Vitamin D plays an important role in calcium homeostasis and bone metabolism, with the capacity to modulate innate and adaptive immune function, cardiovascular function, and proliferation and differentiation of both normal and malignant keratinocytes. 1,25(OH)2D, the biologically active form of vitamin D, exerts most of its functions through the almost universally distributed nuclear vitamin D receptor (VDR). Upon stimulation by 1,25(OH)2D, VDR forms a heterodimer with the retinoid X receptor (RXR). In turn, VDR/RXR binds to DNA sequences termed vitamin D response elements in target genes, regulating gene transcription. In order to exert its biological effects, VDR signalling interacts with other intracellular signalling pathways. In some cases 1,25(OH)2D exerts its biological effects without regulating either gene expression or protein synthesis. Although the regulatory role of vitamin D in many biological processes is well documented, there is not enough evidence to support the therapeutic use of vitamin D supplementation in the prevention or treatment of infectious, immunoinflammatory, or hyperproliferative disorders. In this review we highlight the effects of 1,25(OH)2D on bone and calcium homeostasis, on cancer, and refer to its effects on the cardiovascular and immune systems.

Some degree of external root resorption is a frequent, unpredictable, and unavoidable consequence of orthodontic tooth movement mediated by odontoclasts/cementoclasts originating from circulating precursor cells in the periodontal ligament. Its pathogenesis involves mechanical forces initiating complex interactions between signalling pathways activated by various biological agents. Resorption of cementum is regulated by mechanisms similar to those controlling osteoclastogenesis and bone resorption. Following root resorption there is repair by cellular cementum, but factors mediating the transition from resorption to repair are not clear. In this paper we review some of the biological events associated with orthodontically induced external root resorption.

Burning mouth syndrome (BMS) is a chronic debilitating oral condition characterised by a burning sensation of the oral mucosa in an otherwise apparently normal person. Its aetiology and pathogenesis are obscure, but both psychogenic factors and peripheral and central neuropathies appear to be implicated. There is no cure for BMS, and treatment with either local or systemic medications focuses on the relief of symptoms and on improving quality of life. In recalcitrant cases, psychological/psychiatric intervention may be helpful. In order to improve treatment outcomes, a better understanding of the pathogenesis of this syndrome might provide a basis for the development of more effective management strategies. In this short review, we discuss current knowledge of the diagnosis, aetiopathogenesis, and management of BMS.

Postherpetic neuralgia (PHN) is an unpredictable complication of varicella zoster virus- (VZV-) induced herpes zoster (HZ) which often occurs in elderly and immunocompromised persons and which can induce psychosocial dysfunction and can negatively impact on quality of life. Preventive options for PHN include vaccination of high-risk persons against HZ, early use of antiviral agents, and robust management of pain during the early stage of acute herpes zoster. If it does occur, PHN may persist for months or even years after resolution of the HZ mucocutaneous eruptions, and treatment is often only partially effective. Classical trigeminal neuralgia is a severe orofacial neuropathic pain condition characterized by unilateral, brief but recurrent, lancinating paroxysmal pain confined to the distribution of one or more of the branches of the trigeminal nerve. It may be idiopathic or causally associated with vascular compression of the trigeminal nerve root. The anticonvulsive agents, carbamazepine or oxcarbazepine, constitute the first-line treatment. Microvascular decompression or ablative procedures should be considered when pharmacotherapy is ineffective or intolerable. The aim of this short review is briefly to discuss the etiopathogenesis, clinical features, and treatment of PHN and classical trigeminal neuralgia.

The biologically active form of vitamin D, 1,25 dihydroxyvitamin D (1,25(OH)2D) and its receptor, the vitamin D receptor (VDR), play roles in maintaining oral immunity and the integrity of the periodontium. Results of observational cross-sectional clinical studies investigating the association between vitamin D serum level and the incidence and severity of chronic periodontitis indicate that, perhaps owing to the immunomodulatory, anti-inflammatory, and antibacterial properties of 1,25(OH)2 D/VDR signalling, a sufficient serum level of vitamin D is necessary for the maintenance of periodontal health. In cases of established chronic periodontitis, vitamin D supplementation is associated with reduction in the severity of periodontitis. As cross-sectional studies provide only weak evidence for any causal association and therefore are of questionable value, either longitudinal cohort studies, case controlled studies, or randomized control trials are needed to determine whether or not deficiency of vitamin D is a risk factor for chronic periodontitis, and whether or not vitamin D supplementation adjunctive to standard periodontal treatment is in any way beneficial. In this article, we discuss the relationship between vitamin D, oral immunity and periodontal disease and review the rationale for using vitamin D supplementation to help maintain periodontal health and as an adjunct to standard periodontal treatment.

Orthodontic force-induced stresses cause dynamic alterations within the extracellular matrix and within the cytoskeleton of cells in the periodontal ligament and alveolar bone, mediating bone remodelling, ultimately enabling orthodontic tooth movement. In the periodontal ligament and alveolar bone, the mechanically induced tensile strains upregulate the expression of osteogenic genes resulting in bone formation, while mechanically induced compressive strains mediate predominantly catabolic tissue changes and bone resorption. In this review article we summarize some of the currently known biological events occurring in the periodontal ligament and in the alveolar bone in response to application of orthodontic forces and how these facilitate tooth movement.

2Running title: Implants near the midline mandibular lingual canal Abstract Purpose: To determine the position and occurrence of the midline mandibular canal (MLC) in the various age, sex, population and dentition groups. The average distances from the MLC to a planned mandibular midline implant and the inferior mandibular border were measured. Materials and methods: Cone beam computed tomography (CBCT) was used to scan 122 mandibles (31 black males; 28 black females; 32 white males and 31 white females). Midsagittal sections in the reconstructed images of edentulous mandibles or sagittal sections through the socket of the 41 tooth (FDI nomenclature) in dentate mandibles were made. A measurement of 6 mm across buccolingually (BL) was delineated with the caliper tool indicating the minimum dimensions for placement of an implant. In dentate cases where the BL distance was in excess of 6 mm, the caliper was placed across the deepest part of the socket as a marker to determine the bone dimension available below the socket for implant placement. From these markers a vertical line was dropped to the MLC to measure the available bone. Results: The MLC was a consistent finding within the anterior mandible.A statistical significant difference in bone availability amongst the sexes and with dentition pattern was found indicating that edentulous female patients were particularly at risk of injury to the vessels of the midline lingual canal during implants in that area. Conclusion: Immediate implants in the position of lower central incisors are regarded as a safe procedure as is the placement of interforaminal implants in the anterior mandible. Clinicians should however take note of the position of the midline mandibular lingual canal and approach this area with caution, especially if the alveolar ridge is to be reduced before implant placement.

In immunocompromised subjects, Epstein-Barr virus (EBV) infection of terminally differentiated oral keratinocytes may result in subclinical productive infection of the virus in the stratum spinosum and in the stratum granulosum with shedding of infectious virions into the oral fluid in the desquamating cells. In a minority of cases this productive infection with dysregulation of the cell cycle of terminally differentiated epithelial cells may manifest as oral hairy leukoplakia. This is a white, hyperkeratotic, benign lesion of low morbidity, affecting primarily the lateral border of the tongue. Factors that determine whether productive EBV replication within the oral epithelium will cause oral hairy leukoplakia include the fitness of local immune responses, the profile of EBV gene expression, and local environmental factors.