bluuebunny/crossref_metadata_2025 huggingface dataset:
Histologic Evaluation of New Attachment Apparatus Formation in Humans
Authors: Bowers Gerald M. , Chadroff Brian , Carnevale Robert , Mellonig James , Corio Russel , Emerson Jane , Stevens Mark , Romberg Elaine
Published: October 2010

There is still controversy as to the role of bone grafting materials in the formation of a new attachment apparatus and component tissues (bone, cementum, and periodontal ligament). The purpose of this study was to compare the healing of intrabony defects with and without the placement of decalcified freeze‐dried bone allograft (DFDBA) in a nonsubmerged environment in humans. The most apical level of calculus on the root served as a histologic reference point to delineate root surfaces exposed to the oral environment and to measure new attachment apparatus and new component tissue formation. Free gingival grafts were placed over grafted and nongrafted defects to retard epithelial migration. Biopsies were obtained at 6 months and regeneration was evaluated histometrically. Data from 12 patients with 32 grafted and 25 nongrafted defects were submitted for statistical analysis. Results indicate that in nongrafted defects, a long junctional epithelium formed along the entire length of exposed root surfaces and often extended apical to the calculus reference notch. Free gingival grafts did not enhance regeneration of a new attachment apparatus, new cementum, new connective tissue, or new bone in nongrafted defects. The formation of a new attachment apparatus was observed when intrabony defects were grafted with DFDBA (x1.21 mm); significantly more new attachment apparatus (P <.005), new cementum (P <.005), new connective tissue (P <.05), and new bone (P <.0001) formed in intrabony defects grafted with DFDBA than in nongrafted defects. There was a greater chance for regeneration of a new attachment apparatus and component tissues in grafted defects than in nongrafted defects. New cellular cementum formed on old cementum and dentin but more often formed over both in the same defect). The periodontal ligament was more frequently oriented perpendicular to the root; there was greater loss in alveolar crest height in nongrafted than grafted defects (P <.05); and extensive root resorption, ankylosis, and pulp death were not observed in grafted or nongrafted defects. (Journal of Periodontology, 1989;60:683–693)
Altering the Progression of Human Alveolar Bone Loss With the Non‐Steroidal Anti‐Inflammatory Drug Flurbiprofen
Authors: Williams Ray C. , Jeffcoat Marjorie K. , Howard Howell T. , Rolla Arturo , Stubbs Derek , Teoh Kok W. , Reddy Michael S. , Goldhaber Paul
Published: October 2010

The treatment of human periodontal diseases relies on mechanical and antimicrobial suppression of the etiologic bacteria. The ability to alter the progression of Periodontitis by additionally blocking host pathways involved in the destructive process is an area of current research. Prostaglandins and other metabolites of arachidonic acid are believed to be important host mediators of the bone resorption of diseases such as Periodontitis. We have previously examined the effect of inhibitors of Prostaglandin production, non‐steroidal antiinflammatory drugs (NSAIDs), on inhibiting alveolar bone loss in beagles. The present study was designed to examine the effect of the NSAID, flurbiprofen, on slowing the radiographic loss of alveolar bone in the human.

Fifty‐six individuals with radiographic evidence of alveolar bone loss were recruited for study. Forty‐four patients remained in the study for the data analysis of loss of alveolar bone. Following a 6 month baseline pretreatment period to measure the radiographic progression of bone loss, half of the patients were administered flurbiprofen, 50 mg. b.i.d., while half were administered a placebo. All patients received a subgingival scaling and pumice by a hygienist every 6 months. The rate of alveolar bone loss in a 2‐year treatment period was compared to the baseline 6 month pretreatment period within and between patient groups. Throughout the study, teeth exhibiting obvious loss of bone were exited from study and treated with conventional mechanical therapy. At the end of the pretreatment period both patient groups had a similar mean rate of alveolar bone loss. In individuals given placebo tablets, the rate of bone loss was significantly (P <.05) less than baseline at 6 and 12 months of treatment, but not thereafter. Individuals given flurbiprofen twice daily had a significant (P <.05) decrease in rate of bone loss compared to baseline at 6, 12 and 18 months of treatment. In addition we found that at 12 and 18 months of flurbiprofen use the rate of bone loss in the flurbiprofen treated individuals was significantly less than in the placebo patients. However at 24 months of the treatment period there was no difference in the rate of bone loss between the placebo and flurbiprofen treated patients. These data suggest that the NSAID flurbiprofen, as an inhibitor of cyclooxygenase, can inhibit human alveolar bone loss as measured radiographically. This finding suggests that pharmacologic agents whose main action is the blocking of host responses involved in the disease process may become adjuncts to anti‐infective therapy in the management of bone resorption diseases such as Periodontitis. (J Periodontol 1989;60:485–490)
Class II Furcations Treated by Guided Tissue Regeneration in Humans: Case Reports
Authors: Caffesse R.G. , Smith B. A. , Duff B. , Morrison E.C. , Merrill D. , Becker W.
Published: October 2010

