bluuebunny/crossref_metadata_2025 huggingface dataset:
Influence of Two Different Approaches to Reporting Implant Survival Outcomes for Five Different Prosthodontic Applications
Authors: Morris Harold F. , Ochi Shigeru
Published: February 2005

Background: Over the years, the definition of implant failure has varied, with some investigators accounting for all implants placed, while others discard failures that occurred before clinical loading. The influence of stresses transmitted to various bone densities, by different prosthetic appliances as well as the method used to determine failures, needs to be clearly understood. This paper reports on the influence of two different methods of determining 36‐month survival of implants used to support different dental prostheses.

Methods: More than 2,900 implants with six different designs were placed in 829 patients at 32 study centers and followed for 3 years. The first method of determining survival accounted for all failures from placement through 36 months, while the second method counted only failures from post‐loading of the prosthesis to 36 months. Survival curves were used to determine differences in survival outcomes for the two methods.

Results: For the maxillary single‐tooth prosthetic application, implant survival from placement to 36 months was 94.7% when all failures were counted and increased to 98.3% with the post‐loading method. For upper completely edentulous applications, implant survival was 85.3% with all failures counted and 95.6% with the post‐loading method. This 10.3% difference is clinically important. The survival for implants in lower completely edentulous applications increased by 4.4% simply by using the post‐loading approach. Implants used for upper posterior, partially edentulous applications involved only hydroxyapatite (HA)‐ coated implants, and the survival rates were similar (96.4% for all implants and 98.2% for the post‐loading method). The difference in reported survival rates for implants in the lower posterior, partially edentulous application was 5.8%. Since failures tended to occur in the earlier phases of treatment, the post‐loading approach always resulted in more favorable survival data. With the post‐loading approach, valuable information related to implant performance before loading is lost. In all comparisons, HA‐coated implant survival was always better than non‐HA implants. Clinical investigators should clearly state the method used for determining failures. For all implants included in the study, survival curves illustrated different failure patterns for each method of determining overall survival.

Conclusion: Reporting of implant survival rates based on the post‐loading method provides more favorable survival rates; however, accounting for all implants provides a more accurate method of determining survival. Ann Periodontol 2000;5:90‐100.
Receptor for Advanced Glycation End Products, Inflammation, and Accelerated Periodontal Disease in Diabetes: Mechanisms and Insights Into Therapeutic Modalities
Authors: Lalla Evanthia , Lamster Ira B. , Stern David M. , Schmidt Ann Marie
Published: February 2005

In hyperglycemic states found in diabetics, a nonenzymatic glycation and oxidation of proteins and lipids occurs. As a result, advanced glycation end products (AGEs), particularly N∊‐(carboxymethyl) lysine, accumulate in the plasma and tissues of diabetic subjects. This accumulation has been linked to the development of pathogenic complications of diabetes. Many of the effects of AGEs are receptor‐dependent and involve a multi‐ligand member of the immunoglobulin superfamily of cell surface molecules. The best characterized of these is the receptor for advanced glycation end products (RAGE), which is expressed by multiple cell types including endothelium and mononuclear phagocytes. Based on data from a variety of sources, including studies of RAGE‐deficient mice, it appears that RAGE plays a central role in oral infection, exaggerated inflammatory host responses, and destruction of alveolar bone in diabetes. It is possible that antagonists of RAGE might have a valuable adjunctive therapeutic role for the management of periodontal disease found in diabetics. Ann Periodontol 2001;6:113‐118.
Treatment of Periodontal Disease and Control of Diabetes: An Assessment of the Evidence and Need for Future Research
Authors: Grossi Sara G.
Published: February 2005

Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)‐1β, IL‐6, and tumor necrosis factor (TNF)‐α. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL‐1β, IL‐6, and TNF‐α in the diabetic state have an effect on the liver, stimulate the release of acute‐phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF‐α, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non‐diabetics. Porphyromonas gingivalis, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of P. gingivalis to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions. Ann Periodontol 2001;6:138‐145.
Current Evidence Regarding Periodontal Disease as a Risk Factor in Preterm Birth
Authors: Jeffcoat Marjorie K. , Geurs Nico C. , Reddy Michael S. , Goldenberg Robert L. , Hauth John C.
Published: February 2005

Preterm birth, resulting in babies born too little and too soon, is a major cause of morbidity. Evidence indicates that infections can be major risk factors in preterm birth. Case‐control studies point to an association between periodontal infection and increased rates of preterm birth. This paper summarizes evidence to date and the strategies that ongoing intervention studies are using to answer the fundamental clinical question: can periodontal therapy reduce the risk of preterm birth? Ann Periodontol 2001;6:183‐188.
Role of Nuclear Factor‐Kappa B (NF‐κB) in Inflammation, Periodontitis, and Atherogenesis
Authors: Nichols Timothy C. , Fischer Thomas H. , Deliargyris Efthymios N. , Baldwin Albert S.
Published: February 2005

