Abstract- Bone repair has been studied in order to understand the complex phases involved that result in full conformity of the original bone. Our body has the unique ability to heal a bone fracture without scarring. Bone repair is modulated by different stimulus including growth factors. Transforming Growth Factor-beta (TGF-β) super-family have been studied with strong evidence in vitro and in vivo that TGF-β has significant effects on bone construction and resorption by regulating the duplication and differentiation of chondrocytes, osteoblasts and osteoclasts. Dosage carriers of TGF-β1, 2 or 3 namely HCl was used in vitro to see the effects it has on closure rates using a model wound in cultured monolayers of MG63 bone cells. The wound healing time was investigated using 6.25μl, 12.5μl, 25μl and 50μl concentrations of HCl compared against control. The model wound was made on fully confluent monolayers of MG63 bone cells with an average wound width of 300μm ± 10-30μm. For each concentration of HCl and control after wounding, the wound width was measured over a 30hr period. The results showed that after the 30hr period, the 25μl and 50μl concentrations of HCl enhanced the speed of wound closure in vitro as compared to the control. The culture treated with 25μl concentration of HCl was fully confluent at 25hrs and the 50μl concentration of HCl showed the highest percentage of wound closure but taking the full 30hrs to become confluent. The 6.25μl and 12.5μl concentrations of HCl had slower closure rates than that of the higher concentrations with confluency not achieved at 30hrs. Results from un-treated flasks (control) showed slowest wound closure compared to treated flasks with HCl. Index Terms: Bone monolayer repair; HCl; Transforming Growth Factor (TGF-β3); Wound Healing. Manuscript received March 15, 2010. This work was supported by school of Engineering and School of Pharmacy, University of Bradford, UK. F. Sefat, (Corresponding Author) is with the School of Engineering, Design and Technology-Medical Engineering and Institute of Pharmaceutical Innovation (ipi), University of Bradford, Bradford, BD7 1DP, United Kingdom. (Phone: 01274 234533; Fax: 01274 234525; e-mail: f.sefat@bradford.ac.uk or fsefaty@yahoo.co.uk). C.B. Beggs is with the School of Engineering, Design and Technology-Medical Engineering, University of Bradford, Bradford, BD7 1DP, United Kingdom. (Phone: 01274 233679; Fax: 01274 234525; e-mail: c.b.beggs@bradford.ac.uk). G.D. Meakin, is with the School of Engineering, Design and Technology-Medical Engineering, University of Bradford, Bradford, BD7 1DP, United Kingdom. (Phone: 01274 234533; Fax: 01274 234525; e-mail: gdmeakin@bradford.ac.uk). M.C.T Denyer is with the School of Life Science, Institute of Pharmaceutical Innovation (ipi), University of Bradford, Bradford, BD7 1DP, United Kingdom. (Phone: 01274 234747; Fax: 01274 236060; e-mail: m.denyer@bradford.ac.uk). M. Youseffi is with the School of Engineering, Design and Technology-Medical Engineering, University of Bradford, Bradford, BD7 1DP, United Kingdom. (Phone: 01274 234533; Fax: 01274 234525; e-mail: m.youseffi@bradford.ac.uk). I. INTRODUCTION Bone is unique in nature since it has the ability to heal similarly to its original form without the development of a fibrous scar [1,2]. The regeneration of bone goes under a complex set of four overlapping phases, which are characterized by specific molecular and cellular events [3,4,5]. The four phases include: the haematoma formation/inflammatory phase, the soft callus formation, the hard callus formation and the remodeling process. Bone has the ability to repair itself using different methods depending on the biophysical environment. Ultimitely bone synthesis is achieved through osetoblasts via woven and/or lamellar matrix. Investigations have shown that with an increased ageing population healthcare in the United Kingdom is set to cost over £900 million each year [6,7]. A large percentage of that will go to the 150,000 fractures each year in the United Kingdom due to osteoporosis alone. There are many factors that have effect on bone repair including age, nutrients, hormones, and growth factors, etc. The transforming growth factor-Beta (TGF-β) superfamily has been accepted as the most popular stimulus with strong evidence in both in vitro and in vivo studies that TGF-β has detrimental effects on bone construction and resorption by regulating the duplication and differentiation of chondrocytes, osteoblasts and osteoclasts [8]. Other groups claimed that bone is formed in vivo by osteoblasts when TGF-β has been injected into the fracture site [9,10]. TGF-β has been identified in the fracture haematoma and surrounding periosteal mesenchymal cells with staining techniques [11]. This is thought to orchestrate the cascade of cellular events resulting in fracture repair. The three isoforms (TGF-β1, -β2, -β3) have been found [12] to express overlapping patterns in vivo and with nearly identical biological activities in vitro. TGF-β1 is more potent throughout adult development, whereas TGF- β3 is more potent in tissues with mesenchymal origin. The three isoforms signal through the same kinase receptor with different binding abilities [12]. In order to understand how TGF-β regulates bone repair and formation it is necessary for in vitro experiments using osteoblast cell lines, which are mainly derived from osteosarcomas, and share phenotype similarities to the osteoblast cell. In-vitro experiments have proven that TGF-β stimulates osteoblast chemotaxis, DNA synthesis, cell division, and promotion of bone matrix proteins [13]. The Effect of Different HCl Concentrations on Wound Healing of Bone Cell Monolayer F. Sefat, Member, IAENG, C.B. Beggs, M.C.T. Denyer, G.D. Meakin, and M. Youseffi Proceedings of the World Congress on Engineering 2010 Vol I WCE 2010, June 30 - July 2, 2010, London, U.K. ISBN: 978-988-17012-9-9 ISSN: 2078-0958 (Print); ISSN: 2078-0966 (Online) WCE 2010