The ultrastructure of human gingival langerhans cells in health and disease

Newcomb, G. M.; Powell, R. N.

doi:10.1016/0003-9969(86)90004-x

Cited by 19 publications

(14 citation statements)

References 52 publications

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“…Bos & BucKHARDT (14) have reported that the number of ATPase bearing LC after an itiitial increase following antigen exposure decrease until a homeostasis at about twice the initial number is reached after 20 days. This is in general agreement with recent studies of experimental (15) and chronical gingivitis (17,24). The observed mean density of LC in the coronal clusters in our study was abotit two to three and a half times the mean density of LC in JE.…”

Section: Langerhans Cellssupporting

confidence: 94%

Distribution of Langerhans cells in clinically healthy human gingival epithelium with special emphasis on junctional epithelium

Juhl

Stoltze

Reibel

1988

European J Oral Sciences

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Juhl M, Stoltze K, Reibel J: Distribution of Langerhans cells in chnically healthy human gingival epithelium with special emphasis on junctional epithelium. Scand J Dent Res 1988; 96: 199-208. Abstract -Twenty-one biopsies of clinically healthy marginal gingiva from children, who performed conventional oral hygiene but received no additional professional prophylaxis, were studied in order to obtain information on distribution and density of Langerhans cells (LC) in the oral gingival epithelium (OGE), the sulcular epithelium (SE) and the junctional epithelium (JE). A simple freeze-separation technique was found to create acceptable histomorphology of JE in specimens obtained adherent to teeth, while partially and non-adherent ones were rejected. The majority of LC in OGE, were highly dendritic and stained intensively with OKT6 monoclonal antibodies. The distribution was network-like with a density of 21.0+ 3.2 LC/0.1 mm' crosssectional epithelial area. A similar although less dense distribution was fotmd in SE (8.6 + 3.0 LC/0.1 mm'). These obseri'ations confirm previotis fmdings. In JE 2 groups of LC were identified: 1) Weakly stained LC with very few and short dendrites distributed in a scattered way (2.8+ 1.4 LC/0.1 mm') in the apical three-fourths of JE in most specimens. Present evidence suggests that these cells might be immature cells of Langerhans lineage. 2) Clusters of LC (9.4 + 2.9 LC/0.1 mm') with dendrites of moderate lengths and numbers and a varied fluorescence intensity; they were found in a few specimens in the coronal one-fourth of JE and at the border zone to SE. Such clusters might represent genuine variation in the distribution of LC or reactions to initial/ early plaque formation.Langerhans cells (LC) are dendritic non-cosa including that of gingiva (1-3). Present keratinocytes found suprabasally in most evidence strongly suggests that in tlie epiderstratified squamous epithelia,, such as human mis LC act as peripheral antigen-presenting epidermis and the epithehum of the oral mu-cells during induction of cutaneous immune

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Section: Langerhans Cellssupporting

confidence: 94%

Distribution of Langerhans cells in clinically healthy human gingival epithelium with special emphasis on junctional epithelium

Juhl

Stoltze

Reibel

1988

European J Oral Sciences

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“…In the present study it was found that Langerhans cells in the gingiva of healthy rats were observed generally in the basal layer and with nuclei lobulated or indented and the cytoplasm having either no or few granules, as suggested by Newcomb and Powell. 21 Furthermore, we observed that Langerhans cells were occasionally present in the suprabasal layer, in accordance with previous findings. However, Takehana et al 26 suggested that Langerhans cells were observed mainly in the lower prickle-cell layer of the gingival epithelium.…”

Section: Discussionsupporting

confidence: 91%

“…Langerhans cells were also not seen in the pocket lining the epithelium of periodontally-diseased gingiva. 21,24 Baelum et al 13 examined Langerhans cells in the oral epithelium of chronically inflamed human gingivae and observed such cells in the oral epithelium in all specimens. Most often Langerhans cells were located in the spinous cell layer, although they were also observed in the basal and parabasal layers of the oral epithelium.…”

