Treatment decisions regarding caries and dental developmental defects in children - a questionnaire-based study among Norwegian dentists.

BACKGROUND: Current knowledge on treatment strategies and choice of restorative materials when treating deep caries or severe dental developmental defects (DDDs) in young individuals is scarce. Therefore, the aim was to investigate Norwegian dentists´ treatment decisions and reasons for treatment choice when treating deep caries in primary teeth and severe DDDs in permanent teeth in children. METHODS: A pre-coded questionnaire was sent electronically to all dentists employed in the Public Dental Service (PDS) in Norway (n = 1294). The clinicians were asked about their background characteristics and how often they registered DDDs. Three clinical cases were presented to the dentists and asked to prioritize treatment options and reasons for their choice. RESULTS: After three reminders, 45.8% of the dentists answered. Most clinicians were general practitioners (96.3%), females (77.9%), under 41 year-olds (59.4%), graduated in 2001 or later (61.1%), and representing all regions of Norway. The respondents registered molar incisor hypomineralisation (MIH), other DDDs and dental fluorosis (DF) frequently, 523 (91.1%), 257 (44.8%) and 158 (27.5%), respectively. In case 1a with severe dental caries in a primary molar, the preferred treatment was resin-modified glass ionomer cement (RMGIC) (58.3%), followed by glass ionomer cement (GIC) (17.9%) and zinc oxide-eugenol (ZOE) (13.2%). Extraction, compomer or stainless steel crowns (SSC) were preferred by 0.9, 0.7 and 0.4%, respectively. In case 1b, which was identical to case 1a, but treated under general anaesthesia, the preferred treatment alternatives were RMGIC (37.1%), resin composite (RC) (17.6%) and GIC (17.2%). Extraction and SSC were chosen by 15.1 and 7.2%, respectively. In case 2, showing a severely hypomineralised and symptomatic first permanent molar, the dentists preferred RC (38.4%), followed by RMGIC (26.6%) and GIC (19.0%). Extraction and SSC were chosen by 8.7 and 5.4%, respectively. The treatment choices were not significantly affected by the dentists' background characteristics. The reasons for dentists' treatment decisions varied for each patient case; patient cooperation, prognosis of the tooth and own experience were the dominant reasons. CONCLUSIONS: A notable disparity in treatment choices was shown indicating that Norwegian dentists evaluate each case individually and base their decisions on what they consider best for the individual patient.

Role of Hyperplasia of Gingival Lymphatics in Periodontal Inflammation.

Lymphatic vessels are important for maintenance of tissue fluid homeostasis and afferent antigen transport. In chronic inflammation, lymphangiogenesis takes place and is characterized by lymphatic endothelial cell proliferation and lymphatic hyperplasia. Vascular endothelial growth factor C (VEGFC) is the main known lymphangiogenic growth factor, and its expression is increased in periodontitis, a common chronic infectious disease that results in tissue destruction and alveolar bone loss. The role of lymphangiogenesis during development of periodontitis is unknown. Here, we test if transgenic overexpression of epithelial VEGFC in a murine model is followed by hyperplasia of lymphatic vessels in oral mucosa and if the lymphatic drainage capacity is altered. We also test if lymphatic hyperplasia protects against periodontal disease development. Transgenic keratin 14 (K14)-VEGFC mice had significant hyperplasia of lymphatics in oral mucosa, including gingiva, without changes in blood vessel vasculature. The basal lymph flow was normal but slightly lower than in wild-type mice when oral mucosa was challenged with lipopolysaccharide from Porphyromonas gingivalis. Under normal conditions, K14-VEGFC mice exhibited an increased number of neutrophils in gingiva, demonstrated enhanced phagocyte recruitment in the cervical lymph nodes, and had more alveolar bone when compared with their wild-type littermates. After induction of periodontitis, no strain differences were observed in the periodontal tissues with respect to granulocyte recruitment, bone resorption, angiogenesis, cytokines, and bone-related protein expressions or in draining lymph node immune cell proportions and vascularization. We conclude that overexpression of VEGFC results in hyperplastic lymphatics, which do not enhance lymphatic drainage capacity but facilitate phagocyte transport to draining lymph nodes. Hyperplasia of lymphatics does not protect against development of ligature-induced periodontitis.

Lymphangiogenesis is induced during development of periodontal disease.

Lymphangiogenesis, the formation of new lymphatics, is associated with chronic inflammation and tissue injury, and its role is to enhance lymphatic flow, immune cell transport, and antigen clearance. It is unknown if lymphangiogenesis takes place during periodontal disease development, and we hypothesized that growth of lymphatic vessels occurs in gingiva during development of periodontitis in mice. Inflammation was induced in gingiva with Porphyromonas gingivalis gavage, and bone resorption was verified after 42 days. Growth of lymphatic and blood vessels was measured after immunofluorescent staining with LYVE-1 and CD31. Expression of vascular endothelial growth factors and 2 inflammatory cytokines was investigated 10 days post-infection. Gingival lymphangiogenesis was found 10 days and 42 days post-infection, but proliferation of vessels was observed only in the shortest observation period. Epithelial expression of vascular growth factors (VEGF) A, C, and D was observed in gingiva, and increased numbers of immune cells expressing VEGF-C were found after infection, along with up-regulation of IL-1ß and TNF-α at protein levels. We conclude that lymphangiogenesis takes place in gingiva during periodontal disease development, and that up-regulation of vascular growth factor C in recruited immune cells is likely important for the growth of lymphatic vessels.

Sensory pulpal nerve fibres and trigeminal ganglion neurons express IL-1RI: a potential mechanism for development of inflammatory hyperalgesia.