In the cases reported here, the response of Class II mandibular molar furcation defects to guided tissue regeneration (GTR) versus sham operation was evaluated. Baseline information, including probing pocket depth (PD) and clinical attachment level (CAL) measurements, was recorded after completion of the hygienic phase. Eleven experimental and six control furcations, randomly assigned, are included in this report. The furcations were surgically exposed, using a flap approach and the areas were debrided. On the experimental teeth, Gore‐Tex periodontal material was adapted and sutured, using a suspensory suture. The flaps were then sutured tightly, assuring complete coverage to the material. For 1 month all patients were seen weekly and rinsed their mouths with an 0.12% Chlorhexidine solution daily. After 4 to 6 weeks the Gore‐Tex membranes were removed. Clinical measurements were repeated at 3 and 6 months following surgery. Changes from baseline in PD and CAL were calculated for each case. Results indicated that PD measurements were reduced by both procedures, but the reduction was better for GTR at 3 and 6 months. At six months the test sites showed 2.8 ±1.0 mm pocket reduction, while the control sites showed an average of 1.6 ±0.9 mm reduction in pocket depth. CAL recordings were improved by both treatments, but were better for GTR at 6 months, with an average gain in CAL of 1.8 mm for the GTR and 0.6 mm for the controls. These cases in which GTR was compared to sham‐operated controls indicate that GTR can improve the response to therapy of Class II furcation defects. J Periodontol 1990; 61:510–514.
The Excessive Loss of Branemark Fixtures in Type IV Bone: A 5‐Year Analysis
Authors: Jaffin Robert A. , Berman Charles L.
Published: October 2010

The predictability of branemark implants has been well documented. High success rates in the maxilla and mandible in fully and partially edentulous patients can be expected. A host of factors may be attributed to the etiology of fixture loss. However, the quality of bone stands out as the single greatest determinant in fixture loss. Types I, II, and III bone offer good strength. Type IV bone has a thin cortex and poor medullary strength with low trabecular density. Ninety percent of 1,054 implants placed were in Types I, II, and III bone. Only 3% of these fixtures were lost; of the 10% of the fixtures placed in Type IV bone, 35% failed. Presurgical determination of Type IV bone may be one method to decrease implant failure. J Periodontol 1991; 62:2–4.
Periodontal Disease in Non‐Insulin‐Dependent Diabetes Mellitus
Authors: Emrich Lawrence J. , Shlossman Marc , Genco Robert J.
Published: October 2010

The relationship between diabetes mellitus and oral health status was determined in Pirna Indians from the Gila River Indian Community in Arizona. This tribe of native Americans has the world's highest reported incidence and prevalence of non‐insulindependent (type 2) diabetes mellitus. The probing attachment level, alveolar bone loss, age, sex, Calculus Index, Plaque Index, Gingival Index, fluorosis, and DMFT as well as the diabetic status was assessed in 1,342 Pirna Indians who were at least partially dentate. The prevalence and severity of destructive periodontal disease was determined by measuring probing attachment loss and radiographically apparent interproximal crestal alveolar bone loss, two independent but correlated indicators of periodontal destruction. Only diabetic status, age, and the presence of subgingival calculus were significantly associated with both increased prevalence and greater severity of destructive periodontal disease in this population. Diabetic status was significantly and strongly related to both the prevalence and severity of disease after adjusting for the effects of demographic variables and several indices of oral health including the Plaque Index. Subjects with type 2 diabetes have an increased risk of destructive periodontitis with an odds ratio of 2.81 (95% confidence interval 1.91 to 4.13) when attachment loss is used to measure the disease. The odds ratio for diabetic subjects was 3.43 (95% confidence interval 2.28 to 5.16) where bone loss was used to measure periodontal destruction. These findings demonstrate that diabetes increases the risk of developing destructive periodontal disease about threefold. Furthermore, diabetes increases the risk of developing periodontal disease in a manner which cannot be explained on the basis of age, sex, and hygiene or other dental measures. Periodontitis should be considered a potential complication of diabetes in evaluation of patients. J Periodontol 1991; 62:123–130.
The Effects of Short‐Term Application of a Combination of Platelet‐Derived and Insulin‐Like Growth Factors on Periodontal Wound Healing
Authors: Lynch Samuel E. , Castilla Gustavo Ruiz de , Williams Ray C. , Kiritsy Christopher P. , Howell T. Howard , Reddy Michael S. , Antoniades Harry N.
Published: October 2010

Polypeptide growth factors are a class of potent natural biologic mediators which regulate many of the activities of wound healing including cell proliferation, migration, and metabolism. Platelet‐derived growth factor (PDGF) and insulin‐like growth factor‐I (IGF‐I) have been shown to regulate DNA and protein synthesis in bone cells in vitro and to interact synergistically to enhance soft tissue wound healing in vivo. We have hypothesized that the combination of PDGF and IGF‐I may, therefore, enhance regeneration of both the soft and hard tissue components of the periodontium. To test this hypothesis we performed conventional periodontal surgery on all 4 quadrants of the mouth of 13 beagle dogs with naturally occurring periodontal disease. Following flap reflection, degranulation, and root planing, all premolar teeth in 2 quadrants of each dog received a combination of 3μg of recombinant PDGF‐B and IGF‐I in a methylcellulose gel, while the premolar teeth in the contralateral quadrants received the gel alone. Teeth in 4 additional animals also received 125I‐PDGF or 125I‐IGF‐I in the treated sites. The clearance rate of the 125I‐labeled protein, changes in local bone metabolism, and amount of new bone and cementum with inserting collagen fibers were measured. The clearance studies revealed that the half‐life of the factors at the site of application was 3.0 hours for IGF‐I and to 4.2 hours for PDGF‐B. Greater than 96% of the radio‐labeled proteins was cleared by 96 hours and no radioactivity was detected 2 weeks after application. There was a significant (P < 0.01) 2‐fold increase in uptake of the bone‐seeking radiopharmaceutical Technetium 99‐MDP at 2 and 4 weeks in growth factor treated sites compared to controls, indicating that there was increased metabolic activity within the bone at these sites. Computer‐aided histologic analyses of biopsies obtained at 2 and 5 weeks post‐operatively revealed a significant (P < 0.01), 5 to 10 fold increase in new bone and cementum in PDGF‐B/IGF‐I treated sites at both time points compared to controls receiving the placebo gel. The height and total area of new bone continued to increase from 2 to 5 weeks. The new bone underwent a normal maturation process as judged by histologic appearance. A physiologic periodontal ligament space was also formed between the new bone and new cementum. There was no increase in ankylosis in the treated sites. This study demonstrates that the short term application of the combination of PDGF‐B and IGF‐I can significantly enhance the formation of the periodontal attachment apparatus during the early phases of wound healing following surgery. J Periodontol 1991; 62:458–467.
Tissue Levels of Bone Resorptive Cytokines in Periodontal Disease
Authors: Stashenko Philip , Jandinski John J. , Fujiyoshi Philip , Rynar James , Socransky Sigmund S.
Published: October 2010