Atherosclerosis, the major cause of death and disability in the United States, is a chronic disease with inflammatory components. The first objective of this review is to explain how activation of NF‐κB contributes to atherosclerosis. The second objective is to describe a potential link between inflammation, activation of NF‐κB, and periodontitis. The nuclear transcription factor NF‐κB controls the expression of many genes linked to atherogenesis including those involved with inflammation. We hypothesize that one unifying mechanism in this complex disease is the activation of NF‐κB. The mechanism(s) that activates NF‐κB in atherogenesis is unknown and the effect of inhibiting NF‐κB activation on atherogenesis is untested. Periodontal disease has now been established as a risk factor for atherosclerosis and its thrombotic complications. It is unknown if periodontal disease contributes to the initiation or progression of atherosclerosis. We hypothesize that the chronic and intense inflammatory response accompanying periodontal disease produces an excess burden of circulating mediators of inflammation that initiate or exacerbate the inflammatory components of atherosclerosis. Activation of NF‐κB, then, would be a key step in linking the inflammatory state that accompanies periodontitis and atherogenesis. Further understanding of the mechanisms involved in the activation of NF‐κB in atherosclerosis could lead to important therapeutic applications especially as it relates to the impact of periodontitis.Ann Periodontol 2001;6:20‐29.
Candidate Genes as Potential Links Between Periodontal and Cardiovascular Diseases
Authors: Kornman Kenneth S. , Duff Gordon W.
Published: February 2005

Recent epidemiological associations between periodontal disease and cardiovascular disease have led to a search for biological mechanisms that explain the associations. Genetic factors that influence biological processes involved in both diseases represent one of the potential mechanisms that may link periodontitis and cardiovascular disease. At present, several candidate genes have been investigated in one of the diseases but not the other. Although there are limited data to support a specific candidate gene as the explanation for observed associations between the 2 diseases, a few candidates look promising. One candidate that influences inflammation, interleukin‐1 gene polymorphisms, has been associated with periodontal disease and cardiovascular disease. This review will consider biological mechanisms and genes that may be reasonable candidates for an etiological mechanism that influences the clinical characteristics of both periodontal disease and cardiovascular disease. Ann Periodontol 2001;6:48‐57.
The Relationship Between Infections and Chronic Respiratory Diseases: An Overview
Authors: Terpenning Margaret S.
Published: February 2005

This paper's goal is to review the relationship between infections and chronic respiratory disease, with particular reference to periodontal disease. The link between oral diseases in general, periodontal disease, and respiratory disease remains somewhat controversial. However, with cooperation between dentistry and medicine, the nature of the connection between dental and medical pathology can be better defined. An overview of respiratory disease and some of the factors that can contribute to respiratory infection is presented below, with special reference to infections related to aspiration. Ann Periodontol 2001;6:66‐70.
The Association Between Periodontal Diseases and Cardiovascular Diseases: A State‐of‐the‐Science Review
Authors: Beck James D. , Offenbacher Steven
Published: February 2005

Early case‐control and cross‐sectional studies demonstrating associations between chronic periodontitis and cardiovascular disease (CVD) were quickly followed by secondary analyses of data available from existing longitudinal studies, which indicated that individuals with periodontitis, as determined by clinical measures, were at greater risk for CVD events. Many of these studies contained large numbers of subjects and were adjusted for traditional risk factors. Within the last 18 months, one case‐control study and one longitudinal study have reported finding positive associations that were not statistically significant. The earlier studies stimulated a number of studies focused on identifying potential biological mechanisms that might underlie this association. While still early in that process, such studies have implicated a systemic role for oral microorganisms and for the quality and quantity of the host inflammatory response as key biologic processes that may underlie the association of CVD with the clinical manifestation of periodontitis. It is a positive development when changes in our knowledge regarding biologic mechanisms result in reevaluation of past studies, and this reevaluation leads to new studies that incorporate the design elements demanded by this new knowledge. In that spirit, we conclude that all longitudinal studies reported to date can be characterized as follows: none were initially designed to actually test the association of interest; almost all were restricted to clinical measures of periodontitis to index the exposure and lacked measures of infectious burden and host response; and they used a variety of cardiovascular clinical events to index the outcome and did not include subclinical measures of atherosclerosis. In addition, the longitudinal studies that failed to show a significant association between periodontitis and CVD used the least sensitive and crudest clinical measures of periodontal disease. Based upon the current state‐of‐the‐science, all previous studies should be viewed as lacking sufficiently sensitive and comprehensive measures of periodontal disease as a systemic exposure. Since the potential health care impact of this relationship might be extensive, it is time to enter the next phase of research by conducting molecular epidemiology studies that are appropriately designed to test our current understanding of the molecular and cellular mechanisms involved. Ann Periodontol 2001;6:9‐15.
The Relationship Between Periodontal Diseases and Diabetes: An Overview
Authors: Soskolne W. Aubrey , Klinger Avigdor
Published: February 2005

