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.     

The combination of platelet-derived growth factor-BB and insulin-like growth factor-I stimulates bone repair in adult Yucatan miniature pigs

The combination of insulin-like growth factor-I and platelet-derived growth factor-BB has previously been shown to stimulate healing of soft tissue wounds and the formation of bone and ligament around teeth. The purpose of the present study was to evaluate the effects of platelet-derived growth factor-BB and insulin-like growth factor-I individually and in combination on the healing of osseous wounds. Four standardized cortical wounds were created in each tibia of 11 adult Yucatan miniature pigs. The wounds in one tibia per animal were treated with either purified recombinant human insulin-like growth factor-I, platelet-derived growth factor-BB, or both in a methylcellulose gel. The wounds in each contralateral tibia received placebo gel alone. Coded serial sections of each wound were evaluated by computer-aided histomorphometry 21 days after surgery. The area and perimeter of the newly formed mineralized callus, the thickness of the total callus, and the percentage of mineralized tissue within the callus were significantly increased compared with the values of matched controls only in wounds treated with a combination of insulin-like growth factor-I and platelet-derived growth factor-BB. No significant differences in the measured parameters of callus formation were found in wounds treated with either insulin-like growth factor-I or platelet-derived growth factor-BB alone. Cartilage was present only in sites treated with insulin-like growth factor-I alone. These results suggest that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I stimulates bone formation in wounds in long bones of adult animals and that these growth factors act via different pathways during the repair process.     

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.     

Effects of alkyl chain length on the inhibition of NNK-induced lung neoplasia in A/J mice by arylalkyl isothiocyanates

Six homologous arylalkyl isothiocyanates were evaluated fortheir abilities to inhibit pulmonary adenomas induced by thetobacco-specific nitrosamine 4-(methylnitrosamino)-l-(3-pyridyl)-1-butanone(NNK) in A/J mice. Four consecutive daily doses (5 µmol/mouse)of phenyl isothiocyanate (PITC), benzyl isothiocyanate (BITC),phenethyl isothiocyanate (PETTC), 3-phenylpropyl isothiocyanate(PPITC), 4-phenylbutyl isothiocyanate (PBITC), 4-oxo-4-(3-pyridyl)-butylisothiocyanate (OPBITC) and corn ofl were administered to miceby gavage. Two hours following the final dosing, mice were administeredsaline or 10 µmol of NNK in saline i.p. Pulmonary adenomaswere counted at 16 weeks after NNK administration. The miceadministered only corn oil prior to NNK developed an averagemultiplicity of 9.2 tumors/ mouse. Pretreatment with PITC, BITCand OPBITC had no significant effects on NNK-induced lung neoplasia.However, PEITC pretreatment resulted in a 64% reduction of lungtumor multiplicity, but did not affect the percentage of micethat developed tumors. Both PPITC and PBITC decreased tumormultiplicity by 96% and the percentage of tumor-bearing animalsby >60%. These results, in conjunction with our previouswork, demonstrate a general trend of increasing inhibition ofNNK-induced lung neoplasia by arylalkyl isothiocyanates withincreasing alkyl chain length. This study also demonstratesthe remarkable inhibitory activities of PPITC and PBITC, twoisothiocyanates that had not previously been tested as chemopreventiveagents.