Ridha,

I have to admit that I don't know about pharmacodynamics models. However, we include cellular models within finite element models to simulate the behaviour of whole organs, for example, skeletal muscle contractions (our group), heart pumping (e.g. the group of Peter Hunter in NZ, see Pullan et al. "Mathematically modelling the electrical activity of the heart"), tumor growth (Robert Krause, Uni Stuttgart), the liver (Tim Ricken, Uni Duisburg-Essen), bone fracture healing, among others.

Assuming the pharmacodynamics models are described by ODEs, you have to solve your pharmacodynamics model at each Gauss point of each of your finite elements. Most important will be the transfers operations. You will have to identify quantities to exchange between the microscopic pharmacodynamics model and the macroscopic finite element model.

Hope that helps

Dear Ridha,

 Do you want to model a special drug or drug groups or generally. Usually PK/PD models correlate concentrations in body with efficiency,e.g. you can correlate a vasodilator drug like TNG concentration and effect with its biomechanical effect on arterial and venous pressure and flow. Or you can model the concentration of a drug with its pharmacodynamic effect which the effect is a biomechanical response. e.g. concentration of a moisturizing cream and the improvements of the skin as  a biomechanical response considering time.

hope that gives you more idea

Dear all,

Thank for your interesting responses.

I am under developing a model based on the following ingredients:

1. Develop specific pharmacokinetics models of some drugs against osteoporosis disease in order to predict its absorption, distribution and metabolism in humans. This is based on ODEs equations

2. Develop and implement into a finite element code a multiscale mechanobiological model describing the bone remodeling (adaptation) performed by bone cells. The bone formation and resorption are performed by the bone cells

3. The bone cells activities are modulated by the drugs (step 1)

Perform finite element simulation considering the comprehensive model: drugs (PK) which modulate the bone cells activities which in turn modulate the bone adaptation.

4. The pharmacodynamics effects is predicted by the FE in term of the temporal change of the bone density, shape, resistance, etc…

Regards

Dear Mr Hambli

Bone is living, growing tissue that constantly forms new bone while replacing older bone. Bone continuously renews and changes through a process called remodeling. The bone remodeling cycle consists of two distinct stages: (1) bone resorption (breakdown or removal) and (2) bone formation. During resorption, special cells (osteoclasts) on the bone's surface dissolve bone tissue and create small cavities. During formation, other cells (osteoblasts) fill the cavities with new bone tissue.

Bisphosphonates, calcitonin, denosumab, estrogen and estrogen agonists/antagonists are antiresorptive medicines.

Teriparatide, a form of parathyroid hormone, increases the rate of bone formation.

Bisphosphonates

(Alendronate, Ibandronate, Risedronate and Zoledronic Acid) e.g. Alendronate reduces bone loss, increases bone density and reduces the risk of spine, hip and other broken bones by about 50 percent over two to four years.

If you will try PK parameters and correlation with PD it is good to select Bisphosphonates analogs.

I published recently a paper in JMBBM which demonstrate that we can combine pharmacokinetics of a drug and finite element to investigate the effects of the drug on the bone density.