Numerical simulation of electrically stimulated osteogenesis in dental implants.

Cell behavior and tissue formation are influenced by a static electric field (EF). Several protocols for EF exposure are aimed at increasing the rate of tissue recovery and reducing the healing times in wounds. However, the underlying mechanisms of the EF action on cells and tissues are still a matter of research. In this work we introduce a mathematical model for electrically stimulated osteogenesis at the bone-dental implant interface. The model describes the influence of the EF in the most critical biological processes leading to bone formation at the bone-dental implant interface. The numerical solution is able to reproduce the distribution of spatial-temporal patterns describing the influence of EF during blood clotting, osteogenic cell migration, granulation tissue formation, displacements of the fibrillar matrix, and formation of new bone. In addition, the model describes the EF-mediated cell behavior and tissue formation which lead to an increased osteogenesis in both smooth and rough implant surfaces. Since numerical results compare favorably with experimental evidence, the model can be used to predict the outcome of using electrostimulation in other types of wounds and tissues.

Numerical investigation into blood clotting at the bone-dental implant interface in the presence of an electrical stimulus.

The insertion of a dental implant activates a sequence of wound healing events ending with bone formation and implant osseointegration. This sequence starts with the blood coagulation process and the formation of a fibrin network that detains spilt blood. Fibrin formation can be simplified as the kinetic reaction between thrombin and fibrinogen preceding the conversion of fibrinogen into fibrin. Based on experimental observations of the electrical properties of these molecules, we present a hypothesis for the mechanism of a static electrical stimulus in controlling the formation of the blood clot. Specifically, the electrical stimulus increases the fibrin network formation in such a way that a preferential region of higher fibrin density is obtained. This hypothesis is validated by means of a numerical model for the blood clot formation at the bone-dental implant interface. Numerical results compare favorably to experimental observations for blood clotting with and without the static electrical stimulus. It is concluded that the density of the fibrin network depends on the strength of the static electrical stimulus, and that the blood clot formation has a preferential direction of formation in the presence of the electrical signal.

Mathematical model of electrotaxis in osteoblastic cells.

Electrotaxis is the cell migration in the presence of an electric field (EF). This migration is parallel to the EF vector and overrides chemical migration cues. In this paper we introduce a mathematical model for the electrotaxis in osteoblastic cells. The model is evaluated using different EF strengths and different configurations of both electrical and chemical stimuli. Accordingly, we found that the cell migration speed is described as the combination of an electrical and a chemical term. Cell migration is faster when both stimuli orient cell migration towards the same direction. In contrast, a reduced speed is obtained when the EF vector is opposed to the direction of the chemical stimulus. Numerical relations were obtained to quantify the cell migration speed at each configuration. Additional calculations for the cell colonization of a substrate also show mediation of the EF strength. Therefore, the term electro-osteoconduction is introduced to account the electrically induced cell colonization. Since numerical results compare favorably with experimental evidence, the model is suitable to be extended to other types of cells, and to numerically explore the influence of EF during wound healing.

A mathematical model of medial collateral ligament repair: migration, fibroblast proliferation and collagen formation.

The partial rupture of ligament fibres leads to an injury known as grade 2 sprain. Wound healing after injury consists of four general stages: swelling, release of platelet-derived growth factor (PDGF), fibroblast migration and proliferation and collagen production. The aim of this paper is to present a mathematical model based on reaction-diffusion equations for describing the repair of the medial collateral ligament when it has suffered a grade 2 sprain. We have used the finite element method to solve the equations of this. The results have simulated the tissue swelling at the time of injury, predicted PDGF influence, the concentration of fibroblasts migrating towards the place of injury and reproduced the random orientation of immature collagen fibres. These results agree with experimental data reported by other authors. The model describes wound healing during the 9 days following such injury.

A mechanobiological model of epiphysis structures formation.

Developing bone consists of epiphysis, metaphysis and diaphysis. The secondary ossification centre (SOC) appears and grows within the epiphysis, involving two histological stages. Firstly, cartilage canals appear; they carry hypertrophy factors towards the central area of the epiphysis. Canal growth and expansion is modulated by stress on the epiphysis. Secondly, the diffusion of hypertrophy factors causes SOC growth. Hypertrophy is regulated by biological and mechanical factors present within the epiphysis. The finite element method has been used for solving a coupled system of differential equations for modelling these histological stages of epiphyseal development. Cartilage canal spatial-temporal growth patterns were obtained as well as the SOC formation pattern. This model qualitatively agreed with experimental results reported by other authors.

A phenomenological mathematical model of the articular cartilage damage.

Articular cartilage (AC) is a biological tissue that allows the distribution of mechanical loads and movement of joints. The presence of these mechanical loads influences the behavior and physiological condition of AC. The loads may cause damaged by fatigue through injuries due to repeated accumulated stresses. The aim of this work is to introduce a phenomenological mathematical model of damage caused by mechanical action. It is considered that tissue failure is a consequence of chondrocyte death and matrix loss, taking into account factors modifying fatigue resistance such as age, body mass index (BMI) and metabolic activity. The model was numerically implemented using the finite elements method and the results obtained allowed us to predict tissue failure at different loading frequencies, different damage sites and variations in damage magnitude. Qualitative concordance between numerical results and experimental data led us to conclude that the model may be useful for physicians and therapists as a prediction tool for prescribing physical exercise and prognosis of joint failure.

A finite element method approach for the mechanobiological modeling of the osseointegration of a dental implant.

The aim of this paper is to introduce a new mathematical model using a mechanobiological approach describing the process of osseointegration at the bone-dental implant interface in terms of biological and mechanical factors and the implant surface. The model has been computationally implemented by using the finite element method. The results show the spatial-temporal patterns distribution at the bone-dental implant interface and demonstrate the ability of the model to reproduce features of the wound healing process such as blood clotting, osteogenic cell migration, granulation tissue formation, collagen-like matrix displacements and new osteoid formation. The model might be used as a methodological basis for designing a dental tool useful to predict the degree of osseointegration of dental implants and subsequent formulation of mathematical models associated with different types of bone injuries and different types of implantable devices.

Mathematical model of the coagulation in the bone-dental implant interface.

The healing of the injured tissues after the insertion of a dental implant begins with the formation of a fibrin clot that detains the blood flow and gives initial support to the osteoprogenitor cells. The adequate formation of this clot determines the direct and stable connection between bone and implant, process known as osseointegration. The aim of this work is to introduce a mathematical model of the coagulation in the bone-dental implant interface based on two reaction-diffusion equations representing the kinetic reaction that leads to the production of fibrin and a transformation equation representing the formation of the fibrillar network compounding the clot. The model also includes a parameter associated to the blood platelets concentration that extends the model framework to the analysis of two hematological disorders well reported: thrombocytosis and thrombocytopenia. The solution of the model is performed using the finite element method, obtaining as results the distribution of spatial-temporal patterns in the bone-dental implant interface. These results are in qualitative concordance with experimental results previously reported by other authors. Although the model is a simplified version of the biological process of coagulation, the results here obtained justify the mathematical formulation implemented. It is concluded that the model can be used as a methodological basis for the formulation of a general model of the osseointegration in the bone-dental implant interface.