Negative effects of chronic inflammatory periodontal disease on diabetes mellitus

Periodontal disease is the result of a complex interplay of bacterial infection and host responses, and is often modified by various systemic diseases such as diabetes mellitus. Such diseases are capable of affecting the periodontium and/or the treatment of periodontal disease. However, recent research has changed our concept of how periodontal disease should be treated. Here we present several concerns directed towards the periodontal therapy of patients with diabetes mellitus based on our studies. When treating periodontitis patients who have diabetes mellitus it is important to consider the type of diabetes. Patients with non-insulin dependent diabetes mellitus can be further classified according to the degree of insulin resistance, since recent epidemiological studies have suggested that successful anti-microbial therapy might result in improved insulin resistance in highly insulin resistant patients. Because the major contributing factor for insulin resistance is currently considered to be the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), and because periodontal surgery may cause transient bacteremia which may up-regulate the serum TNF-alpha level, which in turn suppresses insulin action, patients should be strictly treated non-surgically and their serum TNF-alpha levels should be periodically monitored. On the other hand, diabetic patients positive for serum anti-glutamate decarboxylase auto-antibody should be examined for the source of this antibody, since 1) gingival and periodontal ligament fibroblasts were found to express glutamate decarboxylase, and 2) some otherwise healthy periodontitis patients develop anti-glutamate decarboxylase antibody. Thus, chronic periodontitis may influence the level of this antibody which is widely used as a predictive marker for slowly progressive insulin dependent diabetes mellitus. Not only is periodontal disease thereby affected by systemic diseases, but carefully managed periodontal therapy may also have a positive effect on the general health of patients with systemic diseases.     

Learning root debridement with curettes and power-driven instruments. Part II: Clinical results following mechanical,nonsurgical therapy

BACKGROUND, AIMS: In a manikin study we recently assessed how effectively student operators were able to learn scaling with curettes (GRA) and power-driven instruments (PP). Calculating the debrided root area effectiveness was low in both groups without systematic training or without a motivational program. After 10 weeks (20 h) of training, operators reached a high effectiveness of 84.7% (GRA) and 81.6% (PP). The purpose of the present study was to evaluate the clinical outcome of nonsurgical treatment as performed by these student operators. METHODS: In a clinical trial, 19 students trained in the use of Gracey curettes for 10 weeks (=20 h) (GRA10) and Periopolisher system for 1 week (=2 h) (PP1), and 20 students trained in the use of Gracey curettes for 1 week (GRA1) and the Periopolisher for 10 weeks (PP10) treated one patient each in a split-mouth design. At baseline and 6 months, we recorded probing depth (PD), probing attachment level (PAL) and bleeding on probing (BOP) by computer-assisted probing. Statistical analysis was carried out for moderate (category B) and deep sites (category C). Groups were compared using Student's t-tests (p<0.05). RESULTS: Category B sites showed a PD reduction of 1.2/1.0 mm (GRA10/GRA1) and 1.1 mm (PP10/PP1). PAL gain was 0.5/0.3 mm (GRA10/GRA1) and 0.4/0.2 mm (PP10/PP1). In category C sites, PD reduction was 2.1/2.3 mm (GRA10/GRA1) and 2.0 mm (PP10/PP1) with a PAL gain of 0.6/0.9 mm (GRA10/GRA1) and 0.4 mm (PP10/PP1). BOP was significantly lower in all groups. CONCLUSION: The results show that student operators who had received a systematical training on manikins and had attained different effectiveness results were able to treat periodontally diseased patients successfully using both Gracey and Periopolisher instruments.     

Virulence of a polymicrobic complex,Treponema denticola and Porphyromonas gingivalis,in a murine model

The effect of a polymierobic infection employing Treponema denticola and Porphyromonas gingivalis in the murine lesion model was used to determine the synergistic virulence of these two periodontopathic bacteria. At high doses of P. gingivalis W50, addition of T. denticola in the infection mixture had no effect on the formation and size of the spreading lesion caused by this microorganism. However, at low P. gingivalis challenge doses, T. denticola significantly enhanced the virulence of P. gingivalis compared with monoinfection of this microorganism. A potential role of the trypsin-like protease enzyme activity of P. gingivalis in this synergistic virulence was tested using P. gingivalis mutants deficient (i.e., BEI) or devoid (i.e., NG4B19) of this protease activity. These findings demonstrated that T. denticola—P. gingivalis complexes exhibit enhanced virulence in this model and that even using a polymicrobic challenge infection, the trypsin-like protease activity was important to P. gingivalis virulence expression.     

