Nutrient-based diet modifications impact on the gut microbiome of the Javan slow loris (Nycticebus javanicus).

Environment and diet are key factors which shape the microbiome of organisms. There is also a disparity between captive and wild animals of the same species, presumably because of the change in diet. Being able to reverse the microbiome to the wild type is thus particularly important for the reintroduction efforts of Critically Endangered animals. The Javan slow loris (Nycticebus javanicus) is a suitable model, being kept in the thousands within rescue centres throughout Southeast Asia. With next-generation sequencing, we show how a naturalistic diet impacts the gut microbiome of captive slow lorises (Primates: Nycticebus). A comparison of the microbiome of wild animals with captive animals that had been fed a standard captive or improved diet reveals strong microbiome differences between wild and captive animals; however, diet changes failed to alter the microbiome of captive populations significantly. Bifidobacterium was the most abundant genus in wild animals (46.7%) while Bacteroides (11.6%) and Prevotella (18.9%) were the most abundant in captive animals fed the captive and improved diets, respectively. Correlation analyses of nutrients with microbial taxa suggest important implications in using nutrition to suppress potential pathogens, with soluble fibre and water-soluble carbohydrates both being associated with opposing microbiome profiles. The improved diet significantly increased microbe diversity, which exemplifies the importance of high fibre diets; however, wild individuals had lower diversity, which contradicts recent studies. Detection of methanogens appeared to be dependent on diet and whether the animals were living in captivity or in the wild. This study highlights the potential of nutrition in modulating the microbiome of animals prior to release. Unexpectedly, the results were not as significant as has been suggested in recent studies.

Genetic Susceptibility Contributing to Periodontal and Cardiovascular Disease.

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.

Occipital nerve block is effective in craniofacial neuralgias but not in idiopathic persistent facial pain.

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.

Effect of non-working occlusal contacts on vertical condyle position.

The presence of non-working occlusal contacts is often considered harmful for the temporomandibular joint. Thus, the purpose of this study was to investigate the effect of non-working occlusal contacts on the condylar position during submaximal and maximal clenching. The study comprised 22 healthy subjects having a canine-guided occlusion. None of them had a third molar and none of them had a missing tooth or showed tooth mobility. All subjects clenched on (i) the canine, (ii) the canine while a stiff bite registration material was positioned between the second premolar and the first molar on the non-working side. The clenching level was controlled by surface electromyography of the masseter muscle. During clenching, the vertical and horizontal condylar position was predicted using six degrees of freedom ultrasonic motion analyser. Clenching on the canine caused a cranial movement of the non-working side condyle. This movement was reduced by 0.6-0.9 mm when the subjects clenched while the artificial non-working side contacts were in place. These results indicate that the contacts on the non-working side may be able to prevent upward joint movement.

A mutation in the enamelin gene in a mouse model.

Amelogenesis imperfecta is an inherited disorder affecting tooth enamel formation. We previously isolated a mouse strain with an amelogenesis imperfecta phenotype (ATE1 mice) from a dominant ethylnitrosourea screen and mapped the disease-causing defect to a 9-cM region of mouse chromosome 5. In the current study, we tested the hypothesis that there is a mutation in enamelin (ENAM) or ameloblastin (AMBN), both of which are located within the linkage region, by sequencing these two candidate genes. Analysis of our data shows that the amelogenesis imperfecta phenotype is linked to a C > T transition in exon 8 of the enamelin gene. The mutation predicts a C826T transition, which is present in the enamelin transcript and changes the glutamine (Gln) codon at position 176 into a premature stop codon (Gln176X). Conversely, no mutation could be detected in the ameloblastin gene. These results define the ATE1 mice as a model for local hypoplastic autosomal-dominant amelogenesis imperfecta (AIH2), which is caused by enamelin truncation mutations in humans.

Pivot appliances - is there a distractive effect on the temporomandibular joint?

The purpose of this study was to investigate the distractive effect of posterior occlusal pivots on the temporomandibular joint. The study comprised 23 healthy subjects. None of them had a third molar and none of them had a missing tooth or showed tooth mobility. All subjects clenched (i) on 1 mm tin foil positioned between the teeth 17/47 and 27/37; (ii) on a stiff bite registration material of 1 mm thickness that prevented protrusion because of its bold occlusal relief. During clenching on the tin foil and on the protrusion preventing bite registration material, respectively, the vertical and horizontal condylar position was measured using a 6 d.f. ultrasonic motion analyser. Clenching with maximal force on the tin foil lead to a noticeable anterior downward directed movement of the condyle. Clenching on the protrusion preventing pivot, however, caused a statistically significant upward condylar movement of about 0.3 mm. These results indicate that occlusal pivots have no distractive effect on the temporomandibular joint but can lead to unwanted joint compression, if they are designed in a way that is preventing protrusion.

[Otalgia as a result of certain temporomandibular joint disorders]. / Otalgien als Folge bestimmter kraniomandibulärer Dysfunktionen.

