The lymphatic system in dental tissue

The lymphatic system is important for normal immune barrier function and for maintenance of tissue fluid balance. During inflammation, lymphangiogenesis takes place to enhance transport of filtered fluid, proteins and immune cells. In the dental tissue including the pulp, a description of the lymphatic system using specific lymphatic markers is lacking. Objective:We aimed at studying this system and to observe if lymphangiogenesis takes place during inflammation in the rat and mouse dental pulp.

Method: Vital perfused rat and mouse jaws were processed for immunohistochemistry, utilizing LYVE-1 and VEGFR-3 antibodies. For identification of immune cells double labeling was performed with ED-1 (CD 68) or F/80 and OX-6 (RT1B) antibodies. Pulpal inflammation was induced in mice by cavity preparation in 1. molar. The exposures were left open to the oral cavity for 1 week. Sections were evaluated in light, fluorescence and confocal microscope.

Results: Immunostaining with lymphatic endothelium hyaluronan receptor (LYVE-1) and vascular endothelium growth factor receptor-3 (VEGFR-3) showed different localization of lymphatics in molars and incisors. In molars, a dense lymphatic vessel network runs from the coronal pulp to the apical area and bundles of larger vessels exit the root through the apical foramen and side channels. In contrast, in incisors lymphatic vessels are found only in the apical part of the pulp. In interdental bone, transverse lymphatics were found, raising the possibility that an infection can spread from the pulp to the periodontal ligament and to an adjacent neighbour tooth. LYVE-1+ and VEGFR-3+ macrophages were found in both molar and incisor pulps.

Conclusion: we demonstrate different distribution of lymphatic vessels in molars and incisors. Lymphatic vessels communicate horizontally from PDL to PDL in adjacent teeth, providing a potential route of infection. In both molars and incisors, LYVE-1+ and VEGFR-3+macrophages are found and might contribute to lymphangiogenesis during inflammation.