The levels of 3 bone resorptive cytokines, interleukin 1α (IL‐1α), IL‐1β, and tumor necrosis factor α (TNFα), were assessed in tissues from sites of periodontal disease. As determined by ELISA of tissue extracts, IL‐1β and TNFα were detected in all diseased sites, whereas IL‐1α was present in 8/22 sites. IL‐1β was present in highest concentration (mean ± SEM: 11,695 ± 2,888 pg/ml; 672 pM), followed by TNFα (434 ± 135 pg/ml; 26 pM), and IL‐1α (342 ± 160 pg/ml; 20 pM). The levels of all 3 mediators were significantly lower in clinically healthy tissues. There was a highly significant correlation between levels of IL‐1β and TNFα (rs = 0.61, P <0.001), suggesting coordinated expression of these 2 mediators. The numbers of cells containing each mediator was also determined by indirect immunofluorescence on frozen tissue sections. Consistent with findings from tissue extracts, IL‐1β‐containing cells were present in approximately 5‐fold higher numbers than TNFα‐containing cells, and 40‐fold higher numbers than IL‐1α‐containing cells. Taken together with previous findings, these results indicate that IL‐1β is likely to be an important mediator in the pathogenesis of periodontal disease. J Periodontol 1991; 62:504–509.
Guided Tissue Regeneration Versus Mucogingival Surgery in the Treatment of Human Buccal Gingival Recession
Authors: Prato Giampaolo Pini , Tinti Carlo , Vincenzi Giampaolo , Magnani Cristina , Cortellini Pierpaolo , Clauser Carlo
Published: October 2010

A surgical technique involving membranes was used to treat localized human buccal recessions 3 mm to 8 mm. The results on 25 patients (test group) were evaluated 18 months postoperatively and compared with the results obtained in 25 other patients (control group) having undergone mucogingival surgery. In the test group, a trapezoidal flap with a large base was raised beyond the mucogingival junction. The exposed root surface was scaled thoroughly to a concave shape. A membrane was bent and adapted onto the concave root surface. The flap was sutured far coronally and the membrane removed one month later. The control patients underwent a 2‐step procedure, consisting of a free gingival graft and a coronally positioned flap. The amount of root coverage obtained was similar in the 2 groups (test = 72.73%; control = 70.87%), although the clinical attachment gain (test = 5.12 mm; control = 3.56 mm) and pocket variation (test = 1 mm reduction; control = 0.06 mm increase) differed significantly (P < 0.001). The keratinized tissue width was greater in the control group. The regression analysis showed that the amount of covered root surface after treatment was in strict correlation with the depth of the original recession in the test group, while no correlation was found in the control group. The expected root coverage was greater in the test group when the recession was greater than 4.98 mm, while it was greater in the control group when the recession was less than 4.98 mm. These results indicate that a guided tissue regeneration procedure can be used to successfully treat recession. The membrane procedure compared favorably with the mucogingival surgery in the treatment of deep recession. J Periodontol 1992;63:919‐928
A Comparison of ePTFE Membranes Alone or in Combination with Platelet‐Derived Growth Factors and Insulin‐Like Growth Factor‐I or Demineralized Freeze‐Dried Bone in Promoting Bone Formation Around Immediate Extraction Socket Implants
Authors: Becker William , Lynch Samuel E. , Lekholm Ulf , Becker Burton E. , Caffesse Raul , Donath Karl , Sanchez Raquel
Published: October 2010

