Milton R. Sims

Oxytalan Fiber System of Molars in the Mouse Mandible

The periodontal ligament of molars in mice includes an oxytalan fiber system that extends uninterruptedly from the first to the third molar. These fibers are not anchored in bone but they coordinate the movement of the tooth to the periodontal vasculature. The hypothesis is proposed that oxytalan fibers may be part of a mechanism that regulates vascular flow.

Tooth extrusion effects on microvessel volumes, endothelial areas, and fenestrae in molar apical periodontal ligament

Extrusive tooth loads, simulating short-term orthodontic movements, have not previously been used for transmission electron microscopic quantification of their effects on the periodontal ligament vessels. In this study, a continuous extrusive load of 1.0 N, applied to the rat maxillary first molar for 30 minutes, produced statistically significant changes in the microvascular bed of the tensioned apical periodontal ligament. The mean vascular volume, as a percentage of apical periodontal ligament volume, increased (p less than 0.01) in postcapillary-sized venules, venous capillaries, arterial capillaries, and terminal arterioles from 16.6% to 22.3%, 2.0% to 2.7%, 0.4% to 1.0%, and 1.0% to 2.5%, respectively. Mean endothelial surface area per cubic millimeter of apical periodontal ligament tissue increased (p less than 0.01) in postcapillary-sized venules from 16.8 to 25.7 x 10(6) microns 2/mm3, in venous capillaries from 3.0 to 4.8 x 10(6) microns 2/mm3, and in arterial capillaries from 0.7 to 1.5 x 10(6) microns 2/mm3. The number of fenestrae per square micron of endothelium in postcapillary-sized venules, venous capillaries, and arterial capillaries showed a mean increase from 0.02 to 0.07, 0.11 to 0.31, and 0.02 to 0.21 fenestrae/microns 2, respectively (p less than 0.01). Fenestrae per cubic millimeter of periodontal ligament tissue also demonstrated a statistically significant increase with extrusion (p less than 0.01) in postcapillary-sized venules from 0.37 to 1.55 x 10(6) fenestrae/mm3, in venous capillaries from 0.27 to 1.34 x 10(6) fenestrae/mm3, and in arterial capillaries from 0.02 to 0.22 x 10(6) fenestrae/mm3. Fenestrae in control vessels had a mean diameter of 54.2 +/- 0.56 nm (SE) compared with 61.1 +/- 0.7 nm in tensioned vessels (p less than 0.01). This investigation demonstrates multiple ultrastructural changes in the periodontal ligament microvascular bed after tooth extrusion.

An analysis of the effect of tooth intrusion on the microvascular bed and fenestrae in the apical periodontal ligament of the rat molar.

An analysis of the rat apical periodontal ligament (PDL) microvascular bed and fenestrae was conducted to evaluate the effect of a continuous 1.0 N intrusive tooth load for 30 minutes. The microvascular bed consisted of postcapillary-sized venules, venous and arterial capillaries, and terminal arterioles. Intrusion produced significant increases (p less than 0.01) in vascular volume for postcapillary-sized venules and venous capillaries in three of the four animals. Arterial capillaries, overall, showed a statistically significant increase (p less than 0.01). The endothelial surface area (micron2 x 10(6)) per cubic millimeter of PDL responded variably in postcapillary-sized venules and venous capillaries but showed a strong trend to increase in arterial capillaries. After tooth intrusion a significant reduction (p less than 0.01) occurred in the number of fenestrae per square micrometer of endothelium in postcapillary-sized venules and venous capillaries. Fenestrae in the control PDL had a mean diameter of 51.5 nm +/- 0.6 (SE), whereas those on the intrusion side were smaller (p less than 0.05), measuring 49.9 nm +/- 0.4 (SE).