Education – Keeping Australian Dentists in the Loop

What’s the story with gaggers? – The Dental Review

Sam Khoury — Mon, 16 Feb 2026 14:24:25 +0000

How often does a dentist start to tackle a tooth – maybe cracked, but otherwise intact and needs to take a PA xray? But then the patient gags!

Foul thoughts abound and repeated efforts often just make things worse. But maybe it’s time to understand a little more about this important reflex and what it is signalling.

What is gagging? It’s an oral airway protective reflexive response. So why is this important?

The short answer is that it’s signalling the brain’s displeasure of having already lost the ability to nose breathe the impending loss of the oral airway is alarming and it puts measures in place to rectify this situation.

This poses a deeper question – that of what does it mean for a dentist. The answer is often subtle and complex, as all things can be, but as a simple person, I look at life as simply as possible. Simply – if you don’t breathe you die! Then there are all the in-between ranges of airway impairment and the degrees of oxygen saturation. For example where the levels drop slightly in the brain and then recover (Dipping) there is remarkably high adverse inflammatory reaction seemingly out of proportion to the change. But there is less response where the person simply stops breathing for half a minute with greater drop in brain oxygen. Gozal (1) showed the exhaled breath of non-obese snoring 3 year olds has about as many inflammatory chemicals as an adult who recently had a cardiac whereas those who did not snore were near-clean. As most pathology involves inflammation this is a biggie.

How does all this relate to gagging you ask – well hopefully you do ask.

My reading and research of hundreds of cases shows that the underlying cause/s are linked to societal changes. These rose sharply in the second half of the 19^th Century and seem to have peaked in the late 20^th Century. The increase in sugar consumption and in tobacco with their commercialisation in the Caribbean and Southern USA at the turn of the 19^th C. UK sugar levels rose from Shakespeare’s time at around 1lb (500 grams) and seems to have plateaued or peaked in the mid 1990’s at over 200lbs. Sugar is involved in most consumables – even toothpaste. Sugar appears with three ‘friends’ that act epigenetically by inducing HOX genes that in turn dampen the actions of neural crest cells – the fringes of the embryological foetus before the neural plate curls into the neural tube. French and Belgium teams in the 1990’s showed that these factors (sugar – smoking- alcohol and probably maternal sleep fragmentation) combine to impair the midface growth leading to a narrow and ‘shortened’ naso-maxilla. (2-7). This was first signalled in the dental context by Harvold (8-13) as an entity when he blocked one nostril in infant monkeys and induced asymmetrical growth. Equally the lower jaw is generally less impacted with resulting mandibular entrapment and being forced backwards, carrying the tongue into the throat.

These combined mean the nose is frequently out of action and this is noted in some general medicine with people such as Prof Dr. Christian Guilleminault and his request that all dentists ensure 100% nasal breathing – Prof Dr. Giles Lavigne who warns that stopping the dental effects of bruxing with a night-guard may exacerbate the very cause, which is the same as gagging – that is alterations in breathing patterns with gas-levels changing leading to arousal and then parafunction. It is well recognised that Bruxism is preceded by an arousal as seen in sleep studies. (14-19) Lavigne warns the bulk of a night-guard can take away some if not most of the oral airway (20). Many night guards live in the bathroom or found in the bed on waking. So the actions of airway protection are those of the brain protecting its oxygen supply, but equally important is that this is just one aspect of the oral manifestations of a compromised midface growth and impairment of the airways. Gagging, bruxing and sleep apnoea as well as TMJ problems are inextricably entwined.

For those who like lists, this is mine of oral signs starting at the lips.

Lips apart – mouth breathing (important as it draws dry cold dirty air over tonsils and into the lungs and takes out up to six times more carbon dioxide than nose breathing thereby upsetting both pH of blood and of biochemistry as seen in metabolic changes – Type two diabetes is five times more prevalent in ‘snorers’ or more accurately OSA/SDB.

