The effect of geometry on three-dimensional tissue growth

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Abstract

Tissue formation is determined by uncountable biochemical signals between cells; in addition, physical parameters have been shown to exhibit significant effects on the level of the single cell. Beyond the cell, however, there is still no quantitative understanding of how geometry affects tissue growth, which is of much significance for bone healing and tissue engineering. In this paper, it is shown that the local growth rate of tissue formed by osteoblasts is strongly influenced by the geometrical features of channels in an artificial three-dimensional matrix. Curvature-driven effects and mechanical forces within the tissue may explain the growth patterns as demonstrated by numerical simulation and confocal laser scanning microscopy. This implies that cells within the tissue surface are able to sense and react to radii of curvature much larger than the size of the cells themselves. This has important implications towards the understanding of bone remodelling and defect healing as well as towards scaffold design in bone tissue engineering.

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Most cited references 22

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Transmembrane crosstalk between the extracellular matrix--cytoskeleton crosstalk.

B. Geiger, A Bershadsky, R Pankov … (2001)

Integrin-mediated cell adhesions provide dynamic, bidirectional links between the extracellular matrix and the cytoskeleton. Besides having central roles in cell migration and morphogenesis, focal adhesions and related structures convey information across the cell membrane, to regulate extracellular-matrix assembly, cell proliferation, differentiation, and death. This review describes integrin functions, mechanosensors, molecular switches and signal-transduction pathways activated and integrated by adhesion, with a unifying theme being the importance of local physical forces.

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The effect of pore size on cell adhesion in collagen-GAG scaffolds.

F J O'Brien, B A Harley, I V Yannas … (2005)

The biological activity of scaffolds used in tissue engineering applications hypothetically depends on the density of available ligands, scaffold sites at which specific cell binding occurs. Ligand density is characterized by the composition of the scaffold, which defines the surface density of ligands, and by the specific surface area of the scaffold, which defines the total surface of the structure exposed to the cells. It has been previously shown that collagen-glycosaminoglycan (CG) scaffolds used for studies of skin regeneration were inactive when the mean pore size was either lower than 20 microm or higher than 120 microm (Proc. Natl. Acad. Sci., USA 86(3) (1989) 933). To study the relationship between cell attachment and viability in scaffolds and the scaffold structure, CG scaffolds with a constant composition and solid volume fraction (0.005), but with four different pore sizes corresponding to four levels of specific surface area were manufactured using a lyophilization technique. MC3T3-E1 mouse clonal osteogenic cells were seeded onto the four scaffold types and maintained in culture. At the experimental end point (24 or 48 h), the remaining viable cells were counted to determine the percent cell attachment. A significant difference in viable cell attachment was observed in scaffolds with different mean pore sizes after 24 and 48 h; however, there was no significant change in cell attachment between 24 and 48 h for any group. The fraction of viable cells attached to the CG scaffold decreased with increasing mean pore size, increasing linearly (R2 = 0.95, 0.91 at 24 and 48 h, respectively) with the specific surface area of the scaffold. The strong correlation between the scaffold specific surface area and cell attachment indicates that cell attachment and viability are primarily influenced by scaffold specific surface area over this range (95.9-150.5 microm) of pore sizes for MC3T3 cells.

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Biomechanical and molecular regulation of bone remodeling.

Alexander Robling, Alesha Castillo, Charles Turner (2006)

Bone is a dynamic tissue that is constantly renewed. The cell populations that participate in this process--the osteoblasts and osteoclasts--are derived from different progenitor pools that are under distinct molecular control mechanisms. Together, these cells form temporary anatomical structures, called basic multicellular units, that execute bone remodeling. A number of stimuli affect bone turnover, including hormones, cytokines, and mechanical stimuli. All of these factors affect the amount and quality of the tissue produced. Mechanical loading is a particularly potent stimulus for bone cells, which improves bone strength and inhibits bone loss with age. Like other materials, bone accumulates damage from loading, but, unlike engineering materials, bone is capable of self-repair. The molecular mechanisms by which bone adapts to loading and repairs damage are starting to become clear. Many of these processes have implications for bone health, disease, and the feasibility of living in weightless environments (e.g., spaceflight).

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Author and article information

Journal

Journal ID (nlm-ta): J R Soc Interface

Journal ID (publisher-id): RSIF

Title: Journal of the Royal Society Interface

Publisher: The Royal Society (London )

ISSN (Print): 1742-5689

ISSN (Electronic): 1742-5662

Publication date (Electronic): 18 March 2008

Publication date (Print): 6 October 2008

Publication date PMC-release: 18 March 2008

Volume: 5

Issue: 27

Pages: 1173-1180

Affiliations

[1 ]simpleDepartment of Biomaterials, Max Planck Institute of Colloids and Interfaces 14424 Potsdam, Germany

[2 ]simpleEnergy Metabolism Research Group, Department of Organelle Biology, Biotechnology and Molecular Ecophysiology, Max Planck Institute for Molecular Plant Physiology 14424 Potsdam, Germany

Author notes

[* ]Author for correspondence ( fratzl@ 123456mpikg.mpg.de )

[†]

Present address: Ludwig Boltzmann Institute of Osteology, 1140 Vienna, Austria.

[‡]

Present address: Cambridge Centre for Medical Materials, Department of Materials Science and Metallurgy, University of Cambridge, Cambridge CB2 3QZ, UK.

Article

Publisher ID: rsif20080064

DOI: 10.1098/rsif.2008.0064

PMC ID: 2495039

PubMed ID: 18348957

SO-VID: bfd44137-fdfe-4224-9068-dd068d33f39b

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 11 February 2008

Date revision received : 27 February 2008

Date accepted : 28 February 2008

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The effect of geometry on three-dimensional tissue growth

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Most cited references 22

Transmembrane crosstalk between the extracellular matrix--cytoskeleton crosstalk.

The effect of pore size on cell adhesion in collagen-GAG scaffolds.

Biomechanical and molecular regulation of bone remodeling.

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