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  • 1
    Online Resource
    Online Resource
    Infection and inflammatory mechanisms
    Wiley ; 2013
    In:  Journal of Periodontology Vol. 84, No. 4S ( 2013-04)
    Details
    In: Journal of Periodontology, Wiley, Vol. 84, No. 4S ( 2013-04)
    Abstract: This introductory article examines the potential mechanisms that may play a role in the associations between periodontitis and the systemic conditions being considered in the EFP/AAP Workshop in Segovia, Spain. Three basic mechanisms have been postulated to play a role in these interactions; metastatic infections,inflammation and inflammatory injury, and adaptive immunity. The potential role of each alone and together is considered in in vitro and animal studies and in human studies when available. This is not a systematic or critical review, but rather an overview of the field to set the stage for the critical reviews in each of the working groups.
    Type of Medium: Online Resource
    ISSN: 0022-3492 , 1943-3670
    URL: Article
    DOI: 10.1902/jop.2013.1340018
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 2040047-0
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  • 2
    Online Resource
    Online Resource
    The Effect of Nicotine on Reproduction and Attachment of Human Gingival Fibroblasts In Vitro
    Wiley ; 1993
    In:  Journal of Periodontology Vol. 64, No. 7 ( 1993-07), p. 658-665
    Details
    In: Journal of Periodontology, Wiley, Vol. 64, No. 7 ( 1993-07), p. 658-665
    Abstract: T he ability of fibroblasts to reproduce and attach to teeth is of paramount importance in re‐establishing the lost connective tissue attachment after periodontal therapy. This study examined the effect of nicotine, a major component of the particulate phase of tobacco smoke, on human gingival fibroblast (HGF) reproduction and attachment to tissue culture surfaces. Pooled HGF cultures made from expiants of gingival biopsies were utilized between passages 5 and 10 and plated in 96‐well plates at 1.0 × 10 4 cells per well. Cell numbers were determined using 3‐(4,5‐dimethylthiazol‐2‐y)‐2,5‐diphenyl tetrazolium bromide (MTT), which is a reflection of mitochondrial dehydrogenase activity. The concentrations of nicotine used were 0.025, 0.05, 0.1, 0.2, and 0.4 μM, the average serum concentration for a smoker being approximately 0.1 μM. The effect of continuous nicotine exposure on HGF reproduction was determined by incubating cell cultures and media containing nicotine for up to 48 hours. Residual toxicity was determined by preincubating cells with nicotine for 1 or 6 hours. HGF suspensions and increasing concentrations of nicotine were added together to determine the effect on attachment. Results showed an enhanced effect of nicotine on HGF attachment, with increasing numbers of cells attaching with increasing nicotine concentrations, compared to the control. Low concentrations of nicotine had a stimulatory effect on cell replication, while higher concentrations of nicotine appear to have no significant effect on HGF reproduction. The responses of cells to some concentrations of nicotine may persist after its removal. J Periodontol 1993;64:658–665 .
    Type of Medium: Online Resource
    ISSN: 0022-3492 , 1943-3670
    URL: Article
    DOI: 10.1902/jop.1993.64.7.658
    Language: English
    Publisher: Wiley
    Publication Date: 1993
    detail.hit.zdb_id: 2040047-0
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  • 3
    Online Resource
    Online Resource
    Infection and inflammatory mechanisms
    Wiley ; 2013
    In:  Journal of Clinical Periodontology Vol. 40, No. s14 ( 2013-04)
    Details
    In: Journal of Clinical Periodontology, Wiley, Vol. 40, No. s14 ( 2013-04)
    Abstract: This introductory article examines the potential mechanisms that may play a role in the associations between periodontitis and the systemic conditions being considered in the EFP / AAP Workshop in Segovia, Spain. Three basic mechanisms have been postulated to play a role in these interactions; metastatic infections, inflammation and inflammatory injury, and adaptive immunity. The potential role of each alone and together is considered in in vitro and animal studies and in human studies when available. This is not a systematic or critical review, but rather an overview of the field to set the stage for the critical reviews in each of the working groups.