Worn incisors. Secondary to mandibular protrusion, which opens the throat and pharyngeal airway, but not adequately in many and there is still bruxing.

These are typical of incisal wear, often some are far worse than these. Also Buccal ‘erosions’ – arguably abfractions.

Tongue scalloping Lateral borders with indentations of the teeth indicating life-long inadequate tongue space where if there isn’t enough oral space the tongue compromising the pharynx.
Cheek biting. A line or ‘ridge’ along the level of the teeth. Often seen in patients and indicates buccinators activity- again secondary to a poor airway.
Tongue resting on top of lower teeth.
No visible airway. This is most commonly scored 0-4 in the Mallampati Score – a measure developed by an anaesthetist.
Erosion linked to GERD is a reasonable addition as reflux is slightly higher prevalence in Sleep Apnoea, (38% vs 32%) but few studies consider the estimated 9% of juveniles with silent reflux. The most common sign are the cup-like craters on the tips of lower molars. (21-23)

A lot of these manifestations are visible on lateral head xrays including the level of the Hyoid bone and the AP dimension of the throat – above the Glottis.

I also look at the curve of the neck – which should be smooth, but often isn’t. Narrow these airways may be all these patients were awake and compensating. Frequently pharyngometery reveals during sleep these probably halve. These kids will all hate impressions.

Three very different lordotic curves and associated pharyngeal profiles.

A good clue to the core problem of sleep disruption can be hyperactivity in children and Dr. K Bonuck points to this (24-27) as do (28-30) Antonio (Bruxing in children- a warning sign for psychological problems?) Delgado (Bruxism a warning sign) Manfredini & Lobbezoo, very well accepted researchers on current concepts in bruxism. Gagging is often a clue to these patient profiles.

So when your patient gags, perhaps think more of sympathy and check their medical history and medications. A great number of them will have such as reflux – with ‘Losec’ to subdue it and antihypertensives, antidepressants and sleeping tablets, as well as other medications.

A glimpse at their medications can be revealing and a good guide to longevity of restorative work, and via systemic inflammatory processes integrity of bone both regards perio and of course implants.

Maybe you could consider viewing or reviewing the role of the dentist and think of including the airway as part of your daily thought patterns. We all have them and more than half show the results of impairment. Perhaps start with taking impressions in an sitting upright position.

It’s a great new and important field of everyday dentistry.

Dr. David Zimmerman BDS Post Grad Cert Pain and Pain Management.