Section: Discussionmentioning

confidence: 98%

“…If there is no challenge, they remain 'resting' cells, with few or no granules. 21 Six electron-microscopic criteria of specificity for Langerhans cells were determined: 30 (1) indented or lobulate nuclei; (2) Birbeck granules; (3) absence of tonofilaments; (4) clear cytoplasm; (5) absence of desmosomes and (6) Absence of melanosomes and premelanosomes.…”

Section: Discussionmentioning

confidence: 99%

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Ultrastructural determination of gingival Langerhans cells in alloxan‐induced diabetic rats

Özsoy

Gül

Bostanci

et al. 2004

Cell Biochemistry & Function

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The ultrastructure of Langerhans cells has not been fully investigated in diabetes-associated gingival tissues. The present study was carried out to investigate the ultrastructure of gingival Langerhans cells in alloxan-induced diabetic rats. Gingival biopsies were obtained from 22 diabetic and 18 control rats. Langerhans cells were observed by transmission electron microscopy (TEM) in the basal layers of healthy oral epithelium. On rare occasions, Langerhans cells were found in the suprabasal layers of the oral epithelium. Langerhans cells in the oral epithelium of diabetic rats were seen in the basal and suprabasal layers. Usually, Langerhans cells had clear cytoplasm and convoluted or indented nuclei and few or no specific granules. The clear cytoplasm contained mitochondria, lysosomes and a small number of rough-surfaced endoplasmic reticulum regions, but it lacked tonofilament. Occasionally, centrioles were also observed in the cytoplasm. The membrane of Langerhans cells had no junctional complexes such as desmosomes. In diabetic rats, Langerhans cell precursors were developed into specific granule-bearing cells. Both Langerhans cells and their granules were more frequent in the gingiva of diabetic rats than in the control group. These data suggest that Langerhans cells play an important role in explaining the pathogenesis and development of diabetic gingivitis.

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“…The oral mucosa represents an attractive site in this regard, given that it comprises various mucosal niches, each of which contains distinct frequencies of LC and DC subsets (Hovav, 2014). Similar to their equivalents in the epidermis, oral LCs residing in the epithelium express langerin and EpCAM and contain Birbeck granules (Arizon et al, 2012;Kotani et al, 1991;Newcomb and Powell, 1986). Furthermore, several studies have demonstrated a high similarity between the structure and function of the buccal and skin immune systems (Barrett et al, 1993;Etchart et al, 2001;Le Borgne et al, 2006).…”

Section: Introductionmentioning

confidence: 96%

Distinct Murine Mucosal Langerhans Cell Subsets Develop from Pre-dendritic Cells and Monocytes

et al. 2015

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Langerhans cells (LCs) populate the mucosal epithelium, a major entry portal for pathogens, yet their ontogeny remains unclear. We found that, in contrast to skin LCs originating from self-renewing radioresistant embryonic precursors, oral mucosal LCs derive from circulating radiosensitive precursors. Mucosal LCs can be segregated into CD103(+)CD11b(lo) (CD103(+)) and CD11b(+)CD103(-) (CD11b(+)) subsets. We further demonstrated that similar to non-lymphoid dendritic cells (DCs), CD103(+) LCs originate from pre-DCs, whereas CD11b(+) LCs differentiate from both pre-DCs and monocytic precursors. Despite this ontogenetic discrepancy between skin and mucosal LCs, the transcriptomic signature and immunological function of oral LCs highly resemble those of skin LCs but not DCs. These findings, along with the epithelial position, morphology, and expression of the LC-associated phenotype strongly suggest that oral mucosal LCs are genuine LCs. Collectively, in a tissue-dependent manner, murine LCs differentiate from at least three distinct precursors (embryonic, pre-DC, and monocytic) in steady state.

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The ultrastructure of human gingival langerhans cells in health and disease

Cited by 19 publications

References 52 publications

Distribution of Langerhans cells in clinically healthy human gingival epithelium with special emphasis on junctional epithelium

Distribution of Langerhans cells in clinically healthy human gingival epithelium with special emphasis on junctional epithelium

Ultrastructural determination of gingival Langerhans cells in alloxan‐induced diabetic rats

Distinct Murine Mucosal Langerhans Cell Subsets Develop from Pre-dendritic Cells and Monocytes

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