The purpose of this study was to compare bone promotion around implants which were augmented with ePTFE membranes alone or in combination with cortical demineralized freeze‐dried bone (DFDB) or the combination of platelet derived growth factor‐BB (PDGF) and insulin like growth factor I (PDGF/IGF‐I). Membranes were placed over titanium implants which had been inserted into fresh extraction sockets with large buccal dehiscences. Twenty‐four implants were placed in 4 dogs. At 18 weeks clinical bone height measurements were taken, the animals were sacrificed, and all specimens retrieved for histologic evaluation. Clinically, a significant gain in bone levels was present in both the ePTFE membrane alone group (P < 0.005) and PTFE plus PDGF/IGF‐I group (P <0.01), but not in the PTFE plus DFDB group. Results from histometric measurements revealed an approximately 2‐fold increase in the percentage of implant surface in contact with bone, area of bone adjacent to the implant surface, and in the total length of the implant surface in contact with bone in the dehiscence defects treated with ePTFE plus PDGF/IGF‐I compared to the defects receiving ePTFE membranes alone (each P <0.05). The response to the DFDB was highly variable and it did not significantly improve the efficacy of the PTFE membranes for any parameter measured. The distance from the outer surface of the new bone to the implant surface was statistically significant for ePTFE membranes alone and membranes plus PDGF/IGF‐I. The results demonstrated that clinically, ePTFE membranes alone or ePTFE membranes with PDGF/IGF‐I were equally effective in promoting bone growth around the implants. Histologic measurements demonstrated that sites treated with ePTFE membranes plus PDGF/IGF‐I had the highest bone density compared with sites which received ePTFE membranes alone or with ePTFE membranes and DFDB. The results of this study question the use of DFDB and support the use of ePTFE membranes alone or with PDG‐F‐BB/IGF‐I as potential methods of promoting bone formation around dental implants. J Periodontol 1992;63:929– 940.
Regenerative Surgery of Intrabony Periodontal Defects Using ePTFE Barrier Membranes: Scanning Electron Microscopic Evaluation of Retrieved Membranes Versus Clinical Healing
Authors: Selvig Knut A. , Kersten Betty G. , Chamberlain A. Durwin H. , Wikesjö Ulf M. E. , Nilvúus Rolf E.
Published: October 2010

Sixteen intrabony defects in 12 patients were treated by gingival flap surgery including root surface debridement and placement of an expanded polytetrafluoroethylene (ePTFE) membrane. The membranes were removed after 4 to 6 weeks and examined by scanning electron microscopy (SEM) for bacterial contamination and adherent connective tissue elements. Twelve months postsurgery, the defect sites were reexamined for changes in probing attachment level and probing bone level. Comparison of ultrastructural findings and clinical observations revealed that extent of bacterial contamination of the membrane correlated inversely with clinical assessment of attachment gain. The results indicate that the extent of oral exposure and bacterial contamination of the ePTFE membrane at the time of removal may be an indicator of the long‐term success or failure of the regenerative procedure. J Periodontol 1992;63:974–978.
Significance of Early Healing Events on Periodontal Repair: A Review
Authors: Wikesjö Ulf M. E. , Nilvéus Rolf E. , Selvig Knut A.
Published: October 2010

Wound healing in an incisional wound is a highly predictable process which has been studied extensively hour‐by‐hour and day‐by‐day. Healing in a periodontal defect following gingival flap surgery is, conceptually, a more complex process as one wound margin consists of calcified tissue, including the avascular and rigid root surface. Another complicating factor in this wound healing is the transgingival position of the tooth. Experimental studies, however, have indicated that healing at a dento‐gingival interface under optimal conditions occurs at the same rate as in a skin wound. Generally, periodontal healing is characterized by maturation of gingival connective tissue, limited regeneration of alveolar bone and cementum, and the formation of a long junctional epithelium. Such observations have nurtured the hypothesis that the epithelium of the surgical flap needs to be prevented from early access to the root surface during the healing period to achieve connective tissue repair of the root surface‐gingival flap interface. Recent experimental findings suggest, however, that connective tissue repair to the root surface following reconstructive periodontal surgery is a function of the establishment and maintenance of a root surface‐adhering fibrin clot. Since fibrin adherence to the wound margins is a natural event, it is additionally suggested that apical migration of the gingival epithelium in periodontal surgical wounds may only follow interruption of the adherence of the fibrin clot to the root surface. J Periodontol 1992; 63:158‐165.
The Bacterial Etiology of Destructive Periodontal Disease: Current Concepts
Authors: Socransky Sigmund S. , Haffajee Anne D.
Published: October 2010

The interpretation of diagnostic tests for the detection of subgingival bacterial species is dependent on knowledge of the microbial etiology of destructive periodontal diseases. Specific etiologic agents of these diseases have been sought for over 100 years; however, the complexity of the microbiota, an incomplete understanding of the biology of periodontal diseases, and technical problems have handicapped this search. Nonetheless, a number of possible pathogens have been suggested on the basis of their association with disease, animal pathogenicity, and virulence factors. The immunological response of the host to a species and the relation of successful therapy to the elimination of the species have also been used to support or refute suspected periodontal pathogens. Current data suggest that pathogens are necessary but not sufficient for disease activity to occur. Factors which influence activity include susceptibility of the individual host and the presence of interacting bacterial species which facilitate or impede disease progression. Recent studies have attempted to distinguish virulent and avirulent clonai types of suspected pathogenic species and seek transmission of genetic elements needed for pathogenic species to cause disease. Finally, the local environment of the periodontal pocket may be important in the regulation of expression of virulence factors by pathogenic species. Thus, in order that disease result from a pathogen, 1) it must be a virulent clonal type; 2) it must possess the chromosomal and extra‐chromosomal genetic factors to initiate disease; 3) the host must be susceptible to this pathogen; 4) the pathogen must be in numbers sufficient to exceed the threshold for that host; 5) it must be located at the right place; 6) other bacterial species must foster, or at least not inhibit, the process; and 7) the local environment must be one which is conducive to the expression of the species' virulence properties. J Periodontol 1992; 63:322‐331.
Host Responses in Periodontal Diseases: Current Concepts
Authors: Genco Robert J.
Published: October 2010