Gozal. Metabolic alterations and systemic inflammation in OAS among non-obese and obese prepubertal children. Am Jnl Resp and Crit Care [Internet]. 2008; 177:[1142-9 pp.].
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Creuzet S, Schuler B, Couly G, Le Douarin NM. Reciprocal relationships between Fgf8 and neural crest cells in facial and forebrain development. Proc Natl Acad Sci U S A. 2004;101(14):4843-7.
Le Douarin NM, Creuzet S, Couly G, Dupin E. Neural crest cell plasticity and its limits. Development. 2004;131(19):4637-50.
Le Douarin NM, Couly G, Creuzet SE. The neural crest is a powerful regulator of pre-otic brain development. Dev Biol. 2012;366(1):74-82.
Helms JA, Kim CH, Hu D, Minkoff R, Thaller C, Eichele G. Sonic hedgehog participates in craniofacial morphogenesis and is down-regulated by teratogenic doses of retinoic acid. Dev Biol. 1997;187(1):25-35.
Sperber GH. Current concepts in embryonic craniofacial development. Crit Rev Oral Biol Med. 1992;4(1):67-72.
Anderson G, Fields HW, Beck M, Chacon G, Vig KW. Development of cephalometric norms using a unified facial and dental approach. Angle Orthod. 2006;76(4):612-8.
Ball JV, Hunt NP. Vertical skeletal change associated with Andresen, Harvold, and Begg treatment. Eur J Orthod. 1991;13(1):47-52.
Harvold EP, Tomer BS, Vargervik K, Chierici G. Primate experiments on oral respiration. Am J Orthod. 1981;79(4):359-72.
McNamara CM. A retrospective cephalometric study of the effects of the Harvold appliance in the treatment of 20 patients with a Class II division 1 malocclusion. J Ir Dent Assoc. 1989;35(1):36-8.
Tomer BS, Harvold EP. Primate experiments on mandibular growth direction. Am J Orthod. 1982;82(2):114-9.
Woodside DG, Altuna G, Harvold E, Herbert M, Metaxas A. Primate experiments in malocclusion and bone induction. Am J Orthod. 1983;83(6):460-8.
Aguglia U, Gambardella A, Quattrone A. Sleep-induced masticatory myoclonus: a rare parasomnia associated with insomnia. Sleep. 1991;14(1):80-2.
Carra MC, Rompré PH, Kato T, Parrino L, Terzano MG, Lavigne GJ, et al. Sleep bruxism and sleep arousal: an experimental challenge to assess the role of cyclic alternating pattern. J Oral Rehabil. 2011;38(9):635-42.
Herrera M, Valencia I, Grant M, Metroka D, Chialastri A, Kothare SV. Bruxism in children: effect on sleep architecture and daytime cognitive performance and behavior. Sleep. 2006;29(9):1143-8.
Huynh N, Kato T, Rompré PH, Okura K, Saber M, Lanfranchi PA, et al. Sleep bruxism is associated to micro-arousals and an increase in cardiac sympathetic activity. J Sleep Res. 2006;15(3):339-46.
Itani O, Kaneita Y, Ikeda M, Kondo S, Yamamoto R, Osaki Y, et al. Disorders of arousal and sleep-related bruxism among Japanese adolescents: a nationwide representative survey. Sleep Med. 2013;14(6):532-41.
Kato T, Masuda Y, Yoshida A, Morimoto T. Masseter EMG activity during sleep and sleep bruxism. Arch Ital Biol. 2011;149(4):478-91.
Gagnon Y, Mayer P, Morisson F, Rompré PH, Lavigne GJ. Aggravation of respiratory disturbances by the use of an occlusal splint in apneic patients: a pilot study. Int J Prosthodont. 2004;17(4):447-53.
Alfaro EV, Aps JK, Martens LC. Oral implications in children with gastroesophageal reflux disease. Curr Opin Pediatr. 2008;20(5):576-83.
Linnett V, Seow WK. Dental erosion in children: a literature review. Pediatr Dent. 2001;23(1):37-43.
Linnett V, Seow WK, Connor F, Shepherd R. Oral health of children with gastro-esophageal reflux disease: a controlled study. Aust Dent J. 2002;47(2):156-62.
Bonuck K, Parikh S, Bassila M. Growth failure and sleep disordered breathing: a review of the literature. Int J Pediatr Otorhinolaryngol. 2006;70(5):769-78.
Bonuck KA, Chervin RD, Cole TJ, Emond A, Henderson J, Xu L, et al. Prevalence and persistence of sleep disordered breathing symptoms in young children: a 6-year population-based cohort study. Sleep. 2011;34(7):875-84.
Bonuck K, Rao T, Xu L. Pediatric sleep disorders and special educational need at 8 years: a population-based cohort study. Pediatrics. 2012;130(4):634-42.
Bonuck K, Freeman K, Chervin RD, Xu L. Sleep-disordered breathing in a population-based cohort: behavioral outcomes at 4 and 7 years. Pediatrics. 2012;129(4):e857-65.
G AA. Bruxism in children a warning sign for psychological problems. Jnl of Clinical Practise [Internet]. 2006; 72

No2

Delgado Jimenez MC, Pujol Massaguer T. [Bruxism in children: a warning sign?]. Aten Primaria. 1996;17(2):172-3.
Manfredini D, Serra-Negra J, Carboncini F, Lobbezoo F. Current Concepts of Bruxism. Int J Prosthodont. 2017;30(5):437–8.

