Month: July 2015

Diabetes & Periodontitis – A Deadly Combination

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People are unaware that diabetes mellitus, either type 1 or type 2, goes hand in hand with increased susceptibilities to oral health problems. Even diabetics themselves know little about the risks of bacterial infections such as Porphyromonas gingivalis, a primary cause of periodontitis; the correct term for gum disease. Although P. gingivalis is not normally found in subjects with good dental health, the presence of other bacteria is far more common. Streptococcus mutans and Streptococcus gordonii are both found within the oral setting and form biofilms on the tooth surface. Regular brushing and flossing removes these unwanted visitors but if the accumulated bacteria remain undisturbed for a long period of time they can begin to destroy the gum tissue surrounding the teeth. Interestingly this is where the P. gingivalis comes in. A shift in normal ecological balance in the microenvironment allows the bacteria to act as a secondary invader of the gums, and more specifically the gingival sulcus, the part where the tissue contacts the tooth. Colonisation of P. gingivalis arises via its ability to adhere to salivary molecules, matrix proteins in the gum and other bacteria present in the mouth. It is clearly an opportunistic pathogen.

Figure 1 - P.gingivalis: a dental nightmare
Figure 1 – P.gingivalis: a dental nightmare

So, why do diabetics have an increased risk of developing periodontitis? Well, Advanced Glycation End Products (AGEs) arise from chronic hyperglycaemia and therefore are common in diabetes. It is these glycated proteins or lipids which have been shown to impact on periodontal deterioration. Although the exact mechanism behind the interactions of AGE with the disease are unknown there is general consensus suggesting a couple of important points;

  • An accumulation of AGEs affects the host immunological response. The products can disrupt an important nuclear transcription factor called NF-κβ, one which is involved in many inflammatory responses. IL-6 and TNF-α are also just two important pro-inflammatory cytokines which have been shown to be upregulated in the presence of AGEs.
  • AGEs will not only upregulate the production of certain cytokines, they also affect the chemotactic properties of mono and polynuclear cells. This enhances the inflammatory response at a given site of infection, in this case at the gums and surrounding tissue.

One final problem in diabetic patients is a drop in salivary pH. Xerostomia, or hypo-salivation is a main cause of the low pH. Maintaining the correct level of fluid in the body perhaps is the greatest problem for individuals with diabetes mellitus. The presence of AGEs and glycated haemoglobin, the latter being another result of high blood sugar levels, disrupts the balance of fluid and electrolytes in the blood stream. Diabetes is a condition that is associated with polyuria (frequent urination), which occurs because the excessive glucose found in the blood changes the normal osmolarity gradient within the body. Simple GCSE Biology states that water will move from an area of high concentration to low concentration. Therefore the increased movement of water into the bloodstream will effectively force the kidney to produce more urine. It’s a vicious cycle – high glucose levels mean more urine produced, causing the person to become dehydrated which leads onto hypo-salivation, leaving an environment perfect for bacterial infection.

Figure 2 - Periodontitis - A problem for all, but one that is more worrying for diabetics
Figure 2 – Periodontitis – A problem for all, but one that is more worrying for diabetics

The low pH and reduced salivary rate contributes to an increase in tooth decay and as a consequence bacterial/fungal infections are more common in individuals with diabetes mellitus. This is because most oral bacteria and yeast thrive in the acidic conditions of the mouth, the reason why dental experts warn against sugary diet rich in carbohydrates – the main source of food for all mouth dwelling species. This is an alarming problem for experts and scientists worldwide, with an estimated 1 in 3 individuals with either form of diabetes mellitus having some degree of periodontitis during their lifetime. Of course the deterioration of dental health concerns everybody, but more attention must be paid to those that are at a higher risk. Managing the condition as a whole will pay dividends but are there any further precautions which should be taken to preserve the oral wellbeing for diabetics? This remains the most difficult question. Antimicrobial management and regular periodontal treatment is common in the general population, but both should be more prevalent in controlling diabetes related infections.

This post, by author Jason Brown, was kindly donated by the Scouse Science Alliance and the original text can be found here.