Diabetes mellitus, caused by the malfunction of insulin‐dependent glucose and lipid metabolism, presents with the classical triad of symptoms: polydypsia, polyuria, and polyphagia which are often accompanied by chronic fatigue and loss of weight. Complications of diabetes mellitus include retinopathy, nephropathy, neuropathy, and cardiovascular disease. Periodontal diseases are infections affecting the periodontium and resulting in the loss of tooth support. The association between diabetes mellitus and periodontitis has long been discussed with conflicting conclusions. Both of these diseases have a relatively high incidence in the general population (diabetes 1% to 6% and periodontitis 14%) as well as a number of common pathways in their pathogenesis (both diseases are polygenic disorders with some degree of immunoregulatory dysfunction). On the one hand, numerous reports indicate a higher incidence of periodontitis in diabetics compared to healthy controls, while other reports fail to show such a relationship. Clarification of this dilemma is occurring as the diagnostic criteria for periodontitis and diabetes mellitus improve, controlled studies with increased sample sizes are carried out, and the studies take into account major confounding variables that impact on the pathogenesis of both diseases. Current studies tend to support a higher incidence and severity of periodontitis in patients with diabetes mellitus. This overview looks at the bidirectional relationship between periodontitis and diabetes. An analysis of the National Health and Nutrition Examination Survey (NHANES) III data set confirms the previously reported significantly higher prevalence of periodontitis in diabetics than in non‐diabetics (17.3% versus 9%). The analysis of the data also shows that the prevalence of diabetes in patients with periodontitis is double that seen in the non‐periodontitis patients (12.5% versus 6.3%) and that this difference is also statistically significant. The pathogenesis of the 2 diseases is reviewed with an emphasis on common genetic and immune mechanisms. On the basis of the overview, 2 hypotheses for testing the relationship between periodontitis and diabetes are discussed. The first proposes a direct causal or modifying relationship in which the hyperglycemia and hyperlipidemia of diabetes result in metabolic alterations that may then exacerbate bacteria‐induced inflammatory periodontitis. The second hypothesis proposes that a fortuitous combination of genes (gene sets) could result in a host who, under the influence of a variety of environmental stressors, could develop either periodontitis or diabetes or both. Ann Periodontol 2001;6:91‐98.
Periodontitis in Humans and Non‐Human Primates: Oral‐Systemic Linkage Inducing Acute Phase Proteins
Authors: Ebersole Jeffrey L. , Cappelli David , Mathys Erik C. , Steffen Michelle J. , Singer Robert E. , Montgomery Michael , Mott Glen E. , Novak M. John
Published: February 2005

Background: The acute phase response (APR) represents a systemic counterpart to the localized inflammatory response. This report describes patient‐oriented and non‐human primate model studies to determine the effect of periodontal disease on systemic acute phase proteins (APP).

Methods: Patient‐oriented studies included comparison of the levels of APP, using enzyme‐linked immunosorbent assay (ELISA), with the presence and severity of periodontitis in localized chronic periodontitis (LCP), generalized aggressive periodontitis (GAP), and Sjögren's syndrome (SS) patients. The non‐human primate experiments evaluated the serum level of APPs under natural conditions, following mechanical hygiene, experimental gingivitis, and during ligature‐induced periodontitis.

Results: Analysis of the LCP population showed what appeared to be a threshold of periodontal disease severity required for elevating the C‐reactive protein (CRP) and haptoglobin (HG). The results demonstrated a significant elevation in CRP in the GAP versus the control groups, as well as lower levels of all mediators in healthy non‐smokers (HNS) versus smokers (HS), suggesting that these systemic inflammatory markers were altered in response to challenge by noxious materials from smoking. Significantly different levels of CRP, HG, and α1‐antiproteinase were noted in the SS patients suggesting that the autoimmune aspects of Sjögren's syndrome may impact upon oral health and systemic responses. Parallel evidence was also obtained from the primate studies. Providing mechanical oral hygiene, which significantly lowered clinical inflammation and bleeding of the gingiva, decreased the serum APP levels. Both CRP and fibrinogen were significantly elevated during progressing periodontitis, which also appeared to have an impact on serum lipids and lipoproteins.

Conclusions: These findings supported results relating chronic oral infections and the inflammation of periodontitis as contributors to and/or triggers for systemic inflammatory responses. Finally, similarities in the clinical and microbiological parameters of gingival inflammation and periodontitis between humans and non‐human primates was extended to identification of changes in serum APP in the non‐human primates that appeared to be in direct response to the induction of progressing periodontitis. These systemic changes provide additional evidence for the biological plausibility of periodontal infections contributing to various systemic diseases. Ann Periodontol 2002;7:102‐111.
Subtractive Cloning: New Genes for Studying Inflammatory Disorders
Authors: Rebrikov Denis , Desai Sejal , Kogan Yakov N. , Thornton Angela M. , Diatchenko Luda
Published: February 2005