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Science Update: NIH researchers discover cellular protein’s role in bone remodeling

Sam Khoury — Wed, 11 Feb 2026 23:51:10 +0000

Findings could inform efforts to treat osteoporosis and other bone loss disorders

Researchers at the National Institutes of Health have determined that a protein interacting with RNA molecules in cell nuclei plays a role in forming osteoclasts—cells that break down old or damaged bone tissue so it can be replaced with new bone. The findings have implications for understanding degenerative bone disorders like osteoporosis and fibrous dysplasia.

The study was conducted by Jarred Whitlock, Ph.D., and other researchers in the laboratory of senior author Leonid V. Chernomordik, Ph.D., of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and colleagues in the NICHD and the National Institute of Dental and Craniofacial Research, both at the NIH. Their study appears in Nature Communications.

Background

Osteoclasts are a type of bone cell that breaks down bone tissue. They work in balance with osteoblasts—cells that form new bone tissue to replace old tissue that osteoclasts have broken down. Osteoclasts have multiple cell nuclei. They are formed when several progenitor cells that originate in the bone marrow fuse together to form a large cell with multiple nuclei. The more fusions they complete, the larger osteoclasts become and the greater their ability to dissolve bone.

The number and size of osteoclasts are altered in many bone diseases and with the aging process. To gain insight into how the body controls osteoclast size and behavior, the study authors sought to identify the cellular mechanisms that control the fusion of osteoclasts.

Results

With cells isolated from blood donors, the researchers formed progenitor cells and then induced them to form osteoclasts. They discovered that a protein, referred to as La and thought to be present in cell nuclei, disappeared from the progenitor cells and then reappeared as they began to fuse into osteoclasts.

Light micrograph of an osteoclast displaying multiple nuclei.
Credit: Public Domain, Wikimedia Commons, https://commons.wikimedia.org/wiki/File:Osteoclast.jpg

Using a variety of genetic, molecular, and cellular approaches, the researchers demonstrated that surface-bound La controls osteoclast fusion, regulating how large they become. The researchers tested whether blocking La’s surface function in osteoclasts could prevent the formation of excessively large osteoclasts in a disease, fibrous dysplasia. In a mouse model, they showed that blocking the compound resulted in fewer osteoclasts.

Significance

The authors believe that targeting La at the surface of osteoclasts may lead to treatments for bone disorders and age-related changes in osteoclast size and number, including osteoporosis and fibrous dysplasia.

Reference

Whitlock JM, et al. Cell surface-bound La protein regulates the cell fusion stage of osteoclastogenesis. Nature Communications. 2022. https://doi.org/10.1038/s41467-023-36168-x

Reproduced from https://www.nichd.nih.gov/

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Mouth formation during embryonic development

Sam Khoury — Mon, 02 Feb 2026 06:26:44 +0000

Jaw-dropping research explains mouth formation during embryonic development

By Nicole Giese Rura

Whitehead Institute researchers have identified the pre-mouth array—an area of the developing face in embryonic frogs—that “unzips” to surround the mouth opening. Their work highlights the precision necessary to create the mouth and identifies the cellular mechanisms that drive mouth formation during embryonic development.

“All biological holes—openings—that form in the embryo are fascinating because they would become a catastrophic wound if they do not form precisely,” says Whitehead Member Hazel Sive, who is also a professor of biology at MIT. “We call these ‘scheduled holes’ and the mouth is a crucially important example. Mouth formation involves many steps that ensure the opening happens at the right time and at the right place— when the cells are connected with the correct junctions to be exposed to the outside and where the opening connects to a prepared region, in the case of the mouth to the digestive system. But I was so surprised when we found that this process is initiated in frogs several days before the mouth actually opens.”

The Sive lab has studied mouth formation during embryonic development in Xenopus frogs for many years. Because mouth formation occurs early in embryonic development and is highly conserved across species, model organisms, such as frogs and fish, provide fundamental insights into key developmental events that are difficult to observe and study in humans.

