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Updated: Aug 19, 2026

Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva
Published on: April 3, 2018
Keratinocyte growth factor-1 expression in healthy and diseased human periodontal tissues
Min Li1, James D Firth, Edward E Putnins
1Laboratory of Periodontal Biology, Department of Oral Biological and Medical Sciences, The University of British Columbia, Vancouver, British Columbia, Canada.
Objectives:
Keratinocyte growth factor-1 (KGF-1) is up-regulated in chronic inflammation and specifically stimulates epithelial cell proliferation by signaling through the epithelial-specific keratinocyte growth factor receptor (KGFR). We examined KGF-1 and KGFR protein and gene expression in healthy and diseased periodontal tissues.
Methods:
Tissues were collected from patients with periodontal health or disease, immediately frozen and stained for KGF-1 and KGFR protein expression. Laser capture microdissection of epithelial and connective tissue cells with reverse transcription-polymerase chain reaction (RT-PCR) examined KGF-1 and KGFR gene expression profiles and enzymatic digestion with heparitinase, chondroitinase ABC or pre-treatment with suramin examined epithelial surface molecule interactions with KGF-1.
Results:
In tissues collected from healthy patients, KGF-1 protein localized to areas of junctional and basal oral epithelial cells and was significantly increased in periodontal pocket epithelium (p<0.01) and in the oral epithelium (p<0.05) of disease-associated tissues. KGFR localized to the junctional and the parabasal cells of oral epithelium, with the relative staining intensity being increased in disease-associated pocket epithelium (p<0.05). Laser capture microdissection with RT-PCR confirmed KGF-1 and KGFR were specifically expressed by connective tissue and epithelium, respectively. KGF-1 localization to epithelial cells was largely eliminated by suramin pre-treatment, indicating interaction with the KGFR.
Conclusions:
KGF-1 and KGFR proteins are expressed in healthy periodontal tissues but significantly increased in diseased periodontal tissues. We hypothesize up-regulation of KGF-1 and KGFR protein associated with disease regulates epithelial cell behavior associated with onset and progression of periodontal pocket formation.
