IADR Abstract Archives
Periodontal Disease and Tooth Movement: A Frequency-Based Interpretation
Objectives: This study aims to: (1) utilize a bioengineering approach to quantify apposition rates of mineralized tissues within the periodontium, and (2) model the etiology of periodontal disease-related tooth movement by integrating principles of attachment loss, occlusal function, and pathological adaptation.
Methods: Mineral apposition rate (MAR - µm/week) was evaluated in cementum, dentin, and bone in 6 male, Sprague-Dawley rats (3 control, 3 ligated), each administered 10 alternating tetracycline and alizarin red fluorochrome injections over 12 weeks. Hemi-maxillae were dissected, imaged in 3 channels (brightfield-mCherry-Sapphire), and periodic signals analyzed using an innovative Fast Fourier Transform, frequency-domain protocol. MAR values were correlated with direction of respective mineral gradients determined via high-resolution radiography, while 3-D attachment loss (CEJ-ABC) and degrees of freedom (DOF) for ligated molars were quantified via in situ loading and micro-computed X-ray tomography (µCT), respectively. MAR over time (2nd-derivative of signal positions) was quantified via growth rate correlation coefficient (RW).
Results: Cementum formation/MAR was highest in controls, while bone formation/MAR was highest in diseased. RW was lowest in cementum, intermediate in bone, and highest in dentin for both control and ligated specimens (Table 1). By 6 weeks, CEJ-ABC distance was significantly greater in diseased (622±55µm) than in controls (356±41µm), with continued attachment loss/increasing DOF until sacrifice (12 weeks). Ligated specimens also displayed accelerated tooth movement (distal drift), where mesial regions of the maxilla grew faster (17% in dentin, 9% in cementum, 53% in bone) compared to distal regions. Although only 2nd molars were ligated, changes in MAR were most pronounced in the 1st molar (most functionally active site of the maxillary dentition).
Conclusions: Localized inflammatory processes (i.e. periodontitis) cause non-local adaptations (i.e. tooth movement) within the periodontium through an increased susceptibility to normal mechanical forces. Periodontitis is a multi-factorial disease characterized by virulence factors, structural integrity loss, occlusal forces, and ultimately pathological adaptation/function.
Methods: Mineral apposition rate (MAR - µm/week) was evaluated in cementum, dentin, and bone in 6 male, Sprague-Dawley rats (3 control, 3 ligated), each administered 10 alternating tetracycline and alizarin red fluorochrome injections over 12 weeks. Hemi-maxillae were dissected, imaged in 3 channels (brightfield-mCherry-Sapphire), and periodic signals analyzed using an innovative Fast Fourier Transform, frequency-domain protocol. MAR values were correlated with direction of respective mineral gradients determined via high-resolution radiography, while 3-D attachment loss (CEJ-ABC) and degrees of freedom (DOF) for ligated molars were quantified via in situ loading and micro-computed X-ray tomography (µCT), respectively. MAR over time (2nd-derivative of signal positions) was quantified via growth rate correlation coefficient (RW).
Results: Cementum formation/MAR was highest in controls, while bone formation/MAR was highest in diseased. RW was lowest in cementum, intermediate in bone, and highest in dentin for both control and ligated specimens (Table 1). By 6 weeks, CEJ-ABC distance was significantly greater in diseased (622±55µm) than in controls (356±41µm), with continued attachment loss/increasing DOF until sacrifice (12 weeks). Ligated specimens also displayed accelerated tooth movement (distal drift), where mesial regions of the maxilla grew faster (17% in dentin, 9% in cementum, 53% in bone) compared to distal regions. Although only 2nd molars were ligated, changes in MAR were most pronounced in the 1st molar (most functionally active site of the maxillary dentition).
Conclusions: Localized inflammatory processes (i.e. periodontitis) cause non-local adaptations (i.e. tooth movement) within the periodontium through an increased susceptibility to normal mechanical forces. Periodontitis is a multi-factorial disease characterized by virulence factors, structural integrity loss, occlusal forces, and ultimately pathological adaptation/function.
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