Understanding of the biology of interaction between pathogens and host is the central question in studying inflammatory disorders. Subtractive DNA cloning is one of the most efficient and comprehensive methods available for identifying eukaryotic genes regulated under specific physiological conditions, including inflammation and host response. Here we explore the utility of subtractive DNA cloning and describe suppression subtractive hybridization (SSH), a polymerase chain reaction (PCR)‐based DNA subtraction method that has been developed and evolved in our labs over several years. The SSH method possesses a number of advantages as compared to other subtractive cloning techniques, making it one of the most adventitious methods for cloning differentially expressed genes. Besides isolation of differentially expressed eukaryotic mRNAs, subtractive DNA cloning can be used to identify genes that are differentially expressed between diverse bacterial species. These genes can be of great interest, as some may encode strain‐specific traits such as drug resistance, or bacterial surface proteins involved in determining the virulence of a particular strain. Other genes may be useful as markers for epidemiological or evolutionary studies. To demonstrate the potential of the SSH technique, we describe here the comprehensive characterization of 2 SSH subtracted libraries constructed in our laboratories. One library was created using eukaryotic cDNA subtraction and is specific for mRNAs up‐regulated in CD25 positive cells from mouse lymph nodes as compared to CD25 negative cells. The second subtracted library is specific for a methicillin‐resistant Staphylococcus aureus bacterial strain, but not in a methicillin‐sensitive strain. The bacterial genomes of these 2 strains have been completely sequenced and this second library provides an excellent reference for testing the ability of SSH to recover all strain‐specific gene content. The analysis of these 2 subtracted libraries serves as the basis for a discussion of the strength and limitations of the SSH technique. We will also compare and contrast subtractive DNA cloning to other current technologies used to isolate differentially expressed genes. Ann Periodontol 2002;7:17‐28.
Porphyromonas gingivalis Lipopolysaccharide Displays Functionally Diverse Interactions With the Innate Host Defense System
Authors: Bainbridge Brian W. , Coats Stephen R. , Darveau Richard P.
Published: February 2005

Periodontitis is a bacterially induced chronic inflammatory disease and a major cause of tooth loss in the world. The tissue damage and alveolar bone resorption characteristic of the disease are believed to be due to a destructive innate host response to a pathogenic subgingival biofilm. Porphyromonas gingivalis, a Gram‐negative bacterium, is a member of this mixed microbial community that has been designated an etiologic agent of periodontitis. The innate host response to lipopolysaccharide (LPS) obtained from P. gingivalis is unusual in that different studies have reported that it can be an agonist for Toll‐like receptor (TLR) 2 as well as an antagonist or agonist for TLR4. In addition, human monocytes respond to this LPS by secreting a variety of different inflammatory mediators, while endothelial cells do not. We have examined highly purified preparations of P. gingivalis LPS and found that they activate both TLR2 combined with TLR1 and TLR4 in transiently transfected human embryonic kidney (HEK) 293 cells. We have further demonstrated that highly purified P. gingivalis LPS preparations contain at least 3 major different lipid A species. We speculate that P. gingivalis lipid A structural heterogeneity contributes to the unusual innate host response to this LPS and its ability to interact with different TLR molecules. Ann Periodontol 2002;7:29‐37.
Campylobacter Surface‐Layers (S‐Layers) and Immune Evasion
Authors: Thompson Stuart A.
Published: February 2005

Many pathogenic bacteria have evolved mechanisms for evading host immune systems. One evasion mechanism is manifest by the surface layer (S‐layer), a paracrystalline protein structure composed of S‐layer proteins (SLPs). The S‐layer, possessed by 2 Campylobacter species (C. fetus and C. rectus), is external to the bacterial outer membrane and can have multiple functions in immune avoidance. C. fetus is a pathogen of ungulates and immunocompromised humans, in whom it causes disseminated bloodstream disease. In C. fetus, the S‐layer is required for dissemination and is involved in 2 mechanisms of evasion. First, the S‐layer confers resistance to complementmediated killing in non‐immune serum by preventing the binding of complement factor C3b to the C. fetus cell surface. S‐layer expressing C. fetus strains remain susceptible to complementindependent killing, utilizing opsonic antibodies directed against the S‐layer. However, C. fetus has also evolved a mechanism for avoiding antibody‐mediated killing by high‐frequency antigenic variation of SLPs. Antigenic variation is accomplished by complex DNA inversion events involving a family of multiple SLPencoding genes and a single SLP promoter. Inversion events result in the expression of antigenically variant S‐layers, which require distinct antibody responses for killing. C. rectus is implicated in the pathogenesis of periodontal disease and also possesses an S‐layer that appears to be involved in evading the human system. Although studied less extensively than its C. fetus counterpart, the C. rectus S‐layer appears to confer resistance to complement‐mediated killing and to cause the down‐regulation of proinflammatory cytokines. Ann Periodontol 2002;7:43‐53.
Relationships Among Clinical Measures of Periodontal Disease and Their Associations With Systemic Markers
Authors: Beck James D. , Offenbacher Steven
Published: February 2005

Background: Recent investigations of the relationship between periodontitis and systemic disease require that periodontal disease also must be thought of as a disease process that is an exposure for a systemic disease or condition (outcome), rather than as the outcome itself. When viewing periodontal disease as an exposure, investigators must consider the clinical, microbiological, and inflammatory components of periodontitis that potentially convey risk for the systemic outcome of interest, which may or may not be the same as those associated with the assessments used to define tooth‐based disease. Another important consideration is the temporal relationship between the exposure and the outcome of interest.