In periodontal diseases, bacteria trigger inflammatory host responses which, along with the direct destructive effects of the bacteria, cause most of the tissue destruction. Periodontal inflammatory responses are, by and large, immunologic, and our understanding of these reactions has been advanced by the explosion of knowledge in immunobiology, some of which is discussed in this review. Understanding the role of immune cells and their regulatory cell surface molecules such as the MHC, CD antigens, and receptors, as well as knowledge of effector systems set into motion such as phagocytes and cytotoxic T‐cells, and the effector molecules such as antibodies, complement, and cytokines, have led to better understanding of the complex pathogenesis of periodontal disease. The role of mediators including the matrix metalloproteinases, proteoglycans, the kinins and anaphylatoxins, and low molecular weight mediators including products of arachidonic metabolism is beginning to be elucidated in periodontal disease. Important avenues of research for development of diagnostic tests based upon host response are apparent. For example, tissue products released during periodontal inflammation including the metalloproteinases, elastase, cytokines, prostaglandins, antibodies, and complement components may provide the basis for future diagnostic indicator tests. The recognition that the neutrophil/antibody/complement axis is critical for protection against periodontal bacteria and that abnormalities in this system often lead to increased periodontal susceptibility provide approaches for the development of diagnostic tests assessing risk. A group of factors which are negative regulators of inflammation including TGF‐β, gamma‐interferon, and IL‐1 receptor antagonist provide potential for assessment of periodontal disease in remission or in the healing phase. Finally, factors such as HLA associations and the molecular basis for neutrophil abnormalities may provide genetic markers for periodontal disease susceptibility. Diagnostic factors based upon host response measures offer great potential for predicting host susceptibility and will likely be used in combination with microbial diagnostics which identify specific infecting organisms. J Periodontol 1992;63:338‐355.
Mitogenic, Chemotactic, and Synthetic Responses of Rat Periodontal Ligament Fibroblastic Cells to Polypeptide Growth Factors In Vitro
Authors: Matsuda N. , Lin W.‐L. , Kumar N. M. , Cho M. I. , Genco R. J.
Published: October 2010

The mitogenic, chemotactic, and synthetic responses of rat periodontal ligament (PDL) fibroblastic cells to epidermal growth factor (EGF), transforming growth factorβ (TGF‐β), recombinant human platelet‐derived growth factor (rhPDGF)‐AB, rhPDGFBB, natural (n) PDGF‐AB, and insulin‐like growth factor‐I (IGF‐I) were examined in vitro using PDL cells obtained from the coagulum of healing tooth sockets. PDGFs and IGF‐I have potent and comparable mitogenic effects on PDL fibroblastic cells. The maximum mitogenic effect of PDGFs was observed at the concentration of 10 ng/ml, whereas that of IGF‐I was seen at concentrations higher than 100 ng/ml. In contrast, EGF induced moderate, and TGF‐β inhibitory mitogenic responses. The combination of rhPDGF‐AB with either EGF or TGF‐β demonstrated comparable mitogenic potency, equivalent to the level of PDGF alone regardless of the mitogenic effect of other growth factors. The combination of rhPDGF‐AB and IGF‐I, however, showed a synergistic effect revealing the highest mitogenic effect among all individual growth factors as well as any combinations of the growth factors tested. Similarly, PDL fibroblastic cells demonstrated strong chemotactic responses to both IGF‐I and PDGFs. The maximum effect was observed by IGF‐I at concentrations higher than 10 ng/ml, followed by rhPDGF‐BB at 0.1 ng/ml, rhPDGF‐AB and nPDGF at concentrations ranging from 0.1 to 1 ng/ml. TGF‐β revealed no, and EGF slightly increased, chemotactic effects. IGF‐I slightly enhanced the synthesis of total protein, whereas other factors had no significant effect. However, both rhPDGF‐AB and TGF‐β stimulated collagen synthesis. On the other hand, IGF‐I showed no effect on collagen synthesis, while EGF suppressed collagen synthesis. These findings suggest that rhPDGF‐BB and IGF‐I stimulate proliferation and chemotaxis of PDL fibroblastic cells. In addition, the combination of these growth factors further increases the mitogenic effect. rhPDGF‐AB also stimulates collagen synthesis by PDL fibroblastic cells. Thus, rhPDGF‐BB and IGF‐I may have important roles in promotion of PDL healing, and consequently, may be useful for clinical application in periodontal regenerative procedures. J Periodontol 1992;63:515–525.
Periodontal Regeneration of Human Intrabony Defects. IV. Determinants of Healing Response
Authors: Tonetti Maurizio S. , Pini‐Prato Giovanpaolo , Cortellini Pierpaolo
Published: October 2010

