An in vivo study of degranulation of azurophil granules in the neutrophils during phagocytosis of cationized ferritin in the gingival sulcus.

Takano, Teruo; Ayasaka, Norio; Sakano, Akira

doi:10.1267/ahc.21.15

Cited by 6 publications

(2 citation statements)

References 15 publications

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“…Various mechanisms of peripheral host defense have been demonstrated in this epithelium (Schroeder & Listgarten, 1997) (Figure 9): (1) phagocytosis and anti-bacterial activity of neutrophils infiltrating into the junctional epithelium (Yamasaki et al, 1979, Tanaka et al, 1988, (2) outward flow of gingival sulcular fluid through the junctional epithelium (McDougall, 1970;Tanaka, 1984;Tanaka and Sakano, 1987), (3) fast turnover or apoptosis of junctional epithelial cells (Schroeder, 1986, Ekuni et al, 2005, (4) continuous epithelial attachment via the IBL throughout the enamel surface (Squier, 1991;Bartold, et al, 2000), (5) endocytotic capacity of junctional epithelial cells for external pathogens (Yamasaki et al, 1979;Tanaka 1984;Tanaka & Sakano, 1987;Ayasaka et al, 1989, Yamaza et al, 1997, and (6) neurotrophic modulation in the junctional epithelium (Kondo et al, 1995;Tanaka et al, 1996;Kido et al, 1999). Fig.…”

Section: Biological Sealing and Defense Mechanisms In The Transmucosamentioning

confidence: 99%

Biological Sealing and Defense Mechanisms in Peri-Implant Mucosa of Dental Implants

Yamaza¹,

Kido²

2011

Implant Dentistry - The Most Promising Discipline of Dentistry

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Section: Biological Sealing and Defense Mechanisms In The Transmucosamentioning

confidence: 99%

Biological Sealing and Defense Mechanisms in Peri-Implant Mucosa of Dental Implants

Yamaza¹,

Kido²

2011

Implant Dentistry - The Most Promising Discipline of Dentistry

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“…Therefore, the JE is often the initial site of periodontitis caused by periodontal pathogens such as bacteria and toxic bacterial products [29,37]. Various host defense mechanisms exist within the JE, including (1) outward flow of the gingival sulcular fluid through the JE [22,40,41]; (2) phagocytosis of exogenous substances by neutrophils that have infiltrated the JE [3,42,44]; and (3) rapid turnover of JE cells [35]. In addition, JE cells endocytose and digest exogenous molecules via lysosomal systems [4,5,6,19,20,40,41,[46][47][48].…”

Section: Introductionmentioning

confidence: 99%

Localization of the Endogenous Cysteine Proteinase Inhibitor, Cystatin C, and the Cysteine Proteinase, Cathepsin B, to the Junctional Epithelium in Rat Gingiva

Yamaza

Mino

Atsuta

et al. 2005

Acta Histochem. Cytochem

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The junctional epithelium (JE) is a primary site of defense against periodontal pathogens. Cystatin C is an endogenous inhibitor of cysteine proteinases such as cathepsin B and also has antibacterial actions against periodontal pathogens. However, the distribution and role of cystatin C in JE have not been clarified. To investigate the function of cystatin C in the host defense at dentogingival junction, we examined the immunolocalization of cystatin C and cathepsin B in rat gingiva using light and electron microscopy. The JE (particularly the coronal portion) was immunopositive for cystatin C, and immunoelectron microscopy revealed that cystatin C was localized to the vesicular, granular, and vacuolar compartments of JE cells. The pattern of cathepsin B immunoreactivity in JE cells resembled that of cystatin C. Both cystatin C and cathepsin B appeared to be localized to endosomal/lysosomal compartments within JE cells. These findings suggest that cystatin C regulates cysteine proteinase activity and exerts antibacterial effects both in the lysosomal compartments of JE cells and in the intercellular spaces of the JE. Cystatin C is thus able to participate in host defense against periodontal pathogens at the dentogingival junction.

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A fluid‐phase endocytotic capacity and intracellular degradation of a foreign protein (horseradish peroxidase) by lysosomal cysteine proteinases in the rat junctional epithelium

Yamaza

Kido

Kiyoshima

et al. 1997

J of Periodontal Research

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We investigated the co-localization of lysosomal cathepsins B, H and L, and horseradish peroxidase (HRP) in junctional epithelial (JE) cells both as a fluid-phase endocytotic marker to demonstrate the fluid-phase endocytotic capacity of JE cells, and to understand the morphological relationships of the endocytosed foreign substances to lysosomal cathepsins in these cells. The diaminobenzidine (DAB) histochemical and cytochemical methods and immunohistochemical avidin-biotin-peroxidase complex and immunocytochemical post-embedding colloidal gold methods were used. Under light microscopy, DAB reaction products based on HRP were found in JE but were rare or absent in the oral sulcular epithelium and oral epithelium. Immunolabeling for cathepsins B and H was found in the granular structures of the cells, but no cathepsin L was identified. With electron microscopy, DAB reaction products, which indicated both HRP and the azurophil granules of neutrophils, were endocytosed into JE cells. Using a post-embedding technique, gold particles indicating HRP were present on the plasma membrane of JE cells, at the periphery of electronlucent vacuoles, and in the electrondense granules. Gold particles indicating cathepsin B or H were found in the electrondense granules. With different sizes of colloidal golds, the co-localization of cathepsin B or H with HRP was indicated only in the electrondense portion of the larger vacuoles consisting of electronlucent and -dense parts. This study provided the first morphological data which indicate that JE has a fluid phase endocytotic capacity, and which suggest that the lysosomal cathepsins B and H are involved in the intracellular degradation of foreign substances invading through the gingival sulcus in JE cells.

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An in vivo study of degranulation of azurophil granules in the neutrophils during phagocytosis of cationized ferritin in the gingival sulcus.

Cited by 6 publications

References 15 publications

Biological Sealing and Defense Mechanisms in Peri-Implant Mucosa of Dental Implants

Biological Sealing and Defense Mechanisms in Peri-Implant Mucosa of Dental Implants

Localization of the Endogenous Cysteine Proteinase Inhibitor, Cystatin C, and the Cysteine Proteinase, Cathepsin B, to the Junctional Epithelium in Rat Gingiva

A fluid‐phase endocytotic capacity and intracellular degradation of a foreign protein (horseradish peroxidase) by lysosomal cysteine proteinases in the rat junctional epithelium

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