Most dentists and orthodontists are aware of the impact that mouth breathing has on the development of the maxilla. Most are also aware of the fact that even after successful realignment of teeth, unless a retainer is used, relapse usually occurs.

The tongue is nature’s retainer and at the lateral force exertion of 500 Gm provides the balance required against the inward force pull of the cheek muscles, at also around 500 Gm.
In an ideal world, these two forces would balance each other and normal maxillary development would take place. The primary teeth would erupt smoothly and evenly and even in the mixed dentition stage there should not be overcrowding or malalignment of teeth. So what causes mouth breathing to occur and what can be done about it? The answer to this lies in the basic physiology that we all studied during the early part of our careers.
At the time we learned it we were not able to see its overall importance as we had yet to study the full gamut of anatomy and physiology to see how it all inter-related. By the time this happened we had forgotten most of it. So it should not come as any surprise that the information that follows will certainly strike a chord and probably elicit the usual comment “But I knew that!”

Snoring

Snoring is essentially the movement of too much air over the loose tissue at the back of the throat, causing it to rattle. Usually accompanied by open mouth breathing it perpetuates the loss of CO2 and maintains the dysfunctional breathing pattern. In many cases, teaching the patient to reduce the breathing rate and to sleep with closed mouth virtually eliminates the problem.

Sleep Apnea

Sleep apnea is a little different in that it is in many cases caused by a disruption of the pH of the blood due to the decrease in CO2. This causes the blood to become too alkaline leading the brain to think that the body cells are in danger of dying (which they are). The brain’s response to this is to suppress breathing for sufficient time for the CO2 level to rise, for more carbonic acid to be produced to buffer the blood and remove the danger to the cells. Once this has been achieved the signal to breathe is again given.

However, in the case of sleep apnea the ensuing breath is a large gasp and this lowers the CO2 levels again to danger point. This is why sleep apnea is characterised by a pause-gasp cycle which can occur up to 20–50 times an hour. In most cases this can be controlled by restoring CO2 levels to normal, ensuring that the pH integrity is maintained and the need to stop breathing is then removed.

Restoring nasal breathing as the norm

The good news is that it is possible to reverse this situation and re-create functional breathing. This requires several steps which begin with identifying the cause of the original problem.

Unless this is done, and the habit modified, relapse is a real fact of life. It is also necessary to address the breathing mechanics and dynamics so that the optimal levels of retained CO2 can be restored. The moment this happens the medullary response recognizes that retained CO2 levels have risen and starts to re-set the response to the appropriate level.

source: www.dentalnews.com

Background: There is conflicting evidence regarding the association between vitamin D and periodontal disease. The purpose of this study was to explore that relation.

Methods: This cross-sectional study used data from the Canadian Health Measures Survey for respondents 13–79 years of age. Vitamin D status was determined by measuring plasma 25-hydroxyvitamin D (25(OH)D) concentrations. Periodontal disease was defined by gingival index (GI) and calculated loss of attachment (LOA). Statistical analyses included bivariate tests and multiple logistic regression.

Results: At the bivariate level, 25(OH)D concentrations below the cutoff levels of 50 nmol/L and 75 nmol/L were associated with GI. However, multiple regression analyses for GI revealed no association with mean 25(OH)D level or either concentration. Although no significant association between LOA and 25(OH)D status was identified at the bivariate level, a statistically significant association was observed between LOA and 25(OH)D levels < 75 nmol/L on multiple regression analysis. However, mean 25(OH)D concentrations and those < 50 nmol/L were not associated with LOA on multiple regression analysis.

Conclusion: Vitamin D status was inversely associated with GI at the bivariate level, but not at the multivariate level. Conversely, vitamin D status was not associated with LOA at the bivariate level, but it was inversely associated with LOA at the multivariate level. These results provide modest evidence supporting a relation between low plasma 25(OH)D concentrations and periodontal disease as measured by GI and LOA.

Chronic periodontitis is an inflammatory condition of the periodontium initiated by microbial biofilms that form on the teeth.1Bacterial products, as well as the host’s immune response to these products, result in destruction of the tissues that support the teeth, including alveolar bone. Because of this tissue destruction, chronic periodontitis is a major cause of tooth loss in adults.2,3 Prevention of this disease is important because tooth loss can affect one’s nutritional status4 and quality of life.5 Chronic periodontitis has also been associated with systemic conditions, such as cardiovascular disease6 and type II diabetes mellitus.7

Vitamin D is a fat-soluble vitamin obtained from exposure to sunlight, diet and nutritional supplements.8 Vitamin D is metabolized in the liver to 25-hydroxyvitamin D (25(OH)D) and then metabolized in the kidneys to its active form, 1,25-dihydroxyvitamin D (1,25-(OH)2D).8 As the major circulating metabolite in the blood, 25(OH)D is used to determine a patient’s vitamin D status.8 Although there is no consensus on optimal levels of 25(OH)D, most experts define < 50 nmol/L (20 ng/mL) as vitamin D insufficiency.8 Recent evidence suggests that 25(OH)D levels may need to be as high as 75 nmol/L (30 ng/mL) to achieve optimal vitamin D status.8

