Oral health and dental training in Denmark in the early 1960s
The oral health situation in the Scandinavian countries after the 2nd World War was poor. The majority of elderly above 60 years were partly or totally edentulous and children in Denmark had one of the highest caries rates ever recorded. Soon after eruption, the first molars frequently had open cavities and were in many cases extracted. Amongst the poor and in rural areas it was not unusual for all teeth to be extracted when children reached confirmation around the age of 14 years in order to save money on future dental treatment. Until 1958 there was only one dental school in Denmark, and the dentists could not cope with the amount of fillings needed as dental restorations were considered at that time as tertiary prevention. But such restorations (mostly amalgams) had to be constantly replaced. It was claimed that there was a need for better restorative materials, so that failures of fillings and secondary caries could be prevented. This attitude was reflected in the dental curriculum where a department of dental materials was considered, together with restorative and prosthetic departments, as the most important topics to be taught. Nevertheless, in the 1950s, dentistry aimed at being considered part of the medical profession and wished to be seen as a biomedical specialty. The curriculum changed accordingly with the creation of departments of biochemistry, physiology, anatomy and histology, microbiology, pathology, etc.
In Aarhus, a new Royal Dental College was established in 1958 and after military service I started as a student in 1961. Electron microscopy attracted me as a young student. In my spare time, I started working in the electron microscopy laboratories for Hubert Schroeder, a visiting scholar coming from. Zürich where Hans Mühleman had gathered a unique young group including, amongst others, Klaus König and Bernie Guggenheim.
The atmosphere at the dental school in Aarhus was vibrant, making us students feeling that a scientific approach to the numerous questions in oral biology would result in significant improvements in oral health. In particular, Harald Löe’s ability of involving young disciples (national and international) in conducting research had a great impact. He was convinced that removing dental plaque and calculus would prevent periodontal breakdown and would save teeth from being extracted in adult life. Harald taught us that tooth loss was predominantly the result of periodontal breakdown after the age of 30. If any of us questioned his views, we were dismissed. Nevertheless, he opened our eyes to the potentials of international collaboration in science.
Upon graduating, I joined the departments of oral surgery and oral pathology at the Royal Dental College in Aarhus while working part-time in a private practice. After two years I started postgraduate training in general pathology doing postmortem work in the mornings and microscopic diagnosis in the afternoon. My research focus was on mucosal wound healing.
Danish pathologists held regular meetings once a month to discuss their cases and to present their research. During one such event, I presented my first case report of a hamartoma. J.J. Pindborg was present and posing questions to me, and humiliatingly exposed me by informing that he himself had published a similar case to which I had not referred in the literature. Nevertheless, from that evening, he became the one person who, over the next 20 years, was to support me most, encouraging and stimulating me in my work. Without his support I would never have climbed the academic ladder. He was the Nordic dental professor par excellence, a great academic with a very broad intellectual base. I took over responsibility for his small textbook on Odontogenesis after some years and, together with Ivar Mjør from Norway, we developed it into the Histology of the Human Tooth and later Oral Histology and Embryology, both published by Munksgaard Publishers. During the 1980s, he made me associate editor of the Scandinavian Journal of Dental Research, and later editor–in–chief of a journal he had created: Community Dentistry Oral Epidemiology.
Professor in Dental Pathology, Operative Dentistry and Endodontics 1973-93 and Rector for eight years
In 1972, when I turned 29, a lot of things happened simultaneously which totally changed my life and career. I had had a PhD and submitted a thesis to the board of the Royal Dental College to be evaluated for a Doctor Odontology degree. The dental school had been through a turbulent period as Harald Löe had hoped to be Rector, but failed to do be elected by the board. Disappointed, he left for USA and continued his great career there. He had simply become too strong, influential and ambitious for a ‘small’ dental school, but his impact had been enormous. The head of the department of Restorative Dentistry had moved to Norway, and I was asked, much to my surprise, if I would be Acting Chair for a year, while the dental school advertised the vacant Chair internationally.