Distribution of interleukin-2 receptor α-chain and cells expressing major histocompatibility complex class II antigen in chronic human periapical lesions

In situ distribution of CD2⁺ T-lymphocytes, CD4⁺ and CD8⁺ T-cell subsets, CD14⁺ macrophages, interleukin-2 receptor α-chain (IL-2Rα) and class II major histocompatibility complex antigen (major histocompatibility complex class II, HLA-DR) expressing cells were determined in 14 chronic human periapical granulomas by imrnunohistochemical method using monoclonal antibodies. CD2⁺ lymphocytes were rather evenly distributed within the classical granulation tissue and comprised 55% of the mononuclear cells. Macrophages were distributed all over the periapical area, but their proportion was much less than that of T lymphocytes. Both small, lymphocyte-like mononuclear cells and larger mononuclear cells resembling macrophages displayed mild to strong circumferential staining with the anti-HLA-DR antibody. The majority of lymphocytes expressed IL-2Rα indicating the activated state of T cells within the lesion.     

Genetic studies of syndromes with severe periodontitis and palmoplantar hyperkeratosis

The Papillon-Lefevre and Haim Munk syndromes are characterized by the presence of both palmoplantar hyperkeratosis (PPK) and severe early onset periodontitis. It is the early onset periodontal disease component that distinguishes these from other more common forms of PPK. It has been proposed that the periodontal disease component may be a casual association in individuals with PPK. Genetic syndromes with palmoplantar keratosis and severe early onset periodontitis may be due to specific bacterial infections in individuals with PPK. Recently, keratin gene mutations have been identified in several conditions typified by palmoplantar keratosis. The present study sought to test the hypothesis that a keratin gene defect similar to those previously identified in other PPK conditions is responsible for the Haim Munk and the Papillon-Lefevre syndromes. We have performed genetic linkage studies to test for linkage between polymorphic DNA loci within 2 cytokeratin gene families and the disease phenotype in Haim Munk syndrome and Papillon-Lefevre syndrome. Families with individuals segregating for the Haim Munk syndrome and the Papillon-Lefevre syndrome were examined to determine disease status, and genotyped for microsatellite DNA markers closely linked to the acidic (type I) and the basic (type II) cytokeratin genes on chromosomes 12 and 17. Genotype data were evaluated for microsatellite allele homozygosity in affected individuals. Results of these preliminary genetic studies suggest that the gene defect in Haim Munk syndrome is not due to a gene defect in either the type I or the type II keratin gene clusters. These findings suggest that Haim Munk syndrome may be genetically distinct from other more common forms of PPK that have been linked to the cytokeratin gene families, and suggest that mutations in genes other than keratin genes are responsible. Additional family studies are needed to confirm these preliminary findings.     

Chronodynamic evaluation of the stages of osseointegration in zirconium laminar implants

Osteogenesis occurs throughout all stages in life, due to both bone turnover and reparative processes. Thus, osseointegration (OI) can be described as the final step in a cascade of processes involved in bone healing in relation to implants. Ten groups of 5 Wistar rats each (mean = 90 g b.w.) were used. Under ether anesthesia a zirconium laminar implant was placed in the tibia following the method previously described by our laboratory (Cabrini et al Imp Dent 2:264-7, 1993). The animals were killed at Ohs, and 1, 2, 3, 6, 7, 10, 12, 14, and 60 days post-implantation. Tibiae were resected, radiographed and processed for their embedding in methyl methacrylate. Three sections, perpendicular to the major axis of the tibia, were obtained per implant and histologic and histomorphometric studies were carried out. Volume occupied by blood clot, woven bone, percentage of OI and OI bone tissue thickness, were determined. Histologic and histomorphometric studies as function of time revealed: a) at 6 days the presence of non-osseointegrated woven bone around the device is evident increasing in volume from 7 to 10 days post-implantation, and disappearing from day 12 to 14., b) at 14 days after implantation lamellar bone formation on the surface of the zirconium implants (OI) is noticeable. Additional bone growth is observed after 60 days. This study enables quantification of peri-implant reparative process response in an unloaded, necrotic trabeculae free model showing, in the different phases of the osseointegration process, the role of the blood clot and of the appearance and disappearance of woven bone and the final stages of osseointegration. Further investigation will allow comparison of results obtained under the effect of local and/or systemic factors that might affect osseointegration.     

The early development of palatal rugae in the rat

The palatal rugae in rats are contained in two of three zones of morpho-differentiation and develop around the time of palatal closure. Previous studies in humans and pigs have been based on crown-rump lengths but now controlled breeding in rats has allowed exact timing to be established. Twenty-nine female DB IX rats were fertilized and sacrificed in a controlled procedure and foetuses processed for light microscopy and SEM. Serial sagittal sections were made and stained with haematoxylin and eosin and Verhoef's stains. At day 13 the palate was open and no rugae were visible. At day 14 the palatal shelves had started to migrate medially and the ante-molar rugae appeared. At day 15 the palatal shelves were touching and the inter-molar rugae became visible, and at day 16 fusion was all but complete and the definitive rugal pattern established. The development and differentiation is more advanced than in humans and it is concluded that the rugae probably have a role to play in the oral function of animals whereas in humans they are becoming attenuated and the development timetable is retarded because of redundancy.