Occlusal forces as a risk factor for periodontal disease

Most early research on the effects of occlusion on the progression of periodontal disease focused on a cause and effect relationship. Stillman clearly felt that excessive occlusal forces were the cause of periodontal disease and that treatment of the occlusion was the primary method of effective periodontal treatment. As it became evident that bacterial plaque was an integral part of the periodontal disease process, the role of occlusal forces became less clear. Eventually this led to viewing occlusion as a cause of specific types of periodontal destruction. This was described by Glickman as the co‐destructive roles of occlusion and bacterial plaque in the formation of vertical osseous defects and furcation bone loss. Glickman's theory of Co‐Destruction continued to hold to the thesis that occlusion was, in concert with bacterial plaque, a causative factor in periodontal attachment loss and bony destruction. Glickman described an altered pathway of destruction in an attempt to articulate a functional mechanism for the formation of the specific morphology of attachment and bone loss thought to be caused by the co‐destructive action of occlusal forces and bacterial plaque. The altered pathway of destruction still held to the concept that occlusion directly changed the disease process and was thereby, in the presence of bacterial plaque, a causative agent for periodontal destruction. The animal studies on squirrel monkeys and beagle dogs began to shed light on the effect of occlusal forces on the periodontal attachment structures at a cellular level. From these studies it was clear that within these animal models, occlusion had an effect on the periodontium in the form of bone rarefaction, which resulted in the clinical manifestation of mobility. However, it was equally clear that, within the animal models, loss of attachment and thereby periodontal destruction did not occur in the presence of excessive occlusal forces only. Loss of attachment occurred only in the beagle dog model and then only in the presence of excessive occlusal forces and bacterial plaque. While these animal studies gave us an exhaustive insight into the effect of excessive occlusal forces on the periodontal supporting structures of the studied animals, it must be remembered that these studies were performed using animal models that show little or no tendency toward periodontal destruction under natural conditions. The application of the information obtained from these animal models to the periodontal destruction that occurs in humans must be approached with caution. It is probable that these animal studies give us a picture only of the physiologic response of the periodontium to excessive occlusal forces with and without bacterial plaque. It is unlikely that these animal studies give us significant information about the pathophysiology that may occur when excessive occlusal forces are present in humans who may be genetically prone to periodontal destruction and who may also have additional risk factors for periodontal disease beyond occlusal forces and bacterial plaque. Human studies begin to give us some indication of the effect of excessive occlusal forces on the progression of periodontal disease in those patients who show a tendency toward periodontal destruction. While there are many apparently contradictory findings from human studies, there appears to be a trend toward evidence that excessive occlusal forces may play a role in periodontal destruction and the response of the periodontium to periodontal treatment. While the available information suggests a relationship between excessive occlusal forces and progression of periodontal disease, the 1999 International Workshop for Classification of Diseases and Conditions indicated that there was no clear evidence that occlusal forces were a factor in plaque‐induced gingivial disease or connective tissue loss ( 23 ). Since the 1999 Workshop, studies have shown that occlusal interferences have a negative effect on the periodontium and tend to cause more rapid pocket formation and poorer prognosis when compared to teeth that do not have occlusal interference.     

Staph. Epi. Peritonitis in CAPD

Staphylococcus epidermidis is frequently resistant to first-generation cephalosporins. Although I have generally changed the therapy of S. epidermidis CAPD peritonitis to vancomycin when laboratory reports indicate cephalosporin resistance, it frequently appeared that improvement from the cephalosporin was taking place at the time of antibiotic conversion. Should the antibiotics be changed in this setting?     

Pathways of lymph flow through intestinal lymph nodes in the horse

In the horse, several thousand lymph nodes receive lymph from the intestine, part of which is very large and contains microorganisms that enable the animal to utilize refractory dietary constituents such as cellulose. The aim of this study was to describe the pathways by which lymph is delivered into, traverses, and is drained from these lymph nodes. These pathways were studied with either Microfil or methacrylate casting materials and with light and electron microscopy. The afferent lymphatic vessel delivering lymph into one of the nodes divides over the capsular surface and within trabeculae into terminal branches, and these are continuous with the subcapsular and trabecular sinuses through rounded holes up to 30 μm across. Lymph is conveyed from the subcapsular and trabecular sinuses through the cortex by four types of sinuses: trabecular sinuses, cortical tubular sinuses, tubulelike sinuses with a network of stellate cell processes, and sinuses between cortical cords. It is conveyed through the medulla by sinuses both within and between medullary cords. Lymph is drained from these sinuses by initial efferent lymphatics of three types: those between medullary cords, those within the subcapsular sinus overlying medullary or cortical cords, and those within trabeculae. All three types are continuous with surrounding sinuses through holes 5–30 μm across. These three alternative routes for lymph drainage may ensure adequate lymph flow during different intranodal conditions that may exist when the node is responding to microcrganisms or other foreign materials.     

Decreasing the level of translation initiation factor 4E with antisense rna causes reversal of ras-mediated transformation and tumorigenesis of cloned rat embryo fibroblasts

Transformation of cloned rat embryo fibroblasts (CREF) with the T24-ras oncogene results in loss of contact inhibition, growth in soft agar and tumor formation in nude mice. Previously we showed that in such cells (CREF T24), the phosphorylation rate of protein synthesis initiation factor 4E (elF-4E) is increased, correlating with an increase in the general rate of protein synthesis. In the present study, we have expressed antisense RNA complementary to elF-4E mRNA in CREF T24 cells using a stably integrated vector. Cells expressing antisense RNA (CREF T24/AS) contained 30-50% of the normal level of elF-4E and exhibited many of the properties of untransformed cells. CREF T24 had a spindle-shaped, refractile appearance, whereas CREF T24/AS grew in ordered, parallel patterns and exhibited contact inhibition similar to untransformed CREF. The rates of growth and protein synthesis in CREF T24/AS were decreased compared to CREF T24 but were not as low as in CREF. The efficiency of growth in soft agar was 11-fold lower for CREF T24/AS compared with CREF T24. The latency period for tumor formation in nude mice was increased from 8 days for CREF T24 to 17-27 days for CREF T24/AS and various clonal lines derived from them. Cell lines established from these CREF T24/AS-derived tumors were shown to have partially regained the elF-4E levels characteristic of CREF T24. These results demonstrate that many of the phenotypic alterations associated with ras-induced malignant transformation can be reversed by a moderate reduction of the translational initiation capacity and therefore may be mediated through a translational mechanism.     

Gastric ulceration caused by heater probe coagulation

A double-contrast upper gastrointestinal examination on a woman who had undergone endoscopic heater probe therapy one day earlier for multiple arteriovenous malformations revealed shallow, irregular, and linear ulcers at the sites of heater probe coagulation. Multiple shallow ulcers may therefore develop as a direct complication of heater probe therapy. Radiologists should be aware of this complication to avoid diagnostic confusion in these patients.     

Fibula flap reconstruction of the condyle in disarticulation resections of the mandible: a case report and review of the technique.

Segmental resection of the mandible with disarticulation of the temporomandibular joint is occasionally required in the management of extensive tumors. The reconstruction of these deformities is complex, frequently involves staged procedures, and may result in significant deformity and loss of function for patients. The fibula free flap has become a standard treatment option for primary restoration of segmental mandibular deformities. However, little is published about its role in reconstructing the mandibular condyle. This paper describes a simplified technique for primary reconstruction of mandibular defects, including the mandibular condyle, in disarticulation resections of the mandible utilizing the fibula free flap.