Oral Surgery, Oral Medicine, Oral Pathology最新文献

A concensus conference on the timing of facial osteotomies was held in Jönköping, Sweden. Seven teams consisting of a maxillofacial surgeon and an orthodontist representing five countries discussed treatment planning for young patients with maxillomandibular deformities with special emphasis on timing. Patients with severe syndromic facial deformities were not considered. Consensus was reached that for most deformities it is best advised to wait until growth has ceased, as determined by longitudinal cephalometric data. This rule is less tight for Angle Class II than for Class III cases. For asymmetries often there is still not enough scientific evidence to obtain well-founded uniform agreement.

We report the case of a patient in whom oral squamous cell carcinoma and a fatal reactive form of histiocytosis were simultaneously manifested. Our conclusions indicate that such a hematophagocytic syndrome may occur in the setting of oral squamous cell carcinoma as previously described in other malignancies.

Inflammation-induced localized bone resorption in diseases such as marginal and apical periodontitis, rheumatoid arthritis, and osteomyelitis is due to activation and recruitment of osteoclasts by locally produced cytokines and inflammatory mediators. Thus several interleukins (1, 3, 4, 6, and 11), tumor necrosis factors (α, β), colony-stimulating factors (M and GM), leukemia inhibitory factor, γ-interferon, and transforming growth factor-β have effects on bone resorption and bone formation in vivo and in vitro. The kallikrein-kinin system and the coagulation cascade are also activated in inflammation. We have found that peptides produced in the kallikrein-kinin system (bradykinin, kallidin) and thrombin, the end product in the coagulation cascade, can stimulate bone resorption in vitro. The stimulatory effect of bradykinin is linked both to B1 and B2 bradykinin receptors. Both kinins and thrombin stimulate prostaglandin biosynthesis in bone parallel with the bone resorptive effect. The stimulatory effect of bradykinin on bone resorption is completely lost when the prostaglandin response is abolished, whereas thrombin can stimulate bone resorption both via prostaglandin-dependent and independent mechanisms. In addition, bradykinin and thrombin act in concert with interleukin-1 to synergistically stimulate bone resorption and prostaglandin biosynthesis. We also have found that one of the acute-phase reactants, haptoglobin, can stimulate bone resorption in vitro, indicating the possibility of generalized bone loss in chronic inflammatory diseases. Moreover, haptoglobin synergistically potentiates bradykinin-induced and thrombin-induced prostanoid biosynthesis in osteoblasts. These observations indicate that the rate of bone resorption in inflammation-induced bone loss may not be due to a single factor but to the concerted action of several local or systemic factors.

The vascular supply to the temporomandibular joint is not completely understood. To form a base for advancement in this area we developed a method for experimental angiography of the temporomandibular joint that was applied to fresh temporomandibular joint autopsy specimens. Via the external carotid artery the vessels were infused with a mixture of barium and an acrylic resin. The specimens were sectioned and contact radiographs were obtained. These showed the vascularity of the joint and the surrounding structures with great detail. Most of the vascular supply appears to come from the lateral and medial aspects of the condyle head and from the anterior and posterior disk attachments. The method was applied to both normal and abnormal joints and the results suggest that this method could be used to gather further understanding of the vascularity of the temporomandibular joint relative to disease.

A retrospective investigation was carried out of 57 cases of mandibular angle fractures, where a completely or partially impacted third molar was present in the line of fracture. Closed reduction was used in all of the cases, using intermaxillary fixation over a period of 42 days. Antibiotics were given to all patients for a period of 1 week. Thirty-one patients (55%) were treated within the first 24 hours and 43 (75%) within 48 hours. Infection at the fracture site occurred in two patients (3.5%). Both of these patients had been treated within the first 24 hours. It is concluded that closed reduction with retention of the mandibular third molar within the line of a mandibular angle fracture can be carried out with less morbidity compared with cases in which rigid fixation is used and movement of the jaws permitted immediately. Because of the size of the study group, no relationship could be demonstrated between cases with infection and the time from trauma to fixation.

Patients with symptomatic oral lichen planus often require therapy to reduce signs and symptoms of the condition. For this purpose, corticosteroids are frequently used. In this study the effect of another immunosuppressive drug, cyclosporin A was evaluated; it was applied as a topical drug four times daily and contained 0.025% cyclosporin A. The study group was composed of nine symptomatic patients in whom the diagnosis of oral lichen planus was confirmed by histopathologic examination including immunofluorescence. All patients had unsuccessfully undergone previous treatment with topical or systemic corticosteroids. The minimum follow-up period in the present study was at least 4 months. Four patients showed partial response to treatment with respect to signs and symptoms. None of the patients had a complete remission. Five patients showed no response or even complained of an increase of signs and symptoms. No adverse side effects of the drug were recorded during follow-up. Although the number of patients has been small, the results of this study indicate that topical application of cyclosporin A (0.025%) in the treatment of recalcitrant oral lichen planus does not offer a distinct advantage over the use of topical corticosteroids.

Research conducted in the last 10 years has increased our knowledge on pain mechanisms substantially. Although many local tissue mediators, including neuropeptides, are known to exert pro-inflammatory effects, comparatively little is known about the actual tissue levels of these inflammatory mediators and their pharmacologic regulation. This article describes two new methods, clinical microdialysis and superfusion of dental pulp, which provide data on the pharmacology of peripheral neuropeptide and inflammatory mediator release. Collectively, these methods provide a biochemically based approach toward determining the mechanisms and management of orofacial pain.

Multiple mechanisms are involved in the pathologic changes associated with formation of acute and chronic periradicular lesions. Mechanical injury to the periradicular tissues can cause activation of several pathways of inflammation and release of nonspecific mediators. Continuous irritation of periradicular tissues can cause activation of several pathways of inflammation and release of nonspecific mediators. Continuous egress of antigens from a pathologically involved root canal can also result in one or a combination of the various types of immunologic reactions. A number of these reactions participate in the destruction of periradicular tissues. Because of complex interactions between the various components of these systems, the dominance of any one pathway or substance may be difficult to establish.