intravascular filling defects. Autopsy disclosed a mucin-producing small adenocarcinoma (2 cm diameter) and a gallstone in the gallbladder with a few small metastases to peri-aortic, peri-bronchial and mediastinal lymph nodes. Macroscopically, there was no gross thrombotic pulmonary embolism or pulmonary metastases. However, microscopically, more than 60% of the small pulmonary arteries less than 1 mm in diameter were occluded with pulmonary tumor microemboli. This case emphasizes the need to include tumor pulmonary embolism in the differential diagnosis of pulmonary hypertension whether or not there is evidence of an underlying malignant tumor.

Because of the need to make dental records from the standpoint ef patients ， we tried to make a problern oriented dental records （ PODR ） for the oral

No abstract

No abstract