# Static Osteogenesis versus Dynamic Osteogenesis:
## 4 Experimental Evidence for SO and DO Occurrence  
The occurrence of SO and DO explains varied evidence both in experimental conditions and in pathological situations. In one of our experimental studies [35] concerning the timing and manner of bone healing in rat femurs (after drilling transcortical holes, with/without contemporary administration of parathyroid hormone, PTH (1-34)), the interpretation of the results clearly underlined the correlation with the sequential occurrence of the two types of osteogenesis. The final goal was to identify the phase of osteogenesis (static versus dynamic) in which PTH (1-34) can most significantly exert its eventual effect, in order to determine how and when to use the drug with maximum efficacy in improving bone lesion repair strategies. Histomorphometric analysis revealed that 10 days after drilling, despite the holes being temporarily filled by the same amount of newly formed trabecular bone by static osteogenesis independent of the treatment, the extent of the surface of movable osteoblast laminae (covering the SO-trabecular surface) was statistically greater in animals which underwent PTH (1-34) administration as compared to controls. This datum strongly suggests the effect of PTH (1-34) in anticipating the occurrence of dynamic osteogenesis involved in the production of good-quality bone (i.e., lamellar bone, with a more ordered collagen texture, instead of woven-fibered bone) more suitable for mechanical loading. With regard to the translational aspect of basic research, the authors wanted to stress the importance of the two types of osteogenesis in the clinical research to define the best therapeutic approaches/strategies for drug use in orthopedics for recovery from severe skeletal lesions. The two types of osteogenesis were found to be crucial in data interpretation in two of our (successive) investigations [36; 37] for determining whether PTH (1-34) administration during normal diet restoration (after a calcium-free diet) can influence the amounts and sites of bone mass recovery. Besides the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone response to dietary/metabolic alterations, evidence emerged that the most-involved bony architecture is trabecular bone, as it is the most susceptible to the dynamical balance between the two types of homeostasis. Trabecular bone has the ability to respond more readily to mineral homeostasis. This ability of trabecular bone led to: (1) higher bone loss of less-loaded bony trabeculae as a consequence of a calcium-free diet in response to mineral homeostasis, and (2) new bone deposition on the surface of the few remaining overloaded trabeculae by means of dynamic (instead of static) osteogenesis to respond to skeletal homeostasis during normal diet restoration. Once again, the kind of osteogenesis recruited in bone healing is not irrelevant. On the contrary, in some pathologies like human facet joint osteoarthritis (FJOA), remodeling of the subchondral trabecular bone compartment is characterized by increased trabecular number, rather than trabecular thickening [38]; this observation can be explained by the impairment of viability of osteocytes (i.e., the bone mechanosensors) inside the trabecular bone due to osteoarthritis, where static (as compared to dynamic) osteogenesis underpins specific bone remodeling and is activated through the recruitment of osteoporgenitor cells by endothelial-derived growth factors, giving rise to the formation of new trabeculae. The same authors also commented that a histological analysis of osteocyte lacunae in healthy and osteoarthritis specimens could provide further support for the role of static osteogenesis in the pathogenesis of FJOA. Another pathology where static and dynamic osteogenesis explains some evidence is osteogenesis imperfeta (OI), as described by [PERSON] et al. in 2020 [39].