The Role of Nerve Growth Factor (NGF) and Its Precursor Forms in Oral Wound Healing.

Nerve growth factor (NGF) and its different precursor forms are secreted into human saliva by salivary glands and are also produced by an array of cells in the tissues of the oral cavity. The major forms of NGF in human saliva are forms of pro-nerve growth factor (pro-NGF) and not mature NGF. The NGF receptors tropomyosin-related kinase A (TrkA) and p75 neurotrophin receptor (p75) are widely expressed on cells in the soft tissues of the human oral cavity, including keratinocytes, endothelial cells, fibroblasts and leukocytes, and in ductal and acinar cells of all types of salivary glands.

Signal transduction and gene transcription induced by TFF3 in oral keratinocytes.

Trefoil factor family 3 (TFF3) is secreted in saliva. The peptide improves the mechanical and chemical resistance of mucins, and it may act as a motility signal for oral keratinocytes during wound healing. This study aimed to identify novel functions of TFF3 in oral keratinocytes.

Nerve growth factor beta/pro-nerve growth factor and their receptors in normal human oral mucosa.

Nerve growth factor beta (NGF-beta) and its precursor proNGF are important for the differentiation and survival of neurons and dermal keratinocytes. The aim of this study was to determine the role that NGF might play in the differentiation and wound healing of oral mucosa. Cultured normal human oral mucosal keratinocytes expressed mRNA for NGF-beta/proNGF and for their receptors TrkA and p75(NTR).

Survival signalling in keratinocytes of erythematous oral lichen planus.

Background: Keratinocytes in oral lichen (OL) planus have been shown to be exposed to potentially cell death-inducing factors such as tumour necrosis factor-alpha (TNF-alpha) and FasL, produced by the cells of the inflammatory infiltrate and by the keratinocytes themselves. Mostly, however, the lesions do not show ulceration, the clinical manifestation of substantial keratinocyte death. The aim of this study was to find support for the contention that there is activation of protecting anti-apoptotic mechanisms in keratinocytes in a form of chronic OL (erythematous OL; ERY OL), simultaneously with the pathological cell death signals.

Identity of TUNEL-positive cells in the oral buccal epithelium of normal mucosa and lichen lesions.

Background: In situ detection of DNA fragmentation by TdT (terminal deoxynucleotidyl transferase)-mediated dUTP nick end labeling (TUNEL) is a widely used technique to identify apoptotic cells in the terminal phases of cell death. Several studies have shown that there are statistically increased numbers of TUNEL(+) cells within the epithelium of oral lichen (OL). It was suggested that this indicates an increased rate of apoptosis among basal and suprabasal keratinocytes in OL epithelium.

Inhibition of the transforming growth factor-beta/Smad signaling pathway in the epithelium of oral lichen.

The basal cells in epithelium of the erythematous form of oral lichen display hyperproliferation compared with normal oral mucosa. In this study we examined whether this is associated with disrupted production, activation, or signal transduction of the epithelial growth inhibitor transforming growth factor (TGF) beta1. In situ immunostaining showed that most epithelial cells in normal oral mucosa had nuclear and cytoplasmic Smad4 and phosphorylated Smad2/3, but expressed little or no Smad7.

Erythematous and reticular forms of oral lichen planus and oral lichenoid reactions differ in pathological features related to disease activity.

Background: Common clinical forms of oral lichen planus (OLP) and oral lichenoid reactions (OLR) are erythematous (ERY) or reticular (RET). The purpose of this study was to find histopathological changes that differ between these forms.

Methods: Epithelial thickness, epithelial proliferation rate, apoptosis, and HLA-DR expression were compared among 10 reticular and 12 erythematous lesions, and 11 normal oral mucosa samples (NOM).

Highly increased numbers of leukocytes in inflamed gingiva from patients with HIV infection.

Background: HIV infection increases susceptibility for marginal periodontitis, with horizontal and rapid loss of periodontal soft tissues and alveolar bone.

Objectives: To examine whether numbers, distribution and some properties of mast cells, neutrophils and macrophages are normal in chronically inflamed gingiva of HIV-positive patients.

Methods: Gingival biopsies were stained for mast cell tryptase and chymase, neutrophil elastase, CD68, human transforming growth factor beta(1), HLA-DR, Fc gamma RI, Fc gamma RII and Fc gamma RIII and calprotectin.