Periodontal disease (PD) and coronary artery disease (CAD) are common diseases characterized by an overaggressive inflammatory response to diverse stimuli. Whereas PD leads to destruction of the tooth-supporting structures, CAD is a chronic inflammatory condition ultimately causing myocardial infarction via narrowing and occluding of blood vessels. Classical twin studies led to the conclusion that both complex diseases have a similar degree of heritability and that a significant fraction of the genetic factors accounting for this heritability is shared. Recent genome-wide association and large-scale candidate gene studies highlight that variations in >50 genes are associated with premature CAD, while variations in only 4 genes showing nominally significant associations with aggressive periodontitis and/or chronic periodontitis have so far been identified. Remarkably, 3 of the PD loci (75%) show shared associations with CAD ( ANRIL/CDKN2B-AS1, PLG, CAMTA1/VAMP3), suggesting involvement of common pathogenic mechanisms. In this critical review, we highlight recent progress in identifying genetic markers and variants associated with PD, present their overlap with CAD, and discuss functional aspects. In addition, we answer why a significant fraction of the heritability of PD is still missing, and we suggest approaches that may be taken to close the gap.

Trait anxiety is significantly associated with diagnoses of TMD pain.

Metabolic bone disorders arise as primary diseases or may be secondary due to a multitude of organ malfunctions. Animal models are required to understand the molecular mechanisms responsible for the imbalances of bone metabolism in disturbed bone mineralization diseases. Here we present the isolation of mutant mouse models for metabolic bone diseases by phenotyping blood parameters that target bone turnover within the large-scale genome-wide Munich ENU Mutagenesis Project. A screening panel of three clinical parameters, also commonly used as biochemical markers in patients with metabolic bone diseases, was chosen. Total alkaline phosphatase activity and total calcium and inorganic phosphate levels in plasma samples of F1 offspring produced from ENU-mutagenized C3HeB/FeJ male mice were measured. Screening of 9,540 mice led to the identification of 257 phenodeviants of which 190 were tested by genetic confirmation crosses. Seventy-one new dominant mutant lines showing alterations of at least one of the biochemical parameters of interest were confirmed. Fifteen mutations among three genes (Phex, Casr, and Alpl) have been identified by positional-candidate gene approaches and one mutation of the Asgr1 gene, which was identified by next-generation sequencing. All new mutant mouse lines are offered as a resource for the scientific community.

Occipital nerve block (ONB) has been used in several primary headache syndromes with good results. Information on its effects in facial pain is sparse. In this chart review, the efficacy of ONB using lidocaine and dexamethasone was evaluated in 20 patients with craniofacial pain syndromes comprising 8 patients with trigeminal neuralgia, 6 with trigeminal neuropathic pain, 5 with persistent idiopathic facial pain and 1 with occipital neuralgia. Response was defined as an at least 50% reduction of original pain. Mean response rate was 55% with greatest efficacy in trigeminal (75%) and occipital neuralgia (100%) and less efficacy in trigeminal neuropathic pain (50%) and persistent idiopathic facial pain (20%). The effects lasted for an average of 27 days with sustained benefits for 69, 77 and 107 days in three patients. Side effects were reported in 50%, albeit transient and mild in nature. ONBs are effective in trigeminal pain involving the second and third branch and seem to be most effective in craniofacial neuralgias. They should be considered in facial pain before more invasive approaches, such as thermocoagulation or vascular decompression, are performed, given that side effects are mild and the procedure is minimally invasive.