I decided that I would compete for the Chair, but needed to obtain research experience in dental hard tissue pathology. In spring of 1973, therefore, I took up a post-doctoral position at what at the time was one of the strongest dental schools in research on dental caries in Europe, the London Hospital Medical College (part of the University of London). Here I learned polarized light microscopy from Leon Silverstone, and electron microscopy of enamel from Newell Johnson and Ron Fearnhead. The London Hospital had a vibrant research environment on oral diseases and many of those I met –in addition to the above mentioned – there were to become good friends and become some of the most brilliant scientists in their respective fields: Aubrey Sheiham, Brian Burt, Alan Boyde, Jim Elliott, Jeremy Hardie, George Bowden, Christoffer Squire, Brian Clarkson, and Edwina Kidd.
I was interested in dental fluorosis, because in the literature, less was known about this fluoride-induced dental pathology. Thanks to Pindborg, I obtained nine severely fluorotic teeth from Ingolf Møller who had collected these in Morocco. Møller had become professor in Pedodontics in Aarhus for some years before moving to Copenhagen where he did his thesis on fluoride and dental caries in Denmark.
Our studies (Fejerskov, Johnson & Silverstone 1974; Fejerskov, et al. 1975) were an eye-opener and totally changed my view of the role of fluorides in dental caries and in the etiology of dental fluorosis. Most of what I could find in the literature about histopathology of dental fluorosis was not consistent with our findings on fluorosed enamel structure. For the first time I realized how deeply established scientific paradigms can influence and distort peoples way of thinking and of interpreting data, and how true Kuhn (The Structure of Scientific Revolutions 1962, The Univ. Chicago Press) was when stressing how aggressive a scientific community can react when a paradigm has to shift.
Oral health in Denmark from 1970s onwards
There is a long tradition in Denmark of public dental health service programs for children which started as early as in 1910. By 1971, such programs existed in 110 of 275 Danish municipalities, comprising about two-thirds of the population. By law (in accordance with the Act on Child Dental Health in 1972) all children in compulsory education (from seven to 16 years of age) in Denmark were offered free dental service. In about 75% of municipalities, dental health care was provided by the public school dental service. Municipalities were required to establish dental clinics located in larger primary schools and in the remaining municipalities private practitioners were paid by the public purse for treating children in their area. The plan was implemented gradually, so that only children in grade one were included in the school years 1972/73. In each of the following years, one more grade was included so that by 1981 all compulsory grades were covered. This opportunity was later gradually extended to cover up to the age of 18 years. Adults have to pay most of their treatment in private praxis. Between 1981-86, the age groups from birth to 6 had been included.
Dental caries in children in Denmark
Data collected from children in different parts of Denmark indicated that dental caries had already begun to decline by the 1970s. In accordance with the law, school dental services were to score dental caries at cavity level annually from 1972 onwards. They had to submit these data in the beginning by class and later by age to the National Board of Health and Medicine – a unique data-bank. In 1972 each child in grade 1 (combining the DMFS and defs indices) had, on average, 15 surfaces affected, about five of these being filled and on average two teeth extracted. Seven years later, in 1979 the total number of surfaces affected was 11, of which 7 were filled, the number of decayed surfaces reduced from 8 to two, and an average of 2 surfaces missing. What was striking was that there was an improvement year on year amongst those entering school. Thus each subsequent cohort of children presented with a lower caries experience while caries increment remained steady over the school years.
By 2003 the variation of the mean DMFS of 15-yr-olds amongst the 267 Danish municipalities varied from DMFS 1 to DMFS 7 (the D was scored at frank cavity level), with virtually no surfaces missing (data by Dr. Jens Heidmann). By 2012, in some municipalities about 50% of the 15-18 year olds were caries free, about 40% had only 1-3 surfaces affected, reflecting the extreme skewness in distribution when the overall caries experience in a population is very low (Fejerskov, et al. 2013).
By the end of the 1970s at the first international conference on caries decline in Boston we presented the Danish evidence (Fejerskov, Antoft & Gadegaard 1982). Most countries did not believe that dental caries was declining.
During the 1960s and 1970s, there were strong attempts by some at the two dental schools in Denmark, as well as by the school dental service, to introduce artificial water fluoridation. These proposals were inspired by the US and the Tiel-Culemburg water fluoridation program in Holland (Backer-Dirks 1967). But neither politicians nor the public at large supported the idea. Møller, who had now moved to Copenhagen and became affiliated with the oral health program of WHO, introduced fluoride tablet programs instead. However, it soon became evident that compliance from parents was limited. And when tablets were provided at schools, there was limited documented evidence of an associated caries reduction. Rather, it was found that children developed distinct dental fluorosis (Thylstrup, Fejerskov, Bruun & Kann 1979).