References
Goyal, D. et al (2012) Salivary pH and Dental Caries in Diabetes Mellitus. International Journal of Oral & Maxillofacial Pathology. 3(4):13-16
Griffen, AL. et al (1998) Prevalence of Porphyromonas gingivalis and Periodontal Health Status. J Clin Microbiol. 36(11):3239-3242
Lamont, RJ. Jenkinson, H. (1998) Life Below the Gum Line: Pathogenic Mechanisms of Porphyromonas gingivalis. Microbiol. Mol. Biol. Rev. 62(4):1244-1263
Takeda, M. et al (2006) Relationship of Serum Advanced Glycation End Products with Deterioration of Periodontitis in Type 2 Diabetes Patients. J.Periodontol. 77(1): 15-20.

Research provides a window into the depressed mind – but could this really help to improve the view from the inside?

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4241963210_f11f639bed_zThe science blogosphere has been awash this past week with articles exploring a link between depression and damage to part of the brain known as the hippocampus. News outlets, such as IFLS, are claiming that: “Depression Damages Parts of the Brain”. But, where does this assertion come from, is it really so cut and dry, and what impact will this research have on those currently living with major depression?

Firstly, as with many science news stories, the ideas discussed here are far from a new. What is new and exceptionally clever, is the way this study was performed:

As you might imagine, imaging the living brain is not an easy task and different researchers tackle this problem in different ways. This means that data analysis and imaging methods can vary a lot between research groups. Sadly, this lack of standardisation makes it hard to compare data across different studies, which limits the number of patients each study can look at. This is where this new work really shines. Through a massive international collaborative effort, this study has been able to standardise imaging protocols across a number of international labs. The study examines data from a whopping 1728 major depression patients and 7199 healthy controls, meaning that statistically these findings really pack a punch.

Their findings corroborate what other researchers already suspected – that recurrent depressive episodes seem to be accompanied by shrinking of a brain region known as the hippocampus. The hippocampus is best known for its role in memory formation, specifically in the conversion of new experiences to permanent long-term memories (think 50 First Dates or Memento). This region is arguably also integral to our sense of self. Without memories of our pasts how do we know who we are or what we want for the future? So, hippocampal damage could hold far reaching implications beyond that of simple memory loss and perhaps even contribute to many aspects of depression.

Now, the question scientists really want to answer is – what happens in the brain to cause depression? This study finds that hippocampal shrinkage is only significant in patents who have suffered from multiple depressive episodes, while patients who have only experienced a single episode have relatively normal hippocampi. This suggests that depression causes hippocampal shrinkage, rather than hippocampal shrinkage leading to depression.

Could this mean that we need to look beyond this brain region for the cause of depression?

Human hippocampus MRI in 3 different planes (marked by green cross)
Human hippocampus MRI in 3 different planes (marked by green cross)

It’s necessary to keep in mind that this work is not conclusive and may only represent part of a bigger picture. Large scale changes in the brain’s morphology, visible on MRI brain scans (as studied here), indicate significant cell loss. It is quite reasonable to assume that in the early stages of major depression, as with many long-term illnesses, changes in the body/brain may be more subtle – think alterations in brain chemistry and communication rather than large scale cell loss. So, although it’s useful to know that major depression can lead to hippocampal cell loss, we cannot yet rule this region out as a main player in the early stages of depression.

But, most importantly, will this research change anything for the >350 million people suffering from depression worldwide?

Well, actually this work feeds rather nicely into another hypothesis of depression known as ‘the neurotrophic hypothesis of depression’. In brief: It is known that stress and depression cause cell loss in limbic brain regions (including the hippocampus). Neurotrophic factors are proteins in the brain which encourage cell growth and multiplication, these are depleted in depressed patients and animal models of the disorder (often specifically within the hippocampus). Some scientists believe that a reduction in neurotrophins, such as BDNF (Brain Derived Neurotrophic Factor), begins a cascade which ultimately leads to cell damage and death. Therefore, it is possible that repeated episodes of major depression cause an additive loss of BDNF and perhaps subsequent hippocampal damage. Interestingly, a number of studies also suggest that antidepressants may increase BDNF in depressed patients, suggesting the effects of depression on the brain may be reversible.