Methods: To explore which definitions of periodontal disease or clustering of clinical signs are important with regards to systemic exposure to inflammatory stress, we examined the relationship between clinical periodontal disease measures and 2 systemic inflammatory markers of increased risk for cardiovascular disease: serum soluble intercellular adhesion molecule (sICAM), which is a measure of vascular stress and serum C‐reactive protein (CRP), which is a measure of hepatic acute‐phase response. The Dental Arteriosclerosis Risk in Communities (ARIC) study, a cross‐sectional study of the relationship between periodontal disease and cardiovascular disease, forms the basis for the examples used in this investigation.

Results: Our findings demonstrated that while attachment loss, probing depth, (PD) and bleeding on probing (BOP) are individually associated with sICAM and CRP, only BOP remains significant for sICAM when all 3 are in the model and, for CRP, only PD remains significant. Both of these clinical parameters were more robust in estimating the degree of systemic inflammation than traditional classifications of mild, moderate, and severe periodontitis or other measures of disease severity such as attachment loss.

Conclusions: When selecting a definition of “systemic periodontitis” (periodontal disease that represents an exposure for a systemic condition), it is helpful to think of periodontal disease as a chronic oral infection with a number of clinical signs, rather than as the dento‐centrically defined entity, periodontal disease. Thus, “systemic periodontitis” should be defined predicated upon those clinical signs that best represent the underlying mechanisms and temporal sequence that may affect that systemic outcome. Ann Periodontol 2002;7:79‐89.
Bacterial Diversity in Necrotizing Ulcerative Periodontitis in HIV‐Positive Subjects
Authors: Paster Bruce J. , Russell Meaghan K. , Alpagot Tamer , Lee Alice M. , Boches Susan K. , Galvin Jamie L. , Dewhirst Floyd E.
Published: February 2005

Background: Necrotizing ulcerative periodontitis (NUP) is a painful and potentially debilitating affliction that affects about 2% to 6% of HIV‐positive subjects. NUP may be caused by specific microorganisms that are presently unknown or by microbial species not usually thought to cause periodontal infections. The purpose of this study was to define the bacterial species associated with NUP in HIV‐positive patients.

Methods: 16S rRNA bacterial genes of DNA isolated from subgingival plaque of 8 HIV‐positive subjects with NUP were amplified by polymerase chain reaction (PCR) and cloned into Escherichia coli. The sequences of cloned inserts were used to determine species identity or closest relatives by comparison with known sequences. The microbial profiles in subgingival plaque of subjects with NUP, chronic periodontitis, and periodontal health were compared using a battery of over 200 oligonucleotide probes in a PCR‐based, reverse‐capture, checkerboard DNA‐DNA hybridization assay.

Results: Sequence analysis of over 400 clones revealed 108 species; 65 were “uncultivable” phylotypes, of which 26 were novel to NUP subjects. Species or phylotypes most commonly detected were Bulleidia extructa, Dialister, Fusobacterium, Selenomonas, Peptostreptococcus, Veillonella, and the phylum TM7. Based on sequence analysis and checkerboard analysis, NUP did not possess the classical periodontal pathogens such as Porphyromonas gingivalis.Otherwise, the microbial profiles of NUP and periodontitis had many similarities. The microbial profiles of subgingival plaque from periodontally healthy subjects were different and less complex in comparison to the profiles of both disease groups.

Conclusions: Certain species appear to be associated with health and periodontal diseases. The putative pathogens associated with periodontal disease in HIV‐negative subjects are not associated with NUP in HIV‐positive subjects. Ann Periodontol 2002;7:8‐16.
Cellular Responses to Oral Pathogens
Authors: Kuramitsu Howard K. , Miyakawa H. , Qi M. , Kang I.C.
Published: February 2005

Background: Several previous epidemiological studies, along with the results of more recent animal model approaches, have suggested a role for periodontitis in atherosclerosis. Such an association could be mediated by direct interactions of periodontopathic bacteria with host vascular tissues.

Methods:The interactions of Porphyromonas gingivalis with endothelial cells and macrophages in vitro were investigated relative to modification of low‐density lipoproteins (LDL).

Results: P. gingivalis 381, its outer membrane vesicles, and the lipopolysaccharide (LPS) derived from these organisms were all shown to induce modification of LDL in the presence of the murine macrophage J774.A.1. Such alterations led to an increase in the migration of the particles through agarose gels. In addition,u direct modification of LDL by strain 381 was demonstrated in the absence of macrophages. This latter property appears to be related to the potent protease activities of the bacterium. These properties may contribute to modification of LDL to forms which have been strongly implicated in cholesterol lipid accumulation in vascular tissues. P. gingivalis 381 also appears to induce cyclooxygenase‐2 expression in endothelial cells as determined with human umbilical vascular endothelial cells (HUVEC).