Vitamin D is involved in regulating calcium absorption from the intestines, maintaining plasma calcium concentration and bone mineralization.9 Studies have found significant positive associations between 25(OH)D levels and bone mineral density10 as well as between vitamin D supplementation and a lower risk of fractures.11

More recent evidence indicates that vitamin D also has a regulatory effect on the immune response, stimulating immune response at times, while inhibiting it at others. One study12 demonstrated that increased production of the antibacterial proteins cathelicidin and beta-defensins followed exposure to antigens. The authors concluded that the ability to produce active vitamin D improved bactericidal activity. There are many examples of vitamin D’s ability to inhibit the immune response. In vitro studies have shown that 1,25-(OH)2D inhibits the proliferation, maturation and differentiation of dendritic cells from monocytes.13 The active form of vitamin D also inhibits the production of inflammatory cytokines in monocytes.13 Some studies have also reported that 1,25-(OH)2D has the ability to suppress the proliferation and cytokine production of T-lymphocytes.13

Because chronic periodontitis is characterized by bone loss triggered by a host immune response reaction to bacterial plaque, vitamin D deficiency may have an effect on the development and progression of periodontal disease.14-19 Two large cross-sectional studies14,15,17 have found an association between low vitamin D levels and markers of periodontal disease. However, the largest prospective study to date,19 as well as the most recent cross-sectional study,20 found no relation between these two entities. It is clear that further research is needed to determine what impact vitamin D status has on the progression of periodontal disease. The aim of this study was to explore the relation between 25(OH)D concentration and periodontal disease measured by gingival index (GI) and loss of attachment (LOA) using data derived from the Canadian Health Measures Survey (CHMS).

source: www.dentalnews.com

3D printing is still considered to be a possible “game changer”: New treatment methods, new forms of team work, new business models. Dentistry is one of the pioneers. The current opportunities for the practice and laboratory are within grasp – at the International Dental Show, 12 to 16 March 2019, in Cologne.

According to a current analysis, the worldwide market for 3D printing products in the industry is estimated to grow by between 13% and 23% up to a volume of Euro 22.6 billion by 2030.

Specifically in the medical technology sector it is estimated to increase from Euro 0.26 billion (status: 2015) up to Euro 5.59 billion (2030).

According to the estimations of the experts, the development will occur in two phases: primarily the “reinvention” of existing products up until around 2020, then increasingly innovative materials and optimised printing methods. In the industry comparison, 3D printing is experiencing the strongest growth in the medical and dentistry sectors. Hence the dentists, dental technicians and the dental industry are taking on a natural pioneer role.

The printing of bases using the laser-controlled method has long since established itself, whereas dental models are made out of plastic for instance. Market researchers see the biggest opportunities for orthodontic appliances, prostheses, crowns, bridges, aligners and models. Wide sections of which have in the meantime become areas of application in the laboratory and practice.

This manufacturing process continually attracts special attention with spectacular applications. For example, in the prophylaxis segment an individualised, 3D imprinted dental floss holder is one of the advanced developments.
Vivid images prove effective for the communications. A digitally modelled smile agreed upon together with the patient serves here as the template for an imprinted 3D model, this is in turn used to produce a negative of the patient’s teeth in a silicone key and ultimately a thin “veneer simulation” of the actual restoration for an initial aesthetic check in the patient’s mouth.

A robot also managed to implant two 3D imprinted teeth into a patient’s mouth. And to reproduce the original form of the jaw after removing oral tumors, the defect can be scanned today and a template produced using the 3D printing method.

This serves to extract a precisely matching block of bone from another part of the body (i.e. calf) which is subsequently fitted into the mouth – for the patient this is approx. an eight hour “all-in-one OP”.
Talking about 3D printing in the singular form seems to be an under exaggeration today – there are namely so many different methods meanwhile. These include the stereolithography with a precision degree in the lower two-digit micrometre area, which is suitable for instance for drilled templates and which can be used for a wide range of resins in the dentistry sector.

Furthermore, the DLP method is also available: It excels because it is extremely fast because due to the one-time exposure (instead of a dancing laser beam) the respective next layer of the object hardens as quick as lightening. The polyjet method attains an extremely high degree of precision (16 micrometres). It functions most similarly to the familiar office printer and doesn’t require support constructions and material post-processing.
From plastic to metal imprints: Here one is familiar with selective laser melting, selective laser sintering (SLS), direct metal laser sintering (DMLS) or lasercusing: The crowns, bridges and denture bases (“digital model casting bases”) are made out of non-precious metal dental alloys or titanium.

source: www.dentalnews.com