The purpose of this study was to identify factors which might affect the healing response in intrabony defects treated with guided tissue regeneration. Selected sites presented with deep periodontal lesions with 1, 2, and 3 wall combination intrabony component of 6.1 ± 2.5 mm. The significance of patient, tooth, and defect characteristics and surgical parameters as predictor variables affecting the regenerative outcome before and following the removal of the barrier membrane was assessed. Outcome was measured as tissue gain under the membrane, regenerated probing attachment level (PAL), and bone fill. The total depth of the intrabony component and the radiographic defect angle significantly affected the amount of tissue gain. Seventy‐five percent (75%) of the variability of regenerated PAL and bone fill was explained in terms of tissue gain under the membrane, radiographic width of the defect angle, full mouth bleeding score, and presence or absence of flap coverage of the newly formed tissue. Control of the identified predictor variables might improve the extent and predictability of guided tissue regeneration in the treatment of deep intrabony defects. J Periodontol 1993; 64:934–940.
Periodontal Regeneration of Human Infrabony Defects. I. Clinical Measures
Authors: Cortellini Pierpaolo , Prato Giovanpaolo Pini , Tonetti Maurizio S.
Published: October 2010

A series of investigations was undertaken to evaluate the extent and predictability of periodontal regeneration with barrier membranes in deep infrabony defects. This study reports the clinical outcomes in terms of probing attachment level (PAL) gains, probing pocket depth (PPD) reduction, and recession (REC) of marginal gingiva. Forty deep 1, 2, and 3‐wall combination infrabony defects treated with membranes were evaluated 1 year postoperatively following a strict plaque control regimen (mean plaque score = 6.1%, bleeding score = 4% at 1 year). A PAL gain of 6.1 ± 2.5 mm along with a PPD reduction of 5.9 ± 2.5 mm were observed. A PAL gain of 2 mm or more was detected in almost 90% of the treated sites. No site lost attachment. Residual PPD was 3 mm or shallower in 95% of the sites. It is concluded that treatment of deep infrabony defects according to the principles of guided tissue regeneration and a strict plaque control regimen represents an efficacious and predictable treatment alternative. J Periodontol 1993; 64:254–260.
Modulation of Host PGE2 Secretion as a Determinant of Periodontal Disease Expression
Authors: Offenbacher Steven , Heasman Peter A. , Collins John G.
Published: October 2010

An increasing body of evidence supports the concept that host‐produced PGE2 mediates much of the tissue destruction that occurs in periodontal disease. PGE2 levels within the crevicular fluid can serve as a static assessment of ongoing disease activity; i.e., rate of attachment loss and bone resorption. New insights into the mechanisms that regulate PGE2 synthesis provide an altered paradigm of periodontal disease which places the emphasis on host response, rather than the bacterial etiology, as the principal determinant of disease expression. We describe a PGE2 host response model as a hypothetical framework to discuss new, possible explanations for host susceptibility to periodontal disease. J Periodontol 1993;64:432–444.
Role of Matrix Metalloproteinases in Human Periodontal Diseases
Authors: Birkedal‐Hansen Henning
Published: October 2010

Matrix metalloproteinases (MMP) are a family of proteolytic enzymes that mediate the degradation of extracellular matrix macromolecules, including interstitial and basement membrane collagens, fibronectin, laminin, and proteoglycan core protein. The enzymes are secreted or released in latent form and become activated in the pericellular environment by disruption of a Zn++‐cysteine bond which blocks the reactivity of the active site. The major cell types in inflamed and healthy periodontal tissues (fibroblasts, keratinocytes, endothelial cells, and macrophages) are capable of responding to growth factors and cytokines, as well as to products released from the microbial flora by induction of transcription of 1 or more MMP genes. Cytokines that are likely to regulate expression of MMP genes in periodontal tissues include IL‐1, TNF‐α, and TGF‐α. In addition, triggered PMN leukocytes which express only 2 MMP (PMN‐CL and Mr 92K GL) release these enzymes from specific granule storage sites in response to a number of stimuli. The evidence that MMP are involved in tissue destruction in human periodontal diseases is still indirect and circumstantial. Cells isolated from normal and inflamed gingiva are capable of expressing a wide complement of MMP in culture and several MMP can be detected in cells of human gingiva in vivo. In addition, PMN‐CL and Mr 92K GL are readily detected in gingival crevicular fluid from gingivitis and Periodontitis patients. Osteoclastic bone resorption does not appear to directly involve MMP, but a body of evidence suggests that bone resorption is initiated by removal of the osteoid layer by osteoblasts by means of a collagenase‐dependent process. J Periodontol 1993; 64:474–484.
Assessment of Risk for Periodontal Disease. I. Risk Indicators for Attachment Loss
Authors: Grossi Sara G. , Zambon Joseph J. , Ho Alex W. , Koch Gary , Dunford Robert G. , Machtei Eli E. , Norderyd Ola M. , Genco Robert J.
Published: October 2010

Specific risk indicators associated with either susceptibility or resistance to severe forms of periodontal disease were evaluated in a cross‐section of 1,426 subjects, 25 to 74 years of age, mostly metropolitan dwellers, residing in Erie County, New York, and surrounding areas. The study sample exhibited a wide range of periodontal disease experience defined by different levels of attachment loss. Therefore, it was possible to accurately assess associations between the extent of periodontal disease and patient characteristics including age, smoking, systemic diseases, exposure to occupational hazards, and subgingival microbial flora. Age was the factor most strongly associated with attachment loss, with odds ratios for subjects 35 to 44 years old ranging from 1.72 (95% CI: 1.18 to 2.49) to 9.01 (5.86 to 13.89) for subjects 65 to 74 years old. Diabetes mellitus was the only systemic disease positively associated with attachment loss with an odds ratio of 2.32 (95% CI: 1.17–4.60). Smoking had relative risks ranging from 2.05 (95% CI: 1.47–2.87) for light smokers increasing to 4.75 (95% CI: 3.28–6.91) for heavy smokers. The presence of two bacteria, Porphyromonas gingivalis and Bacteroides forsythus, in the subgingival flora represented risks of 1.59 (95% CI: 1.11–2.25) and 2.45 (95% CI: 1.87–3.24), respectively. Our results show that age, smoking, diabetes mellitus, and the presence of subgingival P. gingivalis and B. forsythus are risk indicators for attachment loss. These associations remain valid after controlling for gender, socioeconomic status, income, education, and oral hygiene status expressed in terms of supragingival plaque accumulation and subgingival calculus. Longitudinal, intervention, and etiology‐focused studies will establish whether these indicators are true risk factors. J Periodontol 1994;65:260–267.
Tobacco Use as a Risk Factor
Authors: Bergström Jan , Preber Hans
Published: October 2010

