Human periodontal ligament fibroblast responses to compression in chronic periodontitis

Ahmed R. El-Awady, Carol A. Lapp, Ahmed Y. Gamal, Mohamed M.H. Sharawy, Karl H. Wenger, Christopher W Cutler, Regina L W Messer

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Aim Test whether human periodontal ligament fibroblasts (PDLFs) retain homeostatic responses to a physiological compressive force during chronic periodontitis. Material and Methods Six cell lines were established from periodontally healthy individuals (H-PDLFs) and another six were cultured from patients diagnosed with chronic periodontitis (D-PDLFs). Compressive force at 150 psi was applied to H-and D-PDLFs for 3 h on 2 consecutive days. After compression, comparisons between H-and D-PDLFs were performed by gene expression analysis of IL-6, proteases and 84 inflammation-related targets using real-time PCR. Results Compression of H-PDLFs resulted in a significant increase only in MMP-1 mRNA. In contrast, the same compressive force on D-PDLFs produced significant increases in the expression of MMPs-1,-7,-9 and -16. Moreover, compression of H-PDLFs resulted in down-regulation of IL-6, while IL-6 was significantly up-regulated in compressed D-PDLFs. Compression of H-PDLFs slightly up-regulated 3 and significantly down-regulated 15 inflammation-related genes, while the same treatment strongly up-regulated 21 inflammation-related genes in D-PDLFs. Conclusion These results suggest a fundamental difference in the inflammatory response of healthy versus diseased PDLFs under physiological compression. Maintenance of these characteristics in vitro suggests that these cells may be at least partly responsible for the persistence of inflammation and localized susceptibility in chronic periodontitis.

Original languageEnglish (US)
Pages (from-to)661-671
Number of pages11
JournalJournal of Clinical Periodontology
Volume40
Issue number7
DOIs
StatePublished - Jul 1 2013

Fingerprint

Chronic Periodontitis
Periodontal Ligament
Fibroblasts
Inflammation
Interleukin-6
Matrix Metalloproteinases
Genes
Real-Time Polymerase Chain Reaction
Peptide Hydrolases
Down-Regulation

Keywords

  • compression
  • cytokine(s)
  • Fibroblast(s)
  • gene expression
  • host response
  • inflammatory and innate immunity
  • pathogenesis of periodontal disease(s)
  • real-time PCR arrays

ASJC Scopus subject areas

  • Periodontics

Cite this

Human periodontal ligament fibroblast responses to compression in chronic periodontitis. / El-Awady, Ahmed R.; Lapp, Carol A.; Gamal, Ahmed Y.; Sharawy, Mohamed M.H.; Wenger, Karl H.; Cutler, Christopher W; Messer, Regina L W.

In: Journal of Clinical Periodontology, Vol. 40, No. 7, 01.07.2013, p. 661-671.

Research output: Contribution to journalArticle

@article{91e08b2b91594539ac908fcccce086e1,
title = "Human periodontal ligament fibroblast responses to compression in chronic periodontitis",
abstract = "Aim Test whether human periodontal ligament fibroblasts (PDLFs) retain homeostatic responses to a physiological compressive force during chronic periodontitis. Material and Methods Six cell lines were established from periodontally healthy individuals (H-PDLFs) and another six were cultured from patients diagnosed with chronic periodontitis (D-PDLFs). Compressive force at 150 psi was applied to H-and D-PDLFs for 3 h on 2 consecutive days. After compression, comparisons between H-and D-PDLFs were performed by gene expression analysis of IL-6, proteases and 84 inflammation-related targets using real-time PCR. Results Compression of H-PDLFs resulted in a significant increase only in MMP-1 mRNA. In contrast, the same compressive force on D-PDLFs produced significant increases in the expression of MMPs-1,-7,-9 and -16. Moreover, compression of H-PDLFs resulted in down-regulation of IL-6, while IL-6 was significantly up-regulated in compressed D-PDLFs. Compression of H-PDLFs slightly up-regulated 3 and significantly down-regulated 15 inflammation-related genes, while the same treatment strongly up-regulated 21 inflammation-related genes in D-PDLFs. Conclusion These results suggest a fundamental difference in the inflammatory response of healthy versus diseased PDLFs under physiological compression. Maintenance of these characteristics in vitro suggests that these cells may be at least partly responsible for the persistence of inflammation and localized susceptibility in chronic periodontitis.",
keywords = "compression, cytokine(s), Fibroblast(s), gene expression, host response, inflammatory and innate immunity, pathogenesis of periodontal disease(s), real-time PCR arrays",
author = "El-Awady, {Ahmed R.} and Lapp, {Carol A.} and Gamal, {Ahmed Y.} and Sharawy, {Mohamed M.H.} and Wenger, {Karl H.} and Cutler, {Christopher W} and Messer, {Regina L W}",
year = "2013",
month = "7",
day = "1",
doi = "10.1111/jcpe.12100",
language = "English (US)",
volume = "40",
pages = "661--671",
journal = "Journal of Clinical Periodontology",
issn = "0303-6979",
publisher = "Blackwell Munksgaard",
number = "7",