Conclusions: These in vitro results with vascular cells in culture suggest a molecular basis for a potential role for periodontopathic bacteria such as P. gingivalis in augmenting foam cell formation characteristic of atherosclerotic lesions. Ann Periodontol 2002;7:90‐94.
Guided Tissue Regeneration for the Treatment of Periodontal Intrabony and Furcation Defects. A Systematic Review
Authors: Murphy Kevin G. , Gunsolley John C.
Published: February 2005

Background: Many clinical studies have demonstrated that guided tissue regeneration (GTR) is a successful treatment modality of periodontal reconstructive surgery and it has become an accepted procedure in most periodontal practices.

Rationale: The purpose of this structured review was to assess the efficacy of guided tissue regeneration (GTR) procedures in patients with periodontal osseous defects compared with surgical controls on clinical, radiographic, adverse, and patient‐centered outcomes. It extends the scope of previous GTR systematic reviews, which were limited to randomized controlled studies, by the scope of outcome measures examined, and the duration of the study.

Focused Question: In patients with periodontal osseous defects, what is the effect of physical barriers compared with surgical controls on clinical, radiographic, adverse, and patient‐centered outcomes?

Search Protocol: An electronic search of the Cochrane Oral Health Group Trials Register and MEDLINE databases was performed. Manual searching of journals included Journal of Clinical Periodontology, Journal of Periodontology, and Journal of Periodontal Research up to January 2002. This manual search also included review of relevant bibliographies. Two manufacturers of GTR devices were contacted regarding unpublished data.

Selection Criteria

Inclusion criteria: Studies were selected for review if the evidence level was 3B (cohort) or above, at least 6 months duration, and compared a test GTR intervention with a surgical control.

Exclusion criteria: Studies with experimental design problems; histologic or microbiological investigations; or those with outcome measurements, study populations, or study duration not consistent with the inclusion criteria were excluded. Primary outcome measures for intrabony defects were: clinical attachment level (CAL) gain, probing depth reduction (PD), gingival recession (REC) reduction; for furcation defects: vertical probing attachment level (VPAL) gain, vertical probing depth reduction (VPD), horizontal probing depth reduction (HPD), horizontal open probing attachment level gain (HOPA), and vertical open probing attachment level gain (VOPA). Meta‐analysis was performed to compare GTR procedures to other surgical treatments and to examine the resulting clinical outcomes.

Main Results

For the primary outcome variables, in both intrabony‐defect and furcation‐defect studies, GTR was favored over open flap debridement (OFD) therapies (P 0.0001).

No differences were detected among barrier types, but barrier types could explain some heterogeneity in the results

Augmentation of the GTR barrier with a particulate graft enhanced VPD (P <0.05), VPAL, and HOPA, but none of the intrabony outcomes.

Reviewer's Conclusions: Overall, GTR is consistently more effective than OFD in the gain of clinical attachment and probing depth reduction in the treatment of intrabony and furcation defects.

Ann Periodontol 2003;8:266‐302.
A Six‐Month Comparison of Three Periodontal Local Antimicrobial Therapies in Persistent Periodontal Pockets
Authors: Kinane D.F. , Radvar M.
Published: February 2005

Background: Currently, several local antimicrobial delivery systems are available to periodontists. The aim of this 6‐month follow‐up parallel study was to evaluate the efficacy of three commercially available local delivery systems as adjuncts to scaling and root planing in the treatment of sites with persistent periodontal lesions.

Methods: Seventy‐nine patients with 4 pockets ≥ 5 mm and bleeding on probing and/or suppuration were randomized into 4 treatment groups which included: scaling and root planing alone (S) (20 patients), or in conjunction with the application of 25% tetracycline fibers (S+Tet) (19 patients), or 2% minocycline gel (S+Min) (21 patients), or 25% metronidazole gel (S+Met) (19 patients). Clinical measurements were taken at baseline, 6 weeks, 3 months, and 6 months after antimicrobial application. Treatments were applied using the distributors' recommended protocols.

Results: All 4 therapies resulted in significant improvements from baseline in probing depth, attachment level, bleeding on probing, and the Modified Gingival Index (MGI) scores. The improvements in clinical parameters were greater in all 3 adjunctive treatment groups than scaling and root planing alone. The mean probing depth reductions at 6 months were: scaling + tetracycline = 1.38 mm; scaling + metronidazole = 0.93 mm; scaling + minocycline = 1.10 mm; and scaling alone = 0.71 mm. The probing depth reduction at all time points was significantly greater in the scaling plus tetracycline fiber group than the scaling and root planing alone group (P<0.01). There was also a significant improvement for scaling plus tetracycline fiber application over scaling and metronidazole at both 6 weeks and 3 months, although this did not remain significant at the 6‐month visit. While the frequency of sites with suppuration was markedly reduced following all antimicrobial treatments, the most effective reductions were seen in the scaling plus tetracycline fiber group, followed by the minocycline group.

Conclusions: Although all 3 locally applied antimicrobial systems seem to offer some benefit over scaling and root planing alone, a treatment regimen of scaling and root planing plus tetracycline fiber placement gave the greatest reduction in probing depth over the 6 months after treatment. J Periodontol 1999; 70: 1‐7.
Prognosis Versus Actual Outcome. IV. The Effectiveness of Clinical Parameters and IL‐1 Genotype in Accurately Predicting Prognoses and Tooth Survival
Authors: McGuire Michael K. , Nunn Martha E.
Published: February 2005

Background: Recently, a genetic marker (IL‐1 genotype) that identifies individuals at higher risk for developing severe periodontal disease was discovered. A subgroup of the population reported on earlier was evaluated to determine if knowledge of the patient's IL‐1 genotype would improve accuracy in assignment of prognoses and prediction of tooth loss.

