Dataset Information

Therapeutic interaction of systemically-administered mesenchymal stem cells with peri-implant mucosa.

ABSTRACT:

Objectives

The objective of this study was to investigate the effect of systemically transplanted mesenchymal stem cells (MSCs) on the peri-implant epithelial sealing around dental implants.

Materials and methods

MSCs were isolated from bone marrow of donor rats and expanded in culture. After recipient rats received experimental titanium dental implants in the bone sockets after extraction of maxillary right first molars, donor rat MSCs were intravenously transplanted into the recipient rats.

Results

The injected MSCs were found in the oral mucosa surrounding the dental implants at 24 hours post-transplantation. MSC transplantation accelerated the formation of the peri-implant epithelium (PIE)-mediated mucosa sealing around the implants at an early stage after implantation. Subsequently, enhanced deposition of laminin-332 was found along the PIE-implant interface at 4 weeks after the replacement. We also observed enhanced attachment and proliferation of oral mucous epithelial cells.

Conclusion

Systemically transplanted MSCs might play a critical role in reinforcing the epithelial sealing around dental implants.

SUBMITTER: Kondo R

PROVIDER: S-EPMC3961234 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Publications

Therapeutic interaction of systemically-administered mesenchymal stem cells with peri-implant mucosa.

Kondo Ryosuke R Atsuta Ikiru I Ayukawa Yasunori Y Yamaza Takayoshi T Matsuura Yuri Y Furuhashi Akihiro A Tsukiyama Yoshihiro Y Koyano Kiyoshi K

PloS one 20140320 3

<h4>Objectives</h4>The objective of this study was to investigate the effect of systemically transplanted mesenchymal stem cells (MSCs) on the peri-implant epithelial sealing around dental implants.<h4>Materials and methods</h4>MSCs were isolated from bone marrow of donor rats and expanded in culture. After recipient rats received experimental titanium dental implants in the bone sockets after extraction of maxillary right first molars, donor rat MSCs were intravenously transplanted into the rec ...[more]

PMID: 24651408

Similar Datasets

Project description:Mesenchymal stem cells (MSCs) are a heterogeneous subset of stromal cells currently tested for multiple therapeutic purposes. Their potential to home into tumors, to secrete trophic/vasculogenic factors, and to suppress immune response raises questions regarding their biosafety. Our aim was to evaluate whether systemically administered allogeneic MSCs modify the natural progression of precancerous lesions and whether their putative effect depends on cancer stage and/or cell dose.Oral squamous cell carcinoma (OSCC) was induced in Syrian golden hamsters by topical application of 7,12-dimethylbenz[a]anthracene in one buccal pouch. At hyperplasia, dysplasia, or papilloma stage, animals received intracardially the vehicle or 0.7 ×?106, 7 ×?106, or 21?×?106 allogeneic bone marrow-derived MSCs/kg. OSCC progression was assessed according to the presence of erythroplakia and leukoplakia, extent of inflammation and vascularization, and appearance, volume, and staging of tumors. Also, the homing of donor cells was studied.Precancerous lesions progressed from hyperplasia to dysplasia in 2 weeks, from dysplasia to papilloma in 3 weeks, and from papilloma to carcinoma in 4 weeks. This time course was unmodified by the systemic administration of MSCs at hyperplasia or dysplasia stages. When MSCs were administered at papilloma stage, lesions did not progress to carcinoma stage. Tumors developed in hamsters receiving 0.7 ×?106 or 7?×?106 MSCs/kg at hyperplasia stage were significantly smaller than those found in control animals (25?±?4 or 23?±?4 mm3 versus 72?±?19 mm3, p?<?0.05). Similar results were obtained when 0.7 ×?106, 7 ×?106, or 21?×?106 MSCs/kg were administered at papilloma stage (44?±?15, 28?±?7, or 28?±?5 mm3 versus 104?±?26 mm3, p?<?0.05). For dysplasia stage, only the lower concentration of MSCs reached statistical significance (21?±?9 mm3 versus 94?±?39 mm3, p?<?0.05). Animals receiving 21?×?106 MSCs/kg at hyperplasia stage developed tumors larger than those found in animals that received the vehicle (147?±?47 mm3 versus 72?±?19 mm3, p?<?0.05). Donor cells were rarely found in precancerous lesions.Systemically administered allogeneic MSCs do not aggravate the progression of precancerous lesions. Moreover, they preclude cancer progression and tumor growth.

Project description:Oral health is associated with a symbiotic microbial community and host-microbe homeostasis is maintained by the controlled immune response. Various factors can disrupt this homeostasis. Dysbiosis, which is characterized by increased immune response and a shift in the microbiome, contributes the pathogenesis of peri-implantitis. Peri-implant mucosa and commensal bacteria play important roles in the maintenance of host-microbe homeostasis, but little is known about how they interact. We have therefore investigated the early host-microbe interaction between a commensal multispecies biofilm (Streptococcus oralis, Actinomyces naeslundii, Veillonella dispar, Porphyromonas gingivalis) and peri-implant mucosa at 24 and 48 h. Our in vitro peri-implant mucosa-biofilm model contained organotypic oral mucosa, implant material and biofilm. After 24 h, the biofilm induced a modest innate immune response in the peri-implant mucosa by the upregulation of 5 genes related to immune and inflammatory response and the increased secretion of IL-6 and CCL20. This controlled immune response protected tissue integrity and the peri-implant mucosa remained intact. The secreted antibacterial proteins human β-Defensins-1, -2, and CCL20 controlled the overgrowth of the biofilm by reducing its volume - without affecting the live/dead ratio or bacterial distribution. Thus, host-microbe homeostasis was established within the first 24 h. In contrast, host-microbe homeostasis was disrupted after 48 h. The mucosa was damaged and detached from the implant, due to the induced downregulation of cell adhesion related genes. The immune response was enhanced by upregulation of additional genes related to the immune and inflammatory response and increased secretion of IL-1β, TNF-α, and CCL20. Moreover, bacterial distribution was altered, with an increased proportion of V. dispar. The disrupted host-microbe homeostasis could lead to incipient dysbiosis. This deeper understanding of the early host-microbe interaction at the peri-implant site may provide the basis for new strategies to improve the prevention and therapy of peri-implant diseases.

Dataset Information

Therapeutic interaction of systemically-administered mesenchymal stem cells with peri-implant mucosa.

Objectives

Materials and methods

Results

Conclusion

Publications

Therapeutic interaction of systemically-administered mesenchymal stem cells with peri-implant mucosa.

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