AIM: To localize interleukin-1 receptor type I (IL-1RI) in rat dental pulp and trigeminal ganglion (TG) and to test the hypothesis that pulpal inflammation increases neuronal expression of IL-1RI. METHODOLOGY: Female Wistar rats were subjected to unilateral pulp exposures in the maxillary and mandibular first molars, whereas the contralateral jaws served as untreated controls. Seven days later the animals were transcardiacally perfused and the jaws and the TGs were removed and prepared for immunohistochemistry. Immunoreactivity for IL-1RI was examined alone (DAB) and together with calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY), CD31 or CD34 by multiple-labelling immunofluorescence. Quantification of IL-1RI-immunoreactive (-IR) cells in the maxillary and mandibular division of the ganglion was performed in parasagittal immunoreacted sections of the right and left TGs. Data were analysed with Mann-Whitney Rank Sum test (P < 0.05). RESULTS: Interleukin-1 receptor type I was found on sensory (CGRP-IR) and sympathetic (NPY-IR) nerve fibres and on blood vessels (CD31- and CD34-IR) in the dental pulp. It was also localized on sensory neurons and axons in the TG. Pulpal inflammation significantly increased the expression of IL-1RI in the TG (P < 0.001). CONCLUSIONS: The localization of IL-1RI on sensory nerve fibres and its up-regulation in TG neurons during pulpal inflammation may imply a direct effect of IL-1 in pulpal nociception. The presence of IL-1RI on sympathetic nerve fibres and on blood vessels may indicate a vasoactive role of the same cytokine in the pulp.

Edema in oral mucosa after LPS or cytokine exposure.

Lowering of interstitial fluid pressure (P(if)) is an important factor that explains the rapid edema formation in acute inflammation in loose connective tissues. Lipopolysaccharide (LPS) and the pro-inflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) are pathogenetic in gingivitis. To test if these substances induce lowering of P(if) in rat oral mucosa, we measured P(if) with a micropuncture technique. IL-1beta and TNF-alpha caused lowering of P(if), whereas LPS induced an immediate increase in P(if), followed by lowering after 40 min. Measurements of fluid volume distribution showed a significant change in interstitial fluid volume (V(i)) 1.5 hr after LPS exposure as V(i) changed from 0.41 +/- 0.02 to 0.51 +/- 0.03 mL/g wet weight (p < 0.05), confirming edema. These findings show that LPS, IL-1beta, and TNF-alpha induce lowering of P(if) in the rat oral mucosa and contribute to edema formation in LPS-induced gingivitis.

Effect of denervation on healing after tooth replantation in the ferret.

Studies have shown that the sensory nerves participate in inflammation and immune responses and possess trophic-facilitating wound healing in general. Tooth avulsion represents a pulpal and periodontal injury, and the mechanisms involved in the healing responses subsequent to replantation of teeth are still unclear. The objective of this study was to investigate the healing responses after denervation and replantation of teeth. Unilateral denervation was performed in 15 ferrets by axotomy of the inferior alveolar nerve, 5 days before extraction of the first lower premolars. Six weeks later the mandibles were excised and processed for histological evaluation. Immunohistochemistry was performed using antibodies against the sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP), and measurements of root resorption and ankylosis were performed in four sections from each replanted tooth. After 6 weeks substantial reinnervation was observed in the jaws. Immunoreactivity in the pulp was observed in only two replanted teeth on the denervated side, compared with four on the innervated side. Total pulp necrosis appeared in 10 replanted teeth on the denervated side and in 5 on the innervated, indicating that sensory nerves promote survival of the pulp after replantation. SP-immunoreactive (IR) fibers were more frequently observed in the resorptive lacunae than CGRP-IR fibers. However, resorptive areas lacking IR fibers were frequently found along the root surface. Root resorption averaged 0.062 +/- 0.029 mm2 on the innervated side compared to 0.016 +/- 0.0043 mm2 on the denervated (P< 0.02). Ankylosis was observed in four of the replanted teeth on the innervated side (169.3 +/- 49.7 microm) and in six on the denervated side (332.56 +/- 193.2 microm) (P = 1). It is concluded that the sensory nerves promote root resorption after pulpoperiodontal injuries but have less influence on the osteoblastic activity expressed by ankylosis.

Expression of IL-8 by cells of the odontoblast layer in vitro.

Due to their peripheral location in the dental pulp and their cellular extension into dentin, odontoblasts are the first pulpal cells to encounter dental pathogens. The association of odontoblasts with immunoglobulins and dendritic cells during microbial invasion of dentin implies that these cells may possess a role in the innate and adaptive pulpal immune responses, however this has not been examined. A pivotal step in the innate immune response is the detection of foreign antigen and the recruitment of immune effector cells to the area. IL-8 is a potent chemotactic cytokine that plays an important role in the inflammatory response. The purpose of this study was to determine if odontoblasts are capable of expressing the pro-inflammatory chemokine IL-8. Human odontoblasts from intact, noncarious third molars were maintained in culture and exposed to Escherichia coli lipopolysaccharide (LPS) (serotype 055:B5) on day 4 for 8-10 h in a humidified 5% CO2 incubator. Control and experimental samples were assayed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot for the production of IL-8 mRNA and protein. Analysis of the PCR products revealed that cells of the odontoblast layer maintained in this culture model constitutively expressed low levels of IL-8, which were increased in response to E. coli LPS exposure. Western blotting confirmed that the mRNA was translated into protein. These results imply that odontoblasts are capable of producing of pro-inflammatory mediators, thereby actively participating in the recruitment of neutrophils in response to bacterial by-products.