In the most recent work Sive lab researchers led by Laura Jacox, then a graduate student pursuing a dual DMD-PhD degree through the Harvard School of Dental Medicine and the Harvard-MIT Health Sciences and Technology program, monitored a region of the embryo known as the Extreme Anterior Domain (EAD). Within the EAD, which the Sive group has identified as the earliest element of facial development, they noted that a group of cells reorganizes to form a “pre-mouth array” that indicates where the mouth opening will later form.

The pre-mouth array begins as a square, eight cells wide and high, and morphs into a two-cell wide by twenty tall column. This transformation is a process called convergent extension, a crucial embryonic mechanism of cell reorganization. As the larvae prepares to begin feeding, the two rows of cells unzip down the middle to surround the oral opening that connects the digestive system to the outside.

The team observed that pre-mouth array formation occurs as ‘neural crest’ cells (that later form bones and muscles of the face) come to lie on either side of the EAD. They proposed that these cells send a signal to EAD cells instructing them to reorganize and form the pre-mouth array. Supporting this proposal, they showed that the neural crest and the Wnt/PCP signaling pathway, specifically a Wnt11 signal, triggers pre-mouth array formation.

Jacox acknowledges that this research clarifies a piece of a highly complex, carefully orchestrated process.

“There’s a lot of craniofacial development that we don’t understand,” says Jacox, a co-author of the Cell Reports paper who will soon become a resident in orthodontics at the University of North Carolina Chapel Hill. “If we hope to understand why craniofacial anomalies happen in humans and how to treat them at an earlier point to avoid years of surgery and orthodontics, we need to obtain a better handle on what’s going on. Recognizing what is required to form a mouth and the face and how it’s regulated is a step toward understanding how these processes can be disrupted.”

This work on mouth formation during embryonic development was supported by the National Institute of Dental and Craniofacial Research (NIDCR 1R01 DE021109-01 and F30DE022989) and Harvard University’s Herschel Smith Graduate Fellowship.

* * *

Hazel Sive’s primary affiliation is with Whitehead Institute for Biomedical Research, where her laboratory is located and all her research is conducted. She is also a professor of biology at Massachusetts Institute of Technology.

* * *

Full Citation:

“Formation of a ‘‘pre-mouth array’’ from the extreme anterior domain is directed by neural crest and Wnt/PCP signaling“

Cell Reports, August 2, 2016.

Laura Jacox (1,2,3,4,5), Justin Chen (1,2), Alyssa Rothman (1,2). Hillary Lathrop-Marshall (1,3) and Hazel Sive (1,2).

Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA
Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115, USA
Harvard-MIT Health Sciences and Technology Program, Harvard Medical School, 250 Longwood Avenue, Boston, MA 02115, USA
Biological Sciences in Dental Medicine Program, Harvard Graduate School of Arts and Sciences, 1350 Massachusetts Avenue, Holyoke Center 350, Cambridge, MA 02138, USA

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Immune cells in the healthy mouth

Sam Khoury — Wed, 31 Dec 2025 08:24:41 +0000

Maintaining the body’s barrier defenses at sites such as the skin and mucosal surfaces is critical for health and survival.

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Expansion techniques: how we got from there to here and back

Sam Khoury — Thu, 11 Dec 2025 16:16:35 +0000

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Impression techniques used for single-unit crowns

Sam Khoury — Tue, 11 Nov 2025 07:18:18 +0000

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Gum disease incites deadly oral cancer growth

Sam Khoury — Fri, 07 Nov 2025 06:11:39 +0000

Researchers find byproducts from gum disease incite deadly oral cancer growth

Researchers from Case Western Reserve University have discovered how byproducts in the form of small fatty acids from two bacteria prevalent in gum disease incite deadly oral cancer growth (the growth of deadly Kaposi’s sarcoma-related (KS) lesions and tumors in the mouth).

The discovery could lead to early saliva testing for the bacteria, which, if found, could be treated and monitored for signs of cancer before it develops into a malignancy, researchers say.