    Type of Medium: Online Resource
    ISSN: 0303-6979 , 1600-051X
    URL: Issue
    URL: Article
    DOI: 10.1111/jcpe.2013.40.issue-s14
    DOI: 10.1111/jcpe.12088
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 2026349-1
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  • 4
    Online Resource
    Online Resource
    Hereditary Gingival Fibromatosis Associated With Generalized Aggressive Periodontitis: A Case Report
    Wiley ; 2004
    In:  Journal of Periodontology Vol. 75, No. 5 ( 2004-05), p. 770-778
    Details
    In: Journal of Periodontology, Wiley, Vol. 75, No. 5 ( 2004-05), p. 770-778
    Abstract: Background: Hereditary gingival fibromatosis is a rare, genetically inherited overgrowth condition that is clinically characterized by a benign fibrous enlargement of maxillary and mandibular keratinized gingiva. A syndromic association between gingival fibromatosis and a wide variety of other genetically inherited disorders has been described. However, its coexistence with aggressive periodontitis has not been reported. Methods: A 24‐year‐old African‐American female, patient (proband X, [Px]) reported with a chief complaint of tooth mobility and gingival enlargement. Clinical examination revealed moderate to severe gingival overgrowth on both mandible and maxilla. Generalized attachment loss and mobility of the teeth were observed. Radiographic evaluation demonstrated severe alveolar bone loss. The patient was diagnosed with gingival fibromatosis and aggressive periodontitis based on the clinical and radiographic findings. Her brother (Bx) and her mother (Mx) were evaluated and diagnosed with gingival fibromatosis suggesting that this is a dominant trait in the family and gingival fibromatosis might be of hereditary origin. In addition, the brother also exhibited localized aggressive periodontitis. Medical history revealed no other systemic or local contributory factors associated with the oral findings in any of the subjects. Results: Surgical therapy included internal bevel gingivectomy combined with open flap debridement procedures for Px and Bx. Only internal bevel gingivectomy was performed for Mx since there was mild bone resorption and no intrabony defects. At the time of surgery, gingival biopsies were obtained and fixed in 4% paraformaldehyde. Multiple serial sections were stained with hematoxylin and eosin. Microscopic evaluation of the gingival specimens revealed large parallel collagen bundles associated with scarce fibroblasts in the connective tissue. The collagen bundles reached into the subepithelial connective tissue where elongated rete‐pegs were also observed. Following the completion completion of the treatment, no signs of recurrence or bone resorption were observed over 2‐year follow‐up. Conclusions: This is the first report of hereditary gingival fibromatosis associated with aggressive periodontitis. Combined treatment comprising removal of fibrotic gingival tissue and traditional flap surgery for the elimination of intrabony defects represents a unique treatment approach in periodontal therapy. Two‐year follow‐up revealed that both the gingival overgrowth and the destructive lesions were successfully treated. J Periodontol 2004;75:770‐778 .
    Type of Medium: Online Resource
    ISSN: 0022-3492 , 1943-3670
    URL: Article
    DOI: 10.1902/jop.2004.75.5.770
    Language: English
    Publisher: Wiley
    Publication Date: 2004
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  • 5
    Online Resource
    Online Resource
    Identification of diacylglycerol kinase isoforms in neutrophils from LJP patients
    Elsevier BV ; 1999
    In:  Prostaglandins & Other Lipid Mediators Vol. 59, No. 1-6 ( 1999-12), p. 164-
    Details
    In: Prostaglandins & Other Lipid Mediators, Elsevier BV, Vol. 59, No. 1-6 ( 1999-12), p. 164-
    Type of Medium: Online Resource
    ISSN: 1098-8823
    URL: Article
    DOI: 10.1016/S0090-6980(99)90399-4
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1999
    detail.hit.zdb_id: 2013367-4
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    HIGH DOSE ATORVASTATIN REDUCES PERIODONTAL ACTIVITY IN PROPORTION TO ATHEROSCLEROTIC INFLAMMATION: A POTENTIALLY NOVEL PLEIOTROPIC EFFECT OF STATINS
    Elsevier BV ; 2013
    In:  Journal of the American College of Cardiology Vol. 61, No. 10 ( 2013-03), p. E1055-
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 61, No. 10 ( 2013-03), p. E1055-
    Type of Medium: Online Resource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/S0735-1097(13)61055-4
    RVK:
    XA 17760
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 1468327-1
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  • 7
    Online Resource
    Online Resource
    Partial expression of the Papillon‐Lefèvre syndrome in 2 unrelated families
    Wiley ; 1996
    In:  Journal of Clinical Periodontology Vol. 23, No. 8 ( 1996-08), p. 764-769
    Details
    In: Journal of Clinical Periodontology, Wiley, Vol. 23, No. 8 ( 1996-08), p. 764-769
    Abstract: Abstract The Papillon‐Lefèvre syndrome (PLS) is a rare, autosomal recessive trait that is characterized by palmar plantar keratosis (PPK) and severe, early onset periodontitis. affecting both deciduous and permanent dentitions. The clinical presentation of PLS is variable: the disease occurs so infrequently as to limit clinical cases for study. The exception is a few families with extensive consanguinity in which numerous cases occur. Of particular interest to mapping the genetic origin of the syndrome is the co‐expression of the major traits of hyperkeratosis and periodontitis, and their severity. In this paper, we report 2 families with multiple affected individuals from geographically remote areas. A large extended family, from the Cochin region of India, currently residing in Israel, in which there is documented consanguinity and a family from the southwest region of Germany. In each family, 1 individual presents with hyperkeratotic lesions with the complete absence of periodontal lesions. Further, the difference in severity of the hyperkeratotic lesions between families is marked, and one sibling in the German family expressed rapid, early onset periodontitis in the absence of PPK. The genetic nature and penetrance of the genetic defect are discussed.
