Mechanoresponsive Properties of the Periodontal Ligament are Responsible for Tooth Movement

Objectives: To characterize the response of the periodontal ligament (PDL) to a variety of physiologically relevant mechanical environments. In vivo mitotic activity, changes in cell density and collagen content, and osteogenic protein expression were examined using the PDL associated with the mouse molars as a model.
Methods: The PDL was examined under conditions 1) associated with the eruption of the primary dentition; 2) associated with the adult dentition under normal masticatory load; 3) associated with reduced masticatory loading achieved by feeding the animal either a soft diet or a liquid diet; and 4) conditions associated with experimental tooth movement. Tissues were evaluated using histology coupled with histomorphometry, immunohistochemistry (IHC), and scanning electron microscopy. Additionally, finite element (FE) modeling was performed to identify and characterize the distrubtion of tensile and compressive forces within the mechanically loaded periodontal ligament.
Results: In an unperturbed, uninjured state, BrdU incorporation and IHC for cell proliferation markers demonstrated that the adult molar PDL exhibited almost no cell proliferation. Changes in masticatory load altered mitotic activity and collagen production in the molar PDL. To test the potential relationship between functional loading and cell proliferation masticatory forces were altered by changing the animals’ diet. These data demonstrated that reduced mechanical loading of the PDL altered the density and organization of the collagen fibers. Orthodontic forces were applied to the first molar crown. FE modeling showed the distribution of tensile and compressive forces and histologic/histomorphometric analyses demonstrated that collagen fiber density and cell density were increased in response to experimental tooth movement.
Conclusions: According to our in vivo molecular and cellular analyses, the adult molar PDL is a quiescent tissue. Changes in mechanical loading acted as a stimulus to enhance mitotic activity and increase the amount and orientation of the collagen fibers in the PDL. Both changes appeared to be adaptive responses since a PDL with denser collagen fibers is capable of bearing a greater load before failing, and tissues with greater proliferation are more capable of repairing after damage.