The investigation of glutathione peroxidase, lactoferrin, myeloperoxidase and interleukin‐1β in gingival crevicular fluid: implications for oxidative stress in human periodontal diseases

Wei, Pi-Fen; Ho, Kuen‐Yao; Ho, Ya-Ping; Wu, Yimin; Yang, Yi‐Hsin; Tsai, Chi‐Cheng

doi:10.1111/j.1600-0765.2004.00744.x

Cited by 141 publications

(162 citation statements)

References 46 publications

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“…[13][14][15] Although, the mechanism of bLF modulation of cytokine production is not well understood, this could be important locally at the site of inflammation, such as in the rheumatoid joint or in the periodontal tissue of the periodontitis. [16][17][18] In fact, bLF has been shown to bind 'free' iron in synovial fluid and to reduce inflammation when injected intraarticularly in mice with collagen-induced arthritis. 17 In addition, bLF is of food origin and has high safety.…”

mentioning

confidence: 99%

Inhibitory effects of orally administrated liposomal bovine lactoferrin on the LPS-induced osteoclastogenesis

Yamano

Miyauchi

Furusyo

et al. 2010

Laboratory Investigation

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Bovine lactoferrin (bLF) modulates the production of proinflammatory cytokines including tumor necrosis factor (TNF)-a, and may thus control alveolar bone destruction associated with periodontitis. In this study, the effects of bLF on mRNA expression in lipopolysaccharide (LPS)-stimulated osteoblasts (OBs) and on LPS-induced osteoclastogenesis were examined. The inhibitory effects of oral administration of liposomal-bLF (L-bLF), which improved the robustness of bLF to digestive enzymes, on alveolar bone resorption using LPS-induced periodontitis rat model are also reported. Three groups of 7-week-old male Wistar rats were treated with L-bLF (L-bLF group), bLF (bLF group), or the vehicle (control group) in drinking water (n ¼ 6 in each group). On day 7, LPS was topically applied into the gingival sulcus. Number of osteoclasts and immunoexpression of TNF-a were analyzed. The bLF inhibited the upregulation of TNF-a-mRNA-and upregulation of receptor activator of NFkB (RANKL)-mRNA expression and eliminated downregulation of osteoprotegerin (OPG)-mRNA expression in LPS-stimulated OBs and reduced LPS-induced osteoclastogenesis in co-culture with primary OBs and bone marrow cells. In the control group, the number of osteoclasts increased after LPS treatment. The number of osteoclasts that appeared along the alveolar bone margin was significantly reduced (Po0.01) in the L-bLF but not in the bLF group. Furthermore, L-bLF suppressed upregulation of TNF-a immunoexpression in periodontal tissue and TNF-a and interleukin (IL)-1b-mRNA level in gingival tissue. The results of this study indicate that oral administration of L-bLF significantly reduces alveolar bone resorption induced by LPS stimulation through inhibition of TNF-a production and modulation of RANKL/OPG balance in OBs. It is suggested that L-bLF could be a potent therapeutic and preventive agent for attenuating alveolar bone destruction in periodontitis patients.

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mentioning

confidence: 99%

Inhibitory effects of orally administrated liposomal bovine lactoferrin on the LPS-induced osteoclastogenesis

Yamano

Miyauchi

Furusyo

et al. 2010

Laboratory Investigation

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“…Moreover, the amorphous acidophilic areas which detected in the gland after ELF-MF exposure were described in other study as hyaline degeneration of duct cells [20]. Affection of the parotid ducts are related to accumulation of ROS in their lining cells [21]. Structural and functional affection of the parotid gland were reported with different forms of irradiation including ionizing radiation [22,23].…”

Section: Resultsmentioning

confidence: 99%

“…The previous degenerative changes of parotid gland in light and electron microscope examination could explained by selective damage of EMF to the plasma membrane of the secretory cells of the salivary glands and increase of Na+ influx into the cell followed by water which in turn causes distention of RER and appearance of cytoplasmic vacuoles with leakage of granules and subsequent lysis of acinar cells [21]. Also, free oxygen radicals that produced after exposure to MFs acting as oxidizing agents and able to increase cellular damage [28] and cause decomposition of membranes with leakage of damaging lysosomal hydrolytic enzymes [29].…”

Section: Resultsmentioning

confidence: 99%

Effects of Low Magnetic Irradiation on Morphology and Ultrastructure of Parotid Glands in Rats and Amelioration by Vitamin E

Anan¹,

Gawish²,

Amer³

2012

J Cytol Histol

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“…Oxidative stress is involved in the pathogenesis of a number of diseases, including periodontitis [5], and feeding a high cholesterol diet increases tissue oxidative stress in various organs [6,7]. It is feasible then that tissue oxidative damage caused by high dietary cholesterol, as well as periodontopathic bacteria [8], may play an important role in periodontitis progression.…”

Section: Introductionmentioning

confidence: 99%

Oxidative damage of periodontal tissue in the rat periodontitis model: Effects of a high‐cholesterol diet

et al. 2006

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Studies suggest an association between consumption of a high-cholesterol diet and periodontitis. We addressed the mechanism by which high dietary cholesterol could be detrimental to periodontal health in a rat model. Feeding a high-cholesterol diet augmented the effects of bacterial pathogens and their products (e.g., lipopolysaccharide and proteases) on production of pro-inflammatory cytokines in fibroblasts. High dietary cholesterol also increased mitochondrial 8-hydroxydeoxyguanosine in the periodontal tissues. These results suggest that excessive tissue oxidative damage induced by high dietary cholesterol could potentiate pro-inflammatory cytokine production by fibroblasts stimulated with bacterial pathogens.

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The investigation of glutathione peroxidase, lactoferrin, myeloperoxidase and interleukin‐1β in gingival crevicular fluid: implications for oxidative stress in human periodontal diseases

Abstract: The imbalance between the levels of myeloperoxidase/IL-1beta and glutathione peroxidase/lactoferrin could result in tissue damage of reactive oxygen species (ROS) in periodontitis which is initiated and perpetuated by the chronic insults of periodontopathogens.

Cited by 141 publications

References 46 publications

Inhibitory effects of orally administrated liposomal bovine lactoferrin on the LPS-induced osteoclastogenesis

Inhibitory effects of orally administrated liposomal bovine lactoferrin on the LPS-induced osteoclastogenesis

Effects of Low Magnetic Irradiation on Morphology and Ultrastructure of Parotid Glands in Rats and Amelioration by Vitamin E

Oxidative damage of periodontal tissue in the rat periodontitis model: Effects of a high‐cholesterol diet

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