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Review paper

TGF-1 biomarker level evaluation on fracture healing in a murine model with a bone defect after stromal vascular fraction application

By
Panji Sananta Orcid logo ,
Panji Sananta
Contact Panji Sananta

Orthopedic and Traumatology Department, Faculty of Medicine, Universitas Brawijaya-RSUD Dr. Saiful Anwar , Malang , Indonesia

Respati S Dradjat ,
Respati S Dradjat

Orthopedic and Traumatology Department, Faculty of Medicine, Universitas Brawijaya, RSUD Dr. Saiful Anwar , Malang , Indonesia

Rizqi Daniar Rosandi ,
Rizqi Daniar Rosandi

Orthopedic and Traumatology Department, Faculty of Medicine, Universitas Brawijaya, RSUD Dr. Saiful Anwar , Malang , Indonesia

Lasa Dhakka Siahaan
Lasa Dhakka Siahaan

Orthopedic and Traumatology Department, Faculty of Medicine, Universitas Brawijaya, RSUD Dr. Saiful Anwar , Malang , Indonesia

Abstract

Aim
Bone defect is a challenge even for experienced orthopaedic surgeons and it is a significant cause of morbidity in patients and a source of high economic burden in health care. A severe bone defect is a condition whereby the bone tissue cannot undergo natural healing despite surgical stabilization and requires further surgical intervention. Stromal vascular fraction (SVF) is a heterogeneous cell population derived from adipose tissue that results from minimal manipulation of the adipose tissue itself. TGF is essential in maintaining and expanding mesenchymal stem cells or progenitors of osteoblasts. Furthermore, TGF-β signalling also triggers osteoprogenitor cell proliferation, early differentiation, and maintenance of osteoblasts in the bone healing process. The aim of this study was to determine the effect of administering SVF on bone
defects’ healing process assessed based on the TGF- β1.
Methods
This was an animal study involving twelve Wistar strain Rattus norvegicus. They were divided into three groups: negative
group (normal rats), positive group (rats with bone defect without SVF application), and SVF group (rats with bone defect with SVF application). After 30 days, the rats were sacrificed, the TGF- β1 biomarker was evaluated (quantified using ELISA).
Results
TGF- β1 biomarker expressions were higher in the group with SVF application than in the group without SVF application. All comparisons of the SVF group and positive control group showed significant differences (p=0,000), respectively.
Conclusion
Giving SVF application could aid the healing process in a murine model with bone defect, marked by an increased level
of TGF- β1.

References

1.
Perez J, Kouroupis D, Li D, Best T, Kaplan L, Correa D. Tissue engineering and cell-based therapies for fractures and bone defects. Front Bioeng Biotechnol. 2018;105.
2.
Kim J, Kim H. Rat defect models for bone grafts and tissue engineered bone constructs. Tissue Eng Regen Med. 2013;10310–6.
3.
Adamczyk A, Meulenkamp B, Wilken G, Papp S. Managing bone loss in open fractures. OTA Int. 2020;59.
4.
Roato I, Belisario D, Compagno M, Verderio L, Sighinolfi A, Mussano F, et al. Adipose-derived stromal vascular fraction/xenohybrid bone scaffold: an alternative source for bone regeneration. Stem Cells Int. 2018;4126379.
5.
Bora P, Majumdar A. Adipose tissue-derived stromal vascular fraction in regenerative medicine: a brief review on biology and translation. Stem Cell Res Ther. 2017;145.
6.
Levi B, Longaker M. Concise review: adipose-derived stromal cells for skeletal regenerative medicine. Stem Cells. 2011;576–82.
7.
Alexander R. Understanding adipose-derived stromal vascular fraction (AD-SVF) cell biology and use on the basis of cellular, chemical, structural and paracrine components: a concise review. Journal of Prolotherapy. 2012;855–69.
8.
Kozhemyakina E, Lassar A, Zelzer E. A pathway to bone: signaling molecules and transcription factors involved in chondrocyte development and maturation. Development. 2015;817–31.
9.
Kheirallah M, Almeshaly H. Present strategies for critical bone defects regeneration. Oral health case Rep. 2016;3.
10.
Kamal A, Iskandriati D, Dilogo I, Sirega N, Hutagalung E, Susworo R, et al. Biocompatibility of various hydoxyapatite scaffolds evaluated by proliferation of rat’s bone marrow mesenchymal stem cells: an in vitro study. Med J Indones. 2013;202–8.
11.
Chen G, Deng C, Li Y. TGF-β and BMP signaling in osteoblast differentiation and bone formation. Int J Biol Sci. 2012;272–88.
12.
Gentile P, Piccinno M, Calabrese C. Characteristics and potentiality of human adipose-derived stem cells (hASCs) obtained from enzymatic digestion of fat graft. Cells. 2019;282.
13.
Rodriguez J, Murphy M, Hong S, Madrigal M, March K, Minev B, et al. Autologous stromal vascular fraction therapy for rheumatoid arthritis: rationale and clinical safety. Int Arch Med. 2012;5.
14.
Sananta P, Rahaditya I, Gmo, Suryanto R, Suroto H, Mustamsir E, et al. Adipose-derived stromal vascular fraction prevents bone bridge formation on growth plate injury in rat (in vivo studies) experimental research. Ann Med Surg. 2020;211–7.
15.
Kilkenny C, Browne W, Cuthill I, Emerson M, Altman D. Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research. PLoS Biol. 2010;1000412.
16.
Zuk P. Adipose-derived stem cells in tissue regeneration: a review. ISRN Stem Cells. 2013;1–35.
17.
Todorov A, Kreutz M, Haumer A, Scotti C, Barbero A, Bourgine P, et al. Fat-derived stromal vascular fraction cells enhance the bone-forming capacity of devitalized engineered hypertrophic cartilage matrix. Stem Cells Transl Med. 2016;1684–94.
18.
Prins H, Schulten E, Bruggenkate T, Klein-Nulend C, Helder J, M. Bone regeneration using the freshly isolated autologous stromal vascular fraction of adipose tissue in combination with calcium phosphate ceramics. Stem Cells Transl Med. 2016;1362–74.

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