Epigenetic Orthodontics–Optimising Genetic Potential

   

Andrew Bachour^*

Student, Jaume I University, Brisbane, Australia

^*Corresponding author: Bachour: Andrew Bachour, Student, Jaume I University, Brisbane, Australia. 

Citation: Bachour A. (2023) Epigenetic Orthodontics-Optimising Genetic Potential. J Oral Med and Dent Res. 4(1):1-19.

Received: May 10, 2023 | Published: May 31, 2023

Copyright© 2023 genesis pub by Bachour A. CC BY-NC-ND 4.0 DEED. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non-Commercial-No Derivatives 4.0 International License., This allows others distribute, remix, tweak, and build upon the work, even commercially, as long as they credit the authors for the original creation.

DOI: http://doi.org/10.52793/JOMDR.2023.4(1)-33

Abstract

The field of epigenetics has really come to fruition this century thanks to advances particularly in science and technology. Genetics had taken off in 1865 with Gregor Mendel’s genetic laws. The rise of epigenetics was really a consequence of the Human Genome Project carried out in the late twentieth century, a project dedicated to map the entire human genome. Initial completion took place in 2003 where approximately ninety percent of the genome had been mapped, and 2022 saw the ultimate completion of this project.

Introduction 

A total of 22300 genes had been mapped out, including a large quantity of near identical repetitive segments. This was completely unexpected, initial estimates were estimating at a very minimum four times the number of genes, and likely more to explain the variation we see in the population. Additionally, of these 22300 mapped genes between humans, shows 99.9% of the sequence are identical. The variations we see amongst our species far exceeds what is possible by differences in these genes alone, and thus, the age of epigenetics was truly born. Figure 1 is a great graphic to help visualise the rapid change in epigenetics research from initial completion of the Human Genome Project [1-5]. 

Figure 1: Frequency of articles published against time with “epigenetics” in the title [5].

The term epigenetics was coined in the mid twentieth century by embryologist Conrad Waddington and broken down to mean ‘epi’ (above) and ‘genetics’ (gene), implying control from above the gene, as illustrated in Figure 2. We understand the genome to be our genetic blueprint, the sequence of our genes and what they do. Our epigenome on the other hand refers to how those genes are regulated. In this rapidly evolving field, many ideas or definitions are constantly superseded as our understanding grows. Currently, a widely accepted view is that epigenetics refers to mechanisms altering the phenotype or gene expression of an organism (structural and/or biochemical) without any modification of the genetic blueprint itself. This change is inheritable and may be either physiologic or pathologic [1,6].

Through years of research, we now understand the stable nature of the genome, its sequence, its heritability, and in particular, its resistance to both change and reversibility. This is in contrast to the epigenome, which is found to be highly dynamic, controlling the expression of the genome, its heritability, highly reversible nature and ability to change in response to the surrounding environment. A summary of this can be visualised in Figure 3 [8,9]. 

Figure 3: Genetics vs Epigenetics [8,9].

We see this everywhere in the world around us. Figure 4 is one example of this concept, where each of the four Asian rhinoceros beetles of the same species shown, appear different (body size and horn length). These changes are found due to the amount and quality of food available during their early developmental stages of life (5). 

Figure 4: The Asian Rhinoceros Beetle, Trypoxylus dichotomus [5]. 

We see obvious changes of epigenetics in actions in ourselves. Spending time in the sun will causes melanocytes to increase their production of melanin, aiding in our protection from solar radiation. Consumption of alcohol will stimulate your body to produce more enzymes such as alcohol dehydrogenase to help clearance, Figure 5. We understand neuroplasticity, the re-organisation of our neuronal network due to environmental influences. All cells in our body have the same genetic code, yet are expressed differently, we have different cells in our body such as neurons, glial cells, osteoblasts, erythrocytes, melanocytes, adipocytes to name just a few. Without this ability to for these cells to differentiate from one another with respect to both their function and their identity, we as a species would not exist. This is the essential nature of the epigenome (10). 

Figure 5: The liver responding to consumption of alcohol through epigenetic signaling [7].

 

Epigenetic Coding Mechanisms 

When thinking of the genome and the epigenome, we need to think as if they are two distinct sets of codes. In a way the genome may be thought of as computer hardware (stable in configuration) while epigenome as the software which is running everything and constantly changing through updates. We understand the genome to be the sequence nature of deoxyribonucleic acid (DNA), nucleotide bases (adenine, cytosine, guanine, thymine) paired together to ultimately form a double helix structure. So what does the epigenome look like?  

The epigenome can appear either as 

- Chromatin marking 

- Three dimensional structures or templates 

- Self-sustaining metabolic loops 

- Non-coding ribonucleic acid (RNA) 

Chromatin marking and such as DNA methylation or histone modification and RNA interference are some of the most well studied of the epigenetic mechanisms. Chromatin marking may involve methylation (addition of CH3 methyl group) added to cytosine bases through the enzyme DNA methyltransferase and generally acts to silence the gene, that is to shut down transcription of the gene. The essential nature of this was demonstrated in 1992 by Rudolf Jaenisch et al, pictured in Figure 6. The research team was able to prove the importance of this through inducing a mutation of the gene encoding for DNA methyltransferase. This mutation was shown to be lethal to the embryo (11).