What Can Biological Principles Teach us about Clinical Orthodontics? Dr. GREGORY KING The mechanical environments that orthodontists establish in the periodontal ligament and surrounding alveolar bone can be quite complex and are not well understood. Also, the relationships between mechanics, tissue remodeling and clinical outcome are unclear. Dr. King's presentation focused on the relationships between various biomechanical protocols common in clinical orthodontic practice today, and two important clinical outcome measures: orthodontic tooth movement and root resorption. The role that tissue remodeling plays in these clinical outcomes was examined. The nature of remodeling and the clinical responses to various orthodontic appliance activation protocols can be examined with relative ease and control using well characterized animal models. These studies can be instructive for clinicians. Concepts such as force optimum, minimal effective strain, overload, intermittent versus constant timing are prevalent in several recognized appliance approaches to the treatment of malocclusion. The validity of these concepts was examined by focusing on the consequences of altering the magnitude of initial appliance activation, requirements to initiate movement and recovery from movement and the effects of changing the rhythm of appliance reactivation. Also the clinical consequences of variation in bone density was examined. Even though the classic "pressure-tension" theory is a gross over simplification; Dr. King used it for his discussion. The periodontal ligament is distorted with force and cells respond to this distortion to create tooth movement. The PDL is the key. Witness implants which do not move. When Force is applied teeth move in three stages: 1st - Displacement - instant movement that reflects the facts that bone bends and that the teeth are loosely held in the bone by the PDL 2nd - Delay - a biologically active time where bone resorption is occurring at the pressure sites - no tooth movement occurs. At 3-4 days osteoclasts appear and the pressure sites start to undergo vascular necrosis. Necrotic tissue is started to be removed by cells from the periphery. 3rd - Movement - actual tooth movement - This is remodeling - we see remodeling in all areas except just at pressure point. He has found that teeth move: Without injury -as in tooth eruption and drift With injury - includes all orthodontic tooth movement and occurs at pressure sites even with very light forces However these injuries are temporary and reversible. As a result of vascular necrosis a compensatory hyperemia occurs bringing exceptional blood and nutrient flow to periodontal ligament and pulp. Because of the inter connection of tissues in the dental support apparatus, this hyperemia is widely seen in the surrounding area. Root resorption occurs along with bone resorption but has no healing mechanism and is irreversible. Microscopic evidence shows root resorption occurs most extensively and generalized on the surface of the root at pressure sites. We notice it on the root tips mostly because we can see it on an x-ray. 1. Vascular shut down 2. Bone is bent 3. PDL fibers relaxed 4. Necrosis at CS All adjacent tissue goes into hyperfunction and a massive hyperemia occurs. The appearance of osteoclasts is the 1st step in remodeling and they start to appear in 3-4 days. Cementoclasts, macrophages also are present. Necrotic tissue is removed from the periphery. So remodeling is wound healing in bone. First 1-2 weeks is devoted to removal of bone. Bone replacement is a lower process. So resorption is fast and remodeling is slow. Coupling - exactly the same amount of bone is replaced as was taken away. Bone Modeling - on the tension side osteoblasts lay down new bone. Here the PDL is loaded and on the pressure side unloaded. Growth and development occurs with modeling. Osteoclasts die in two ways, it takes 3-4 days to see them and they start to disappear in 5-7 days: Necrosis - they increase in size and blowup: an environmental death. Apoptosis - genetically programmed cell death, normal death as cells break apart. Also occurs in 5-7 days. Apoptosis is very important today in cancer cell research and neuro degeneration diseases such as Alzheimer's disease. Dr. King related clinical topics to cell biology. 1. Bone Density 2. Force Magnitude 3. Intermittent Force 4. Timing of Activation BONE DENSITY Although there is controversy surrounding the effect of bone density on root resorption and tooth movement Dr. King believes: 1. Teeth move more rapidly through less dense bone 2. Tooth movement in less dense bone places roots at less risk for resorption 3. Reducing bone density prior to tooth movement could offer significant clinical advantages. Possibly a future treatment option. FORCE MAGNITUDE 1. Increasing force will increase tooth movement and root resorption 2. Excessive force increases risk of RR and bone loss without increasing tooth movement so no advantage. Bone resorption is extended and recovery is delayed. Perhaps so much necrosis is created that cells can't get in for clearance. 3. Tissue changes persist after force removal. INTERMITTENT FORCES: Intermittent forces stimulate the same number of osteoclasts as continuous forces. When force is removed these cells stay around 7-10 days - so process keeps going. Intermittent forces, such as headgear may be good. Bone remodeling can be initiated with a few short duration activations: 1. Longer duration force intervals are required to move teeth -forces need to be applied approximately 50% of time at least. 2. Using intermittent forces may reduce the risk of root resorption. TIMING OF APPLIANCE REACTIVATION 1. Reducing the reactivation interval reduces tooth movement and extends the period of bone remodeling. Tooth movement will go slower with more frequent activations. Best to wait till remodeling cycle is over. 2. Appliance reactivation should be at more than four week intervals. 3. Root resorption is unaffected by activation schedules over the short term.