Tobacco, particularly tobacco smoking, has a substantial influence on periodontal health and disease. It is associated with an increased disease rate in terms of periodontal bone loss, periodontal attachment loss, as well as periodontal pocket formation. In addition, it exerts a masking effect on gingival symptoms of inflammation. Risk assessment based on an increasing body of investigations over the past few years suggests that the tobacco attributable risk is considerable, estimated odds ratios being of the order 2.5 to 6.0 or even greater. Although the mechanisms by which tobacco exerts its influence are obscure, information available to date does not support the view that its action simply relates to other environmental factors such as the dental plaque or some specific microflora. It seems more likely that it primarily has a systemic influence affecting host response or susceptibility. The chief novelty of the present report is that current data suggest that, although the overall disease prevalence is decreasing, the proportion of periodontal disease attributed to tobacco is stable or even increasing. This seems to be analogous to what has been observed for other smoking‐associated chronic diseases. This, in turn, indicates that periodontal disease behaves like several other chronic diseases and, further, that tobacco should be considered a major risk factor for chronic periodontal disease. J Petiodontol 1994;65:545–550.
Assessment of Risk for Periodontal Disease. II. Risk Indicators for Alveolar Bone Loss
Authors: Grossi S.G. , Genco R.J. , Machtet E.E. , Ho A.W. , Koch G. , Dunford R. , Zambon J.J. , Hausmann E.
Published: October 2010

This study examined the risk indicators for alveolar bone loss associated with periodontal infection. A cross‐section of 1,361 subjects aged 25 to 74 years, from Erie County, NY were evaluated for interproximal alveolar bone loss and potential explanatory variables including age, gender, history of systemic diseases, smoking, and presence of 8 subgingival bacteria. Interproximal alveolar bone loss was measured from the alveolar crest to the CEJ and a mean computed for each subject. The mean bone loss per subject (BL) ranged from 0.4 to 8.8 mm, and this outcome variable was grouped into 4 ordered categories. The degree of association between the explanatory variables and BL was examined utilizing an ordinal stepwise logistic regression model. Factors which were positively associated with more severe bone loss included subgingival colonization with B. forsythus (O.R. 2.52; 95% CI: 1.98 to 3.17) or P. gingivalis (O.R. 1.73; 95% CI: 1.27 to 2.37), race (Native American, Asian, or Pacific Islanders) with an O.R. 2.40 (95% CI: 1.21 to 4.79), and gender with males having higher odds than females. Smokers had greater odds for more severe bone loss compared to non‐smokers ranging from 3.25 (95% CI: 2.33 to 4.54) to 7.28 (95% CI: 5.09 to 10.31) for light and heavy smokers, respectively. Individuals at older ages also showed more severe levels of bone loss. History of kidney disease (O.R. 0.55; 95% CI: 0.35 to 0.89) and history of allergies (O.R. 0.76; 95% CI: 0.59 to 0.98) were inversely associated with severity of bone loss. Severity of alveolar bone loss is associated with increasing age, smoking, race, and colonization with subgingival B. forsythus or P. gingivalis. This and other studies directed to identifying true risk factors associated with periodontal disease may lead to preventive measures directed to reducing the deleterious effects of modifiable risk factors. J Periodonol 1995;66:23–29.
Periodontal Infection as a Possible Risk Factor for Preterm Low Birth Weight
Authors: Offenbacher Steven , Katz Vern , Fertik Gregory , Collins John , Boyd Doryck , Maynor Gayle , McKaig Rosemary , Beck James
Published: October 2010

Periodontal diseases are Gram‐negative anaerobic infections that can occur in women of childbearing age (18 to 34 years). In the present investigation we sought to determine whether the prevalence of maternal periodontal infection could be associated with preterm low birth weight (PLBW), controlling for known risk factors and potential covariates. A case‐control study of 124 pregnant or postpartum mothers was performed. PLBW cases were defined as a mother with a birth of less than 2,500 g and one or more of the following: gestational age <37 weeks, preterm labor (PTL), or premature rupture of membranes (PROM). Controls were normal birth weight infants (NBW). Assessments included a broad range of known obstetric risk factors, such as tobacco use, drug use, alcohol consumption, level of prenatal care, parity, genitourinary infections, and nutrition. Each subject received a periodontal examination to determine clinical attachment level. PLBW cases and primiparous PLBW cases (n = 93) had significantly worse periodontal disease than the respective NBW controls. Multivariate logistic regression models, controlling for other risk factors and covariates, demonstrated that periodontal disease is a statistically significant risk factor for PLBW with adjusted odds ratios of 7.9 and 7.5 for all PLBW cases and primiparous PLBW cases, respectively. These data indicate that periodontal diseases represent a previously unrecognized and clinically significant risk factor for preterm low birth weight as a consequence of either PTL or preterm PROM. J Periodontol 1996;67:1103–1113.
Periodontal Disease and Cardiovascular Disease
Authors: Beck James , Garcia Raul , Heiss Gerardo , Vokonas Pantel S. , Offenbacher Steven
Published: October 2010