Methods: This subgroup consisted of 42 patients (1,044 teeth) in maintenance care for 14 years; 16 tested IL‐1 genotype‐positive (IL‐1GP). Nine were smokers, and 30 had a history of smoking, with an average of 29.44 pack years. A multiple Cox regression model and Kaplan‐Meier survival plots were fit to the subset of patients to evaluate tooth loss.

Results: Both IL‐1GP and heavy smoking were significantly related to tooth loss. A positive IL‐1 genotype increased the risk of tooth loss by 2.7 times, and heavy smoking by 2.9 times. The combined effect of IL‐1GP and heavy smoking increased the risk of tooth loss by 7.7 times. The value of clinical parameters traditionally used to assign prognosis was found to be dependent on IL‐1 genotype and smoking status. In the model that included IL‐1 genotype and heavy smoking, none of the clinical parameters added significantly to the model for tooth loss while mobility, probing depth, crown‐to‐root ratio, and percent bone loss added significantly to the model, which included IL‐1 genotype in non‐smokers. IL‐1GP patients and patients who smoked heavily demonstrated a much worse tooth survival rate when compared to IL‐1 genotype‐negative patients and non‐smokers, respectively.

Conclusions: Knowledge of the patient's IL‐1 genotype and smoking status will improve the clinician's ability to accurately assign prognosis and predict tooth survival. Clinical implications are as follows. Investigators were unable to judge which patients would be IL‐GP or negative based on their clinical presentation or family history of tooth loss due to periodontal disease. Since periodontal diseases are multifactorial, knowledge of the patient's genotype is more important in predicting future risk than explaining past disease. Knowledge of IL‐1 genotype status would be important in developing a treatment plan and predicting tooth survival for a new patient who smokes and presents with periodontal disease, especially if restorative care is needed. Knowledge of a maintenance patient's IL‐1 status would help target therapy for non‐responding areas; one would be less likely to take a “wait and see approach” with IL‐1GP patients. IL‐1 positive non‐smokers can be successfully treated and maintained over long periods of time. J Periodontol 1999;70: 49‐56.
Leiomyosarcoma Presenting as a Mandibular Gingival Swelling: A Case Report
Authors: Goldschmidt Paul R. , Goldschmidt Jeffrey D. , Lieblich Stuart E. , Eisenberg Ellen
Published: February 2005

We report a case of primary low‐grade leiomyosarcoma of the mandible in an otherwise healthy young woman. The neoplasm presented as a painful, pericoronal gingival swelling that mimicked an acute periodontal infection. It was managed accordingly, with curettage, debridement, and antibiotics. When the lesion failed to respond to this treatment approach, a biopsy was performed. Microscopy revealed a malignant mesenchymal neoplasm which, on immunohistochemistry analysis, demonstrated reactivity for smooth muscle actin (SMA) and vimentin. This established the diagnosis of leiomyosarcoma; subsequently, an en bloc resection of mandibular bone and overlying soft tissue was performed. Close follow‐up for over 10 years has revealed no evidence of recurrent or metastatic disease. Since the patient was taking oral contraceptives prior to the onset of the lesion, a possible link between estrogen and smooth muscle tumors is considered. J Periodontol 1999;70: 84‐89.
Full‐Arch Restoration of the Jaw With Fixed Ceramo‐Metal Prosthesis: Late Implant Placement
Authors: Chaushu Gavriel , Schwartz‐Arad Devorah
Published: February 2005

Background: The completely edentulous patient has few treatment options in conventional dentistry. When implants are considered, treatment plans range from a 2‐implant overdenture to a completely implant‐supported prosthesis. Fixed prosthesis is often the preferred selection of the edentulous patient. This study assesses the 5‐year cumulative survival rate of implants placed to support full‐arch fixed restoration.

Methods: During 1990 to 1995, 171 implants were placed in 22 completely edentulous jaws of 20 patients. All patients were discharged wearing immediate dentures. The implants were analyzed as to the number of implants per jaw, implant location, length, and diameter.

Results: The 5‐year cumulative survival rate was 89.9%. The mean number of implants per jaw was 7.7 for the maxilla and 8 for the mandible. In the maxilla, the preferred implant locations were the canines, centrals, laterals, and first premolars; in the mandible, they were the canines, laterals, and first molars. The mean implant length was 14.2 mm for the mandible and 13.2 mm for the maxilla. The mean implant diameter was 3.6 mm for the maxilla and 3.8 for the mandible.