Fluoride containing toothpaste had become widespread in Denmark from 1963 and, by the early 1970s, almost all toothpastes in the market contained fluoride. Children and their parents were told by the school dental service to perform proper oral hygiene and to restrict sweets to once a week. Parents in the higher socioeconomic strata tended somewhat to implement this regime, but the overall per capita consumption of sugars remained fairly unchanged around 40-50 kg/year ove the period. Moreover, in the school dental services the application of bi-weekly fluoride mouth rinses had become widespread (Heidmann, et al. 1992).
Dental caries prevalence had gradually declined year by year, although with some variation across the country, with the smallest decline observed in the low socioeconomic regions (data from Dr Jens Heidmann). Studies showed that there was an association between the magnitude of the decline in dental caries prevalence and the extent to which public dental staff engaged with the public.
Societal changes in the post 2nd World War period
It is important here to remind ourselves of the dramatic changes for the majority of people that occurred in Europe and in Denmark in particular in the post 2nd World War period. The establishment of the welfare state ensured a social safety-net, enabled universal access to education, health and social services, and widespread sanitation. Most families lived in decent accommodation with heating, inside bathrooms and toilets. There were significant improvements in hygiene, access to foods and commodities, changes in diet, vaccinations, etc. for the majority of people. Denmark was to become one of the richest countries in the world. Such factors must have influenced the occurrence of oral diseases, even if social gradients persist in high-income countries (Sabbah, et al. 2007).
Dental plaque and oral health
Harald Löe’s paradigm was that periodontal diseases were plaque induced and hence could be treated and prevented by plaque and calculus removal. He worked for the establishment of schools for dental hygienists as such cadres could perform the scaling and polishing at regular intervals for all age groups. His view was that periodontal pockets should be kept shallow and deep pockets surgically removed.
At one stage, chlorhexidine mouthwashes were introduced and for more than a decade seen by periodontologists as the ultimate solution. The battle against microbial plaque was almost entirely focused on preventing gingivitis and periodontal disease, as these were claimed to be responsible for the majority of tooth-loss in adults and elderly.
Research on the role of the microflora in dental caries had been focused on a few microorganisms, in particular mutans streptococci. There were even some researchers who tried to convince the WHO about the need to develop a vaccine against S. Mutans. Fortunately, attempts to test a vaccine on the population in Iceland was not approved by the health authorities – and later data showed a dramatic decline in dental caries in this population within a short period in the 1980’ies without a change in salivary prevalence of S. Mutans (Bjarnason, et al. 1993). Periodontology had been so successful in ‘monopolizing’ dental plaque that there have even been claims that it plays only a minor role, if any, in the development of caries. So, even today some WHO representatives claim at a consultation meeting with Ministry of Health in Bogota (Bogota, Colombia meeting, March 2016) that oral hygiene and plaque removal plays a limited if any role in controlling dental caries.
Caries prevention in Denmark
Around 1980 much of the focus on caries prevention had been on the role of fluorides, with a wealth of fluoridated products introduced into the market internationally ( gels, foams, lozenges, varnishes, fluoridated tooth picks and dental floss, chewing gum, many different fluoridated toothpastes with different – and often increasing concentrations of fluoride, tablets, rinsing solutions, fluoridated milk, salt, school waters, etc). All of this was based on the claims made in the US: ‘if little is good more is better’ and ‘dental caries is a result of fluoride deficiency’. In the Scandinavian countries, some researchers even claimed that teeth in water fluoridated areas were better mineralized and pearl-like and that teeth in these areas had rounded cusps and shallow occlusal fissures. Some went so far to say that in fluoridated areas there was less plaque, less bone fractures and less periodontal breakdown. Fortunately, in Denmark the two dental schools coordinated their work on the mechanisms of action of fluoride in caries prevention for more than 20 years during the 1980s and 1990s (Fejerskov, Thylstrup & Larsen 1981) in a successful attempt to avoid most of these products. They sought to encourage fluoride preventive programs to be as cost-effective, and as simple, as possible. This evidence based approach proved to be highly successful as apparent in the caries decline referred to above.