“These new findings provide one of the first looks at how the periodontal bacteria create a unique microenvironment in the oral cavity that contributes to the replication the Kaposi’s sarcoma Herpesvirus (KSHV) and development of KS,” said Fengchun Ye, the study’s lead investigator from Case Western Reserve School of Dental Medicine’s Department of Biological Sciences.

The discovery is described in The Journal of Virology article, “Short Chain Fatty Acids from Periodontal Pathogens Suppress HDACs, EZH2, and SUV39H1 to Promote Kaposi’s Sarcoma-Associated Herpesvirus Replication.”

The research focuses on how the bacteria, Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn), which are associated with gum disease, contribute to cancer formation.

Ye said high levels of these bacteria are found in the saliva of people with periodontal disease, and at lower levels in those with good oral health—further evidence of the link between oral and overall physical health.

The deadly oral cancer growth KS impacts a significant number of people with HIV, whose immune systems lack the ability to fight off the herpesvirus and other infections, he said.

“These individuals are susceptible to the cancer,” Ye said.

Deadly oral cancer growth KS first appears as lesions on the surface of the mouth that, if not removed, can grow into malignant tumors. Survival rates are higher when detected and treated early in the lesion state than when a malignancy develops.

Also at risk are people with compromised immune systems: those on medications to suppress rejection of transplants, cancer patients on chemotherapies and the elderly population whose immune systems naturally weaken with age.

The researchers wanted to learn why most people never develop this form of cancer and what it is that protects them.

The researchers recruited 21 patients, dividing them into two groups. All participants were given standard gum-disease tests.

The first group of 11 participants had an average age of 50 and had severe chronic gum disease. The second group of 10 participants, whose average age was about 26, had healthy gums, practiced good oral health and showed no signs of bleeding or tooth loss from periodontal disease.

The researchers also studied a saliva sample from each. Part of the saliva sample was separated into its components using a spinning centrifuge. The remaining saliva was used for DNA testing to track and identify bacteria present, and at what levels.

The researchers were interested in Pg’s and Fn’s byproducts of lipopolysaccharide, fimbriae, proteinases and at least five different short-chain fatty acids (SCFA): butyric acid, isobutryic acid, isovaleric acid, propionic acid and acetic acid.

After initially testing the byproducts, the researchers suspected that the fatty acids were involved in replicating KSHV. The researchers cleansed the fatty acids and then introduced them to cells with quiescent KSHV virus in a petri dish for monitoring the virus’s reaction.

After introducing SCFA, the virus began to replicate. But the researchers saw that, while the fatty acids allowed the virus to multiple, the process also set in motion a cascade of actions that also inhibited molecules in the body’s immune system from stopping the growth of KSHV.

“The most important thing to come out of this study is that we believe periodontal disease is a risk factor for Kaposi sarcoma tumor in HIV patients,” Ye said.

With that knowledge, Ye said those with HIV must be informed about the importance of good oral health and the possible consequences of overlooking that area.

The research was supported by a career development grant at Center for AIDS Research at Case Western Reserve University, and a National Institute of Dental and Craniofacial Research grant.

Contributing to the study were Case Western Reserve University researchers Abdel-Malek Shahir and Nabil Bissada, from the Department of Periodontics; Xiaolan Yu, Jingfeng Sha, Zhimin Feng, Betty Eapen, Stanley Nithianantham, and Aaron Weinberg, from the dental school’s Department of Biological Sciences; and Biswajit Das and Jonathan Karn, from the Department of Molecular Biology & Microbiology at the School of Medicine.

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Providing oral care for people with intellectual disability

Sam Khoury — Thu, 06 Nov 2025 14:26:28 +0000

Providing oral care to people with intellectual disability requires adaptation of the skills you use every day. In fact, most people with mild or moderate intellectual disability can be treated successfully in the general practice setting.

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Chemotherapy and your mouth

Sam Khoury — Wed, 05 Nov 2025 12:01:01 +0000

Chemotherapy is the use of drugs to treat cancer. These drugs kill cancer cells, but they may also harm normal cells, including cells in the mouth. Side effects include problems with your teeth and gums; the soft, moist lining of your mouth; and the glands that make saliva (spit).