So, it seems that when it comes to depression, scientists are slowly piecing together large parts of the puzzle. Although many uncertainties still exist (the brain is a tricky organ to understand), with continued research it is hoped that better treatments may be just around the corner.

Post by: Sarah Fox

Why do mangos taste like pines?

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4818759374_29e1e0a716_qHaving grown up in a South Eastern European country, where fruits are abundant and make up probably about half of our diet during the summer, I’m used to many different kinds of fruit. However, a banana was probably the most exotic fruit that I came across until the age of about sixteen.  So, I was pretty intrigued when a couple of months ago a friend of mine bought a mango for us to try. We googled ‘how to eat a mango’, cut it into those cute hedgehogs like they do and tasted it. But, since neither of us had ever tried this fruit before, we didn’t realise that it wasn’t ripe, so the taste was far from nice. Except for the part just around the pit it was like chewing on pine needles. Since then I have learned how to pick more or less ripe mangos and developed quite a taste for them but, I still can’t help noticing a hint of pine in the flavour. Every time this makes me ask myself, what is it that makes two plants that are so different in terms of their habitat and their taxonomic position taste or smell similar?

To get to the bottom of this lets start by looking at how the sense of taste operates and how it is linked to the sense of smell. The flavour of our food is determined by these two senses
combined: try holding your nose whilst eating, you’ll find even familiar foods don’t taste right. Our tongue, the roof, sides and the back of our mouth are covered with taste buds – small receptors sensitive to so called flavorants. The receptors that allow us to detect and recognise odors are somewhat similar to these taste receptors. The two systems rely on chemoreception, which means that the receptors involved are able to capture the chemical compounds that make up a certain smell or taste and transform this information into a nerve impulses in the brain. Information regarding both taste and smell combine in your brain allowing you to enjoy a multi-sensory flavour experience.

4402795295_013a780bbb_zNow back to the mango/pine problem. I decided to start my investigation by finding out what chemicals produce the familiar smell of pine. A quick trip to the nearest pharmacy and a scan through the ingredients of pine-scented essential oils revealed that the main components were: α-pinene, β-pinene, limonene, myrcene, camphene cadinene with very little variation from one brand to another. These compounds belong to a larger group known as terpenes, or more precisely monoterpenes, which are most commonly, but not exclusively, found in the resin of coniferous trees.

More than thirty different chemicals make up the flavour of mango and, surprisingly enough, α-pinene, β-pinene, limonene, myrcene and camphene are among them. So, five out of six compounds that are found in pine needles are also found in mango pulp.

Due to their strong smell, high viscosity and antiseptic properties, terpenes act as a repellent that drives away herbivores and insects, thus protecting the plant from predation. The native land for mangos is South and South East Asia and, while there are several varieties of pines that grow in the same part of the world, these plants are only distantly related. Pines are gymnosperms – even though they produce seeds, they develop neither a flower nor a fruit. Mangos on the other hand are flowering plants. From an evolutionary point of view they are considered to be more advanced than gymnosperms since they have flowers that facilitate pollination and their seed is protected by a fruit. Flowering plants diverged from gymnosperms more that 200 million years ago. So how did such different plants develop such a similar defense mechanism?

The first thing that pops to mind is convergent evolution. It is very common in nature for different animals which occupy very different habitats and never even come near each other to develop similar adaptations when faced with a similar obstacle. A classic example is the structure of an eye of vertebrates (e.g. mammals) and cephalopods (e.g. octopus): both these groups have independently developed camera eyes astonishingly similar in their structure and way of functioning. Therefore, an efficient system is very likely to develop in parallel across unrelated species.

So, in the case of pines and mangos, terpenes provide not only a reliable defense against predators but also a mind-bending taste anomaly.

Guest Post by: Daria Chirita.

unnamedOriginally from Moldova, I am currently in my second year at university in France, Université Jean Monnet , St Etienne, studying Biology. My scientific interests include Molecular Biology and Genetics, in which I am hoping to pursue a Master’s degree. Other than that I enjoy learning and speaking foreign languages, knitting and cinema.