It is our central hypothesis that periodontal diseases, which are chronic Gramnegative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. We further suggest that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (especially TxA2, IL‐1β, PGE2, and TNF‐α) which serve to initiate and exacerbate atherogenesis' and thromboembolic events. A cohort study was conducted using combined data from the Normative Aging Study and the Dental Longitudinal Study sponsored by the United States Department of Veterans Affairs. Mean bone loss scores and worst probing pocket depth scores per tooth were measured on 1,147 men during 1968 to 1971. Information gathered during follow‐up examinations showed that 207 men developed coronary heart disease (CHD), 59 died of CHD, and 40 had strokes. Incidence odds ratios adjusted for established cardiovascular risk factors were 1.5, 1.9, and 2.8 for bone loss and total CHD, fatal CHD, and stroke, respectively. Levels of bone loss and cumulative incidence of total CHD and fatal CHD indicated a biologic gradient between severity of exposure and occurrence of disease. J Periodontol 1996;67:1123–1137.
Periodontal Regeneration of Human Intrabony Defects With Bioresorbable Membranes. A Controlled Clinical Trial
Authors: Cortellini Pierpaolo , Prato Giovanpaolo Pini , Tonetti Maurizio S.
Published: October 2010

The purpose of this controlled clinical trial was to compare the clinical efficacy of 3 treatment modalities in the treatment of deep interproximal intrabony defects. Thirty‐six (36) defects in 36 patients. were randomly assigned to 1 of 3 treatment groups by blocking to prognostic variables. The test group was treated with bioresorbable membranes positioned coronal to the interproximal bone crest; the second group (membrane control) was treated with conventional non‐resorbable (ePTFE) barrier membranes applied coronal to the alveolar crest; the third group (flap control) was treated with an access flap procedure (MWF). No differences were observed in terms of baseline oral hygiene and defect characteristics among the 3 groups, indicating that the blocking approach was effective. A stringent infection control program was enforced for 1 year. The results indicated that: 1) at 1 year all treatment modalities resulted in clinically significant improvements in clinical attachment levels (CAL) and reductions in probing depths; 2) a statistically significant treatment effect (P < 0.0001, ANOVA) was observed comparing the test (4.6 ±1.2 mm), the membrane control (5.2 ± 1.4 mm), and the flap control groups (2.3 ± 0.8 mm) in terms of CAL gains; 3) differences in terms of CAL gain between the test (bioresorbable) and the membrane control (ePTFE) groups were not statistically significant (P = 0.19, t‐test); 4) both the test and the membrane control groups gained significantly more CAL at 1 year than the MWF group (P < 0.0001, t‐test). CAL gains ≥ 4 mm were observed in 83.3% of cases in both GTR groups, while CAL gains of this magnitude were not detected in the MWF group. We concluded that clinically significant CAL gains can be obtained.with GTR procedures using both bioresorbable and non‐resorbable membranes. Patients' morbidity, however, was lower in the group treated with bioresorbable membranes. J Periodontol 1996;67:217–223.
Treatment of Periodontal Disease in Diabetics Reduces Glycated Hemoglobin
Authors: Grossi Sara G. , Skrepcinski Fred B. , DeCaro Thomas , Robertson Don C. , Ho Alex W. , Dunford Robert G. , Genco Robert J.
Published: October 2010

Periodontal disease is a common infection‐induced inflammatory disease among individuals suffering from diabetes mellitus. The purpose of this study was to assess the effects of treatment of periodontal disease on the level of metabolic control of diabetes. A total of 113 Native Americans (81 females and 32 males) suffering from periodontal disease and non‐insulin dependent diabetes mellitus (NIDDM) were randomized into 5 treatment groups. Periodontal treatment included ultrasonic scaling and curettage combined with one of the following antimicrobial regimens: 1) topical water and systemic doxycycline, 100 mg for 2 weeks; 2) topical 0.12% chlorhexidine (CHX) and systemic doxycycline, 100 mg for 2 weeks; 3) topical povidone‐iodine and systemic doxycycline, 100 mg for 2 weeks; 4) topical 0.12% CHX and placebo; and 5) topical water and placebo (control group). Assessments were performed prior to and at 3 and 6 months after treatment and included probing depth (PD), clinical attachment level (CAL), detection of Porphyromonas gingivalis in subgingival plaque and determination of serum glucose and glycated hemoglobin (HbAlc). After treatment all study groups showed clinical and microbial improvement. The doxycycline‐treated groups showed the greatest reduction in probing depth and subgingival Porphyromonas gingivalis compared to the control group. In addition, all 3 groups receiving systemic doxycycline showed, at 3 months, significant reductions (P ≤ 0.04) in mean HbAlc reaching nearly 10% from the pretreatment value. Effective treatment of periodontal infection and reduction of periodontal inflammation is associated with a reduction in level of glycated hemoglobin. Control of periodontal infections should thus be an important part of the overall management of diabetes mellitus patients. J Periodontol 1997;68:713–719.