}

TY - JOUR

T1 - Human periodontal ligament fibroblast responses to compression in chronic periodontitis

AU - El-Awady, Ahmed R.

AU - Lapp, Carol A.

AU - Gamal, Ahmed Y.

AU - Sharawy, Mohamed M.H.

AU - Wenger, Karl H.

AU - Cutler, Christopher W

AU - Messer, Regina L W

PY - 2013/7/1

Y1 - 2013/7/1

N2 - Aim Test whether human periodontal ligament fibroblasts (PDLFs) retain homeostatic responses to a physiological compressive force during chronic periodontitis. Material and Methods Six cell lines were established from periodontally healthy individuals (H-PDLFs) and another six were cultured from patients diagnosed with chronic periodontitis (D-PDLFs). Compressive force at 150 psi was applied to H-and D-PDLFs for 3 h on 2 consecutive days. After compression, comparisons between H-and D-PDLFs were performed by gene expression analysis of IL-6, proteases and 84 inflammation-related targets using real-time PCR. Results Compression of H-PDLFs resulted in a significant increase only in MMP-1 mRNA. In contrast, the same compressive force on D-PDLFs produced significant increases in the expression of MMPs-1,-7,-9 and -16. Moreover, compression of H-PDLFs resulted in down-regulation of IL-6, while IL-6 was significantly up-regulated in compressed D-PDLFs. Compression of H-PDLFs slightly up-regulated 3 and significantly down-regulated 15 inflammation-related genes, while the same treatment strongly up-regulated 21 inflammation-related genes in D-PDLFs. Conclusion These results suggest a fundamental difference in the inflammatory response of healthy versus diseased PDLFs under physiological compression. Maintenance of these characteristics in vitro suggests that these cells may be at least partly responsible for the persistence of inflammation and localized susceptibility in chronic periodontitis.

AB - Aim Test whether human periodontal ligament fibroblasts (PDLFs) retain homeostatic responses to a physiological compressive force during chronic periodontitis. Material and Methods Six cell lines were established from periodontally healthy individuals (H-PDLFs) and another six were cultured from patients diagnosed with chronic periodontitis (D-PDLFs). Compressive force at 150 psi was applied to H-and D-PDLFs for 3 h on 2 consecutive days. After compression, comparisons between H-and D-PDLFs were performed by gene expression analysis of IL-6, proteases and 84 inflammation-related targets using real-time PCR. Results Compression of H-PDLFs resulted in a significant increase only in MMP-1 mRNA. In contrast, the same compressive force on D-PDLFs produced significant increases in the expression of MMPs-1,-7,-9 and -16. Moreover, compression of H-PDLFs resulted in down-regulation of IL-6, while IL-6 was significantly up-regulated in compressed D-PDLFs. Compression of H-PDLFs slightly up-regulated 3 and significantly down-regulated 15 inflammation-related genes, while the same treatment strongly up-regulated 21 inflammation-related genes in D-PDLFs. Conclusion These results suggest a fundamental difference in the inflammatory response of healthy versus diseased PDLFs under physiological compression. Maintenance of these characteristics in vitro suggests that these cells may be at least partly responsible for the persistence of inflammation and localized susceptibility in chronic periodontitis.

KW - compression

KW - cytokine(s)

KW - Fibroblast(s)

KW - gene expression

KW - host response

KW - inflammatory and innate immunity

KW - pathogenesis of periodontal disease(s)

KW - real-time PCR arrays

UR - http://www.scopus.com/inward/record.url?scp=84878573079&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84878573079&partnerID=8YFLogxK

U2 - 10.1111/jcpe.12100

DO - 10.1111/jcpe.12100

M3 - Article

C2 - 23560813

AN - SCOPUS:84878573079

VL - 40

SP - 661

EP - 671

JO - Journal of Clinical Periodontology

JF - Journal of Clinical Periodontology

SN - 0303-6979

IS - 7

ER -