INTRODUCTION: Different hypotheses of reasons for common incidence of temporomandibular disorders (TMD) and otalgia have been discussed. The hypothesis of this study was, that the high prevalence of otalgia in patients with TMD may result in part from pain in the M. masseter pars prof. or in the temporomandibular joint (TMJ) which, due to the close anatomic neighborhood, can feel like ear pain. MATERIAL AND METHODS: [corrected] We retrospectively analyzed the anamneses of 720 of our TMD-patients with regard to main treatment motivation: how many patients quoted "pain in the ear" as main treatment motivation and how many of them had no objective findings in the ear but muscle tenderness of the M. masseter prof. or objective findings in the TMJ. Using all pairwise multiple comparison procedures (Dunn's Method) we compared the frequency of muscle and joint findings in patients with ear complaints to two controls: Tinnituspatients and patients seeking orthodontic treatment. RESULTS: 51 of 720 patients quoted ear pain as main treatment motivation. 25 of them (49 %) had findings in the masseter muscle, 9 (18 %) in the joint and 15 (29 %) had findings in both the joint and the muscle. The frequency of findings in the controls was significantly (p < 0.001) lower. CONCLUSION: A significant fraction of patients seeking treatment due to pain in the ear have no findings in the ear, but in the TMJ and in the masseter muscle.

[Influence of botulinum toxin on myogenous facial pain]. / Beeinflussung muskulärer Gesichtsschmerzen durch Botulinumtoxin A.

OBJECTIVE: Can chronic pain of the masticatory muscles be positively affected by low dose injection of botulinum toxin (BTX-A)? METHODS: Twenty patients suffering chronic myofacial pain were questioned and examined after injection of 25-50 U Dysport into the affected muscles over a period of 8 weeks. RESULTS: Four weeks after injection of BTX-A patients reported a significant reduction of pain (p <0.001, paired t-test. Power of performed test with alpha 0.050:1.000). Then the pain remained constant over the next 4 weeks. Concurrently a significant increase of mandubular range of movement was observed (p <0,05, Wilcoxon signed rank test). CONCLUSIONS: Even though lacking placebo control the findings suggest that patients suffering chronic myofacial pain may benefit from injection of low dose BTX-A into the affected muscles.

Amelogenesis imperfecta in a new animal model--a mutation in chromosome 5 (human 4q21).

Candidate genes for amelogenesis imperfecta (AI) and dentinogenesis imperfecta (DI) are located on 4q21 in humans. We tested our hypothesis that mutations in the portion of mouse chromosome 5 corresponding to human chromosome 4q21 would cause enamel and dentin abnormalities. Male C3H mice were injected with ethylnitrosourea (ENU). Within a dominant ENU mutagenesis screen, a mouse mutant was isolated with an abnormal tooth enamel (ATE) phenotype. The structure and ultrastructure of teeth were studied. The mutation was located on mouse chromosome 5 in an interval of 9 cM between markers D5Mit18 and D5Mit10. Homozygotic mutants showed total enamel aplasia with exposed dentinal tubules, while heterozygotic mutants showed a significant reduction in enamel width. Dentin of mutant mice showed a reduced content of mature collagen cross-links. We were able to demonstrate that a mutation on chromosome 5 corresponding to human chromosome 4q21 can cause amelogenesis imperfecta and changes in dentin composition.

Impact of posterior occlusal support on the condylar position.

The purpose of this study was to investigate condylar displacement related to the loss of posterior occlusal support. Each of 23 subjects received one occlusal adjusted splint that covered all teeth from the right to the left second mandibular molar. None of the subjects had a third molar and none of them had a missing tooth or showed tooth mobility. The splint was inserted and vertical and horizontal condylar position was measured by an ultrasonic motion analyser. The splint was then unilateraly shortened tooth-by-tooth up to the canine tooth and the measurement was repeated after each shortening. Cutting off the splint's second molar on one side lead to a slight ipsilateral cranial motion of the condyle if subjects clenched with maximum voluntary force. If the second and first molar were cut off, a noticeable cranial condylar movement of about 0.3 mm was observed even when teeth occluded with low force. These results suggest that loss of posterior occlusal support as it happens in routine oral rehabilitation leads to a noticeable cranial condyle movement during registration, even if the clenching force is low.

[The "Costen Syndrome" - Which Symptoms Suggest that the Patient may Benefit from Dental Therapy?]. / Das "Costen Syndrom" - welche Befunde lassen aus HNO-ärztlicher Sicht die Zusammenarbeit mit einem Zahnarzt sinnvoll erscheinen?

INTRODUCTION: Since the thirties the hypothesis of a direct connection between temporomandibular disorders (TMD) and tinnitus/otalgia has been discussed. The thesis of this possible connection is often named after one of the earliest and most vehement supporters as "Costen Syndrome". This review is aimed to elucidate the present state of the discussion from the Dentist's point of view. DIAGNOSIS/EPIDEMIOLOGY/THERAPY OF TMD: Diagnostic research criteria which define TMD are not standardized. Despite high prevalence and strong demand for treatment of TMD there is still a lack of a commonly accepted standard therapy and the potential benefit from a therapeutic point of view is still controversial. TMD AND TINNITUS/OTALGIA:: Concurrence of TMD and tinnitus by a common underlying cause is still unproven. By contrast a causal link between certain forms of TMD and otalgia is obvious. CONCLUSION: A lack of clear definitions and standards for the diagnosis of TMD is the main hinderance to prove a causal relationship especially between TMD otalgia. However patients seeking care for otalgia with no identifiable otologic cause may benefit from dental therapy. Therefore future studies should focus on well defined subgroups of TMD to investigate a link between otalgia/tinnitus and TMD.