Impact on dental services
In response to the decline in dental caries, some politicians tried in 1983 to close one of the Danish dental schools. However, such attempts failed. Instead, the government implemented a reduction in total number of students enrolled at the two dental schools each year. Today, only about 170 students are enrolled per year. Despite a dramatic reduction in dental caries experience, and with the declining number of edentulous adults since the 1980s, the number of dentists in Denmark has remained fairly stable. The adult populations are served by private dentists working either alone or most often in small dental offices where they have 2-5 other dentists employed together with auxiliary staff. In principle a dentists can only owe one dental office however in the last year we have experienced large venture capital firms buying a larger number of these small clinics to create chains across the country. These chain-clinics aim at generating money for the firms and employ dentists and worse of all sets the standard for how much trade turnover each clinic should have (restorations, porcelain crowns, bridges and implants, etc.). This will result in commercialization of adult dental care and hardly result in improved oral health in the future adult and elderly populations.
In the public services, about one third of children receive orthodontic treatment. In the adult population, cosmetic dentistry had grown; crowns and bridges had once been frequent, but now gradually being replaced by implants. In practice, dentists make their living from replacing fillings and restorations and ensuring frequent recalls of the so-called ‘high caries cohorts’ from decades ago. However, they will soon experience the new almost caries-free generations (Fejerskov et al., 2013). They have the potential for keeping caries increment very low if applying the concepts of caries control amongst adults and elderly in decades ahead and to prevent loss of teeth – but if so their income will decline dramatically.
In Sweden Hugoson followed cohorts of adults and elderly in the town of Jönköbing from 1973-2003 (Hugoson & Koch 2008; Hugoson, et al. 2000) while applying the principles of caries control. Amongst 70 years olds there were about 40% edentulous in 1973 contrasting 2% thirty years later.
If we combine the valuable information from data from Danish children available from 1972 until now with those arising from Hugoson’s longitudinal studies on adults in Sweden, we need to consider how, in a Nordic context, we best serve the future of oral health care of our populations. Can dentists continue to make a living from the emerging caries-free cohorts without providing unnecessary restorative interventions? And are we, as a profession, serving the need of the populations in the coming years? Are we training the right type of oral health care workers? I shall return to this at the end of the paper where I will outline what I think is needed if we are to take full account of the impact of rapidly declining need for restorative care. In addition, I will outline what I think needs to change in the way we have been training dentists in the past.
But before doing so, let me outline what, for almost 30 years, became my main areas of research that has involved working with highly skilled and specialized colleagues without whom I would never have been able to pursue my visions of combining basic laboratory-based research, animal experiments, epidemiological field studies and approaches to oral health in East Africa and Peoples Republic of China.
Understanding knowledge from basic sciences to explain and interpret epidemiological findings
We are all a product of the training which we received both at dental school and under the influence of mentors who guided our first years of research. I was lucky to be exposed to some of the most academically and intellectually brilliant mentors of high personal integrity. So, whenever I encountered situations where our results and clinical observations did not fit with conventional wisdom (paradigms), we learned to trust our data and try to expose them for critique in publications and at international conferences.
When I became head of the restorative department in Aarhus, an outstanding associate professor had already established a small fluoride chemistry laboratory where he conducted solubility studies on dental enamel (Larsen 1974). The effect of fluoride on forming dental enamel and on dental caries became our mutual focus over the next 30 years. A young colleague, Anders Thylstrup, had undertaken his PhD thesis based on epidemiological studies of dental caries amongst the populations of the Faroe Islands. On his return to Denmark, he asked to be included in the small group that was working on fluoride. A classmate from the dental school, Kaj Josephsen had become an associate professor in Oral Anatomy and wanted to join our rat experimental studies on dental fluorosis. So from its early period, the small group comprised unique people with a broad spectrum of expertise and approaches.
The results obtained from the structural studies of the fluorotic teeth that I had been involved with at the London Hospital were novel and different from what had hitherto been described in the literature. We therefore published a critical review entitled Dental fluorosis–possible pathogenic mechanisms (Fejerskov, Thylstrup & Larsen 1976). ). This sat the stage for the hypotheses which we pursued in rat (Fejerskov, et al. 1979; Larsen, Fejerskov & Jensen1980; Fