The mass action kinetics approach is discussed in Section 3.2, and its general application to the bone volume and cells of the BMU is shown in Section 3.3. Extensions of , aside from those based on , integrate physiologically based models for calcium homeostasis or integrate pharmacokinetics/pharmacodynamics (PKPD) to study the treatment of multiple myeloma and osteoporosis . So the signals and biological mechanisms added to models following focus on modifications necessary to capture disease dynamics or calcium homeostasis. For example, Mathematical models of bone remodeling to study anti-sclerostin treatments for osteoporosis and derives a π term for sclerostin inhibition of the Wnt pathway based on mass action kinetics, assuming a constant Wnt concentration. While most models extend , reduces the model to a system of two dependent variables (osteoblasts and osteoclasts) and uses dimensional analysis to determine important aspects of the model that control the dynamics. The reduction is achieved by changing the cell concentrations to vary with respect to the initial values given in , casting the system into dimensionless variables, eliminating variables, and applying a quasi-steady-state approximation. The work also demonstrates negligible differences from the model for slow processes such as aging and estrogen deficiency. Like other models following , the reduced model is further extended to study postmenopausal osteoporosis and its treatment in other models including ; .