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Chewing away at the question of oral immunity

Sam Khoury — Sun, 02 Nov 2025 08:17:18 +0000

Oral immunity is dependent on the immune system performing a remarkable balancing act by fighting off dangerous pathogens while tolerating the presence of the normal flora.

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Re-establishing a physiologic vertical dimension for an overclosed patient

Sam Khoury — Fri, 31 Oct 2025 08:28:55 +0000

The term neuromuscular occlusion has become associated with certain limited methodologies that are used to obtain a muscle-compatible occlusal relationship. In reality, there are several different approaches that can be used to determine a "neuromuscular" maxillo-mandibular relationship, even with a fully edentulous case.

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Normal bacterial colonies in human body linked to presence of cancer of the mouth and throat

Sam Khoury — Wed, 15 Oct 2025 08:33:52 +0000

In a sample study, researchers at Johns Hopkins say they have found an association between the makeup of an individual’s normal bacterial colonies and head and neck cancer, a finding that potentially advances the quest for faster and more accurate cancer diagnosis and therapy.

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Plant-made antimicrobial peptide targets dental plaque and gum tissues

Sam Khoury — Fri, 03 Oct 2025 09:43:20 +0000

Katherine Unger Baillie has found that protein drugs, which derive from biological sources, represent some of the most important and effective biopharmaceuticals on the market. Some, like insulin, have been used for decades, while many more based on cloned genes are coming to market and are valued for their precise and powerful functions.

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Gum disease genes identified

Sam Khoury — Wed, 15 Jan 2025 07:14:30 +0000

Identification of gum disease genes may speed quest for compounds to treat severe periodontitis

Researchers at Columbia University College of Dental Medicine (CDM) Columbia University Medical Center (CUMC) have identified 41 master regulator genes that may cause gum disease (gum disease genes), also known as periodontal disease. The study was the first of its kind to employ genome-wide reverse engineering to identify the gene pathways that contribute to periodontitis.

Identification of the genes represents a vital step toward developing compounds that can be used in targeted, individualized treatment of severe periodontitis, before loss of teeth and supportive bone occurs.

Findings of the study were published recently in the Journal of Dental Research.

In gene expression studies, investigators find those genes that are most commonly expressed in either healthy or diseased tissue. But such studies cannot identify a causal link between these genes and the disease, and often miss genes that affect a larger number of genetic pathways, which may have a large impact on the disease process.

In this study, a team led by Panos N. Papapanou, DDS, PhD, professor and chair of oral, diagnostic and rehabilitation sciences at the College of Dental Medicine at CUMC, “reverse-engineered” the gene expression data to build a map of the genetic interactions that lead to periodontitis and identify individual genes that appear to have the most influence on the disease. “Our approach narrows down the list of potentially interesting regulatory genes involved in periodontitis,” says Dr. Papapanou. “This allows us to focus on the handful of genes that represent the most important players in the process rather than the whole transcriptome.”

To identify the genes, Dr. Papapanou partnered with CUMC investigators including Ryan Demmer, PhD, assistant professor of epidemiology, at the Mailman School of Public Health, and researchers in Systems Biology who had previously developed algorithms to identify regulatory genes that fuel cancer growth. The researchers examined RNA from healthy and diseased gum tissues of 120 patients with periodontitis. They applied one algorithm to study the interactions among the genes and used another algorithm to identify genes that disrupt healthy tissue and drive the disease process.

Many of the genes identified by Dr. Papapanou and his team are implicated in immune and inflammatory pathways, confirming laboratory and clinical observations of the development of periodontal disease.

Identification of the master regulator genes will allow investigators to test compounds that interrupt their action, creating treatments that stop periodontal disease at its source. “Now it’s important to do the downstream work of validating these master regulators in the lab before we can test these genes in experimental models,” says Dr. Papapanou.

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