Figure 1
- Muscles and tendons apply loads over mineralized bone structures which, with a view to meeting functional demands, have thickness of trabecular and cortical bones increased while subject to stimuli that characterize the dynamics of bone remodeling.
Figure 2
- Bone structures. The following are highlighted: trabeculae, a thin layer of osteoid, osteoblasts and especially osteoblasts, which constitute, via canaliculi and with a number of cytoplasmic extensions, a cell-to-cell network with mediators and trabecular as well as cortical bones, thus actively affecting bone remodeling (HE, 25X).
Figure 3
- On the surface, osteoblasts form new bone layers as they are stimulated by mediators released by local neighboring cells and which travel through the blood, or by osteocytes travelling through connected canaliculi (HE, 25X).
Figure 4
- Osteocytes and their typical shape, with dozens of extensions forming an effective network within the mineralized bone matrix. Lacunae where osteocytes are located are termed osteoplasts.
Figure 5
- Osteocytes within the mineralized matrix, revealing a number of cytoplasmic extensions inside the intercommunicating canaliculi (HE; A = 25X, B = 40X).
Figure 6
- Osteocytes were replaced by resin which, after polymerization, formed the shape of lacunae and canaliculi visible by scanning electron microscopy once the mineralized portion was completely removed by acids. As evinced, this network helps us comprehend how sensitive osteocytes in capturing bone deformation, albeit discreet.
Figure 7
- Flow of mononuclear cells towards the bone surface exposed by local displacement of osteoblasts, resulting from the action of mediators and changes in local conditions, such as pH reduction due to cellular stress. Note discreet Howship lacunae, with special attention to osteocytes within the mineralized bone matrix (HE, 25X).
Figure 8
- Two bone modeling units (BMUs) in Howship lacunae, with special attention to osteocytes, osteoblasts and macrophages as important components.
Figure 9
- On periodontal ligament bone surface, bone modeling units (BMUs), as it occurs in the entire body, continuously renew the bone structures, thus causing minimal natural tooth movement throughout one's life. Cementoblasts on root surface, without membrane receptors for bone mediators, do not take part in bone remodeling (B = Mallory, 25X, C = HE, 25X).
Figure 10
- At the bone environment, there are mediators intrinsic to bone modeling units. They speed up or inhibit bone remodeling according to stimuli extrinsic to these units, and are represented by bone remodeling local and systemic mediators. A few mediators stimulate osteoblasts, osteocytes and other local cells to release RANKL which, in turn, stimulates clastic activity. Other mediators, however, stimulate the production of osteoprotegerin, or OPG, which reduces the effect of RANKL by connecting to the molecules and preventing them to interact with clastic membrane receptors or RANKL.
Figure 11
- Various bone modeling units and their clasts in their respective Howship lacunae, and a network of osteocytes associated with the resorptive phenomenon, potentially releasing mediators and directly affecting local bone remodeling (HE, 25X).
Figure 12
- Diagram illustrating the function and organization of a bone modeling unit. Each BMU is controlled by osteoblasts and secondarily by macrophages via RANKL mediators. At the active or brush border, acids and enzymes are released by an effective sealing zone formed by molecular fusion between membrane and bone proteins. Note the relationship established with osteocytes.
Figure 13
- The bone crest periodontal surface of a tooth subject to induced tooth movement reveals areas without osteoblasts, in addition to stress and inflammation of ligament (asterisks) at the periphery. Subsequently, bone modeling units, or BMUs, settle down and begin the process of bone resorption. In B, note the BMU components in function, with clasts and mononuclear cells located at the periphery while representing osteoblasts and macrophages (A and B = HE, 10 and 40X).
Figure 14
- Stimuli or aggressive agents frequently found in the bone and teeth subject to force application. They are responsible for releasing mediators key to the biological process of bone remodeling.
Figure 15
- Cells with cytoskeleton proteins evinced by immunofluorescence, and diagram in B. Proteins, in red and green, reveal the structure that maintains cell shape and which provides the cell with mobility, whenever necessary. Cytoskeleton proteins are connected with integrins within the cell membrane and with the nuclear membrane at the center (in blue).
Figure 16
- Diagram illustrating how osteocytes actively participate in bone remodeling as mechanotransductors. Deformation of the network of osteocytes induces mechanical stress. RANKL local levels are raised, with a higher number of active clasts and greater release of sclerostin by osteocytes. Once the response to stimulus is adequate, there is a reduction in the number and activity of clasts, and a reduction in sclerostin levels by osteocytes.
Figure 17
- The periosteum, within the area corresponding to induced tooth movement (arrow in B), receives mechanical stimuli also provided by mediators released by osteocytes subject to deformation and acting as mechanotransductors by reacting with deposition of new bone layers on the cortical surface (arrows in C), thus changing the shape, volume and size of the jaws, in addition to affecting teeth positioning (HE; 25X).
Figure 18
- Clay modeling is performed with force application intended to adapt the material to the design planned by the artist. It is analogy to the application of forces by means of mini-implants and miniplates on the tridimensional network of osteocytes which will cause the bone structure to adapt, thus determining a new shape and tensegrity for the modified structure.
Figure 19
- Tooth movement performed by means of conventional orthodontic appliance, regardless of the type of bracket, might be compared to forces transmitted by the reins placed on the head of a horse controlled by a horseman who directly affects command of what is ahead of him. The head and the body immediately move around him. The horseman on the horse might be compared to the bracket bonded to the anchorage tooth.
Figure 20
- Analogy: Miniplates correspond to larger carriages, with various animals. The reins or wires must be well calibrated and secured, the coachman must be properly and the carriage must be stable. Miniplates can control, albeit afar, the shape of the network of osteocytes in the bone that gives support to anterior incisors and canines, in addition to influencing midline position and relationship.
Figure 21
- Miniplates offer anchorage to a number of elastics and devices, which allows the shape of the maxilla and mandible to be remodeled and have their relationship with all other anatomical structures to be changed. This example of miniplates clinical use allows the analogy with reins to be applied. Clinical case granted by Dr. Ertty Silva.
Figure 22
- Miniplates provide greater anchorage, as they are secured to a wider base with two to three screws fixed in thicker bone areas where ordinary bone remodeling tends to occurs slowly when compared to other areas, as depicted by the images. Clinical case granted by Dr. Ertty Silva.