Conclusions: The results of the present study indicate that fixed full‐arch ceramo‐metal restorations can be a predictable implant treatment modality for the edentulous patient. J Periodontol 1999; 70: 90‐94.
Selecting a Practice Location: Factors That Periodontists May Consider
Authors: Waldman H. Barry
Published: February 2005

Background: The decision to locate a periodontal practice is based upon a complex series of interrelated variables. An understanding of this process is essential if planning for the distribution of periodontists is to be considered.

Methods: Non‐parametric statistical tests were used to determine the relationships between the rankings of states by periodontist‐to‐population ratios and 1) the availability of a periodontal training program, and 2) selected population demographic characteristics.

Results: A statistically significant positive relationship was found between the ranking of states by periodontist‐to‐population ratios and 1) the availability of a periodontal training program; 2) per capita income; 3) per capita spending for health services; 4) availability of health insurance; and 5) the percentage of the population that is African‐American, Hispanic, and Asian‐American.

Conclusions: This study provides a broad analysis of some of the factors in the practice location decision process. Further analysis at the local level (and for individual practitioners) is needed to better understand the decision process in the selection of a practice site. J Periodontol 1999; 70: 95‐99.
Effects of Occlusal Loading on Ankylosis, Bone, and Cementum Formation During Bone Morphogenetic Protein‐2‐Stimulated Periodontal Regeneration In Vivo
Authors: King Gaston N. , Hughes Francis J.
Published: February 2005

Background: The purpose of this study was to investigate the influence of occlusal loading on recombinant human bone morphogenetic protein‐2 (BMP‐2)‐induced bone and cementum formation in a previously established rat model of periodontal regeneration during the early and late stages of wound healing.

Methods: 64 Wistar rats were divided into 8 groups and had surgically created fenestrated defects on the right side of the mandible involving the removal of bone and exposure of the first and second molar roots. Four groups had their right maxillary molars extracted 2 weeks prior to surgery. Ten μl of 100 ug/ml BMP‐2 in a collagen membrane was placed in extracted (hypofunctional) and non‐extracted (functional) groups (BMPe and BMPf, respectively) while control groups had collagen membrane only (CONe and CONf). Groups were sacrificed at 10 (BMPe, BMPf, CONe, CONf) or 35 days (BMP35e, BMP35f, CON35e, CON350 postoperatively and tissues processed for histological examination. Transverse 5 μm sections were stained for identification of new bone, ankylosis and cementum formation.

Results: At 10 days, CONe developed greater bone growth compared with CONf (P <0.05), while both BMP groups developed greater bone compared with controls, However, BMPe developed more ankylosis compared with both CONe and CONf while BMPf was significantly greater than CONf only (P < 0.05 ) . BMPf only developed significantly greater new cementum compared with controls. At 35 days, BMP35f developed greater bone growth compared with all other groups including BMP35e (P <0.05) and unlike results at 10 days, no differences were apparent between CON35f and CON35e. Unwanted bone growth beyond the defect margin anteriorly was significantly greater in BMP35f.

Conclusions: Results suggest hypofunction stimulates early bone formation. Furthermore, hypofunction and BMP‐2 increase the development of transient ankylosis. However, after wound healing is complete, function augments the early effects of BMP‐2‐induced new bone growth indicating remodeling to physiological levels does not occur. Finally, occlusal loading is both an important stimulus for remodeling and establishment of the periodontal ligament space during early wound healing a s well a s enhancing BMP‐2‐induced cementogenesis. J Periodontol 1999;70:1125‐1135.
Human Periodontal Ligament Fibroblast Behavior on Chemically Conditioned Dentine: An In Vitro Study
Authors: Rompen Eric H. , Goffinet Gerhard H. , Nusgens Betty
Published: February 2005

Background: Chemical root conditioning is widely used in an attempt to improve the outcome of regenerative periodontal surgery, but its effect on connective tissue cell proliferation and biosynthetic activity has been poorly studied. The goal of the present study was to test in vitro the consequences of conditioning human dentine by citric acid or minocycline on the behavior of attached human periodontal ligament (HPDL) cells in terms of proliferation, protein synthesis and morphological appearance.

Methods: HPDL cells were seeded on powdered human dentine, either untreated or conditioned for 3 minutes with 3% citric acid or 2.5% minocycline HCl. Scanning (SEM) and transmission (TEM) electron microscopic observations were performed, and 3H‐thymidine and 3H‐proline incorporation tests were used to evaluate the proliferative and the biosynthetic activities.

Results: Cell spreading was already evident and the penetration of cytoplasmic processes into dentinal tubules were frequently observed on all dentine types after 2 hours of attachment. After 24 hours of incubation, citric acid conditioning promoted an intense spreading of the cells, while minocycline HCl conditioning induced the formation of a dense feltwork of cellular processes. HPDL fibrolasts adherent to both types of surface‐conditioned dentine exhibited a significantly higher rate of proliferation (P <0.01) as well as a significantly higher level of total protein and of collagen synthesis (P <0.01) than on untreated dentine.

Conclusions: These data suggest that during periodontal surgery a conditioning of the root surface by citric acid or by minocycline HCl could promote the attachment, the proliferation, and the biosynthetic activity of HDPL, prerequisites to periodontal regeneration. J Periodontol 1999;70:1144‐1152.