    Type of Medium: Online Resource
    ISSN: 0303-6979 , 1600-051X
    URL: Issue
    URL: Article
    DOI: 10.1111/cpe.1996.23.issue-8
    DOI: 10.1111/j.1600-051X.1996.tb00607.x
    Language: English
    Publisher: Wiley
    Publication Date: 1996
    detail.hit.zdb_id: 2026349-1
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  • 8
    Online Resource
    Online Resource
    Neutrophil Defects as Risk Factors for Periodontal Diseases
    Wiley ; 1994
    In:  Journal of Periodontology Vol. 65, No. 5S ( 1994-05), p. 521-529
    Details
    In: Journal of Periodontology, Wiley, Vol. 65, No. 5S ( 1994-05), p. 521-529
    Abstract: T here are several hypotheses proposed for the etiologic mechanisms causing periodontal diseases. These include a paradigm in which all individuals are equally susceptible to one or several pathogenic bacteria; a second paradigm that holds that all bacteria are equally virulent and that host susceptibility determines onset of disease; or a combination of the above. In this review, we analyze the role of neutrophil dysfunction as a risk factor for the onset of periodontitis. Both intrinsic or genetically inherited abnormalities of neutrophils and acquired neutrophil abnormalities are considered. While a large body of data implicates neutrophil dysfunction, either intrinsic or acquired (bacterially or extrinsically induced), as a significant risk factor for the periodontal diseases, clear, prospective, longitudinal epidemiologic studies to evaluate this association remain to be performed. J Periodontol 1994; 65:521–529 .
    Type of Medium: Online Resource
    ISSN: 0022-3492 , 1943-3670
    URL: Article
    DOI: 10.1902/jop.1994.65.5s.521
    Language: English
    Publisher: Wiley
    Publication Date: 1994
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  • 9
    Online Resource
    Online Resource
    The American Journal of Cardiology and Journal of Periodontology Editors' Consensus: Periodontitis and Atherosclerotic Cardiovascular Disease
    Wiley ; 2009
    In:  Journal of Periodontology Vol. 80, No. 7 ( 2009-07), p. 1021-1032
    Details
    In: Journal of Periodontology, Wiley, Vol. 80, No. 7 ( 2009-07), p. 1021-1032
    Abstract: Acknowledgment: This Editors' Consensus is supported by an educational grant from Colgate‐Palmolive, Inc., New York, New York, and is based on a meeting of the authors held in Boston, Massachusetts, on January 9, 2009. Disclosure: Dr. Friedewald has received honoraria for speaking from Novartis, East Hanover, New Jersey. Dr. Kornman is a full‐time employee and shareholder of Interleukin Genetics, Waltham, Massachusetts, which owns patents on genetic biomarkers for chronic inflammatory diseases. Dr. Genco is a consultant to Merck, Whitehouse Station, New Jersey. Dr. Ridker has received research support from AstraZeneca, Wilmington, Delaware; Novartis; Pfizer, New York, New York; Roche, Nutley, New Jersey; Sanofi‐Aventis, Bridgewater, New Jersey; and Abbott Laboratories, Abbott Park, Illinois. Dr. Ridker has received non‐financial research support from Amgen, Thousand Oaks, California. Dr. Ridker is a co‐inventor on patents held by Brigham and Women's Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease. Dr. Ridker is a research consultant for Schering‐Plough, Kenilworth, New Jersey; Sanofi‐Aventis; AstraZeneca; Isis, Carlsbad, California; Novartis; and Vascular Biogenics, Tel Aviv, Israel. Dr. Van Dyke is a co‐inventor on patents held by Boston University, Boston, Massachusetts, that relate to inflammation control, including consulting fees. Dr. Roberts has received honoraria for speaking from Merck, Schering‐Plough, AstraZeneca, and Novartis. All other individuals in a position to control content disclosed no relevant financial relationships.
    Type of Medium: Online Resource
    ISSN: 0022-3492 , 1943-3670
    URL: Article
    DOI: 10.1902/jop.2009.097001
    Language: English
    Publisher: Wiley
    Publication Date: 2009
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  • 10
    Online Resource
    Online Resource
    Change of antibiotic susceptibility following periodontal therapy : A pilot study in aggressive periodontal disease
    Wiley ; 2003
    In:  Journal of Clinical Periodontology Vol. 30, No. 3 ( 2003-03), p. 222-229
    Details
    In: Journal of Clinical Periodontology, Wiley, Vol. 30, No. 3 ( 2003-03), p. 222-229
    Type of Medium: Online Resource
    ISSN: 0303-6979
    URL: Article
    DOI: 10.1034/j.1600-051X.2003.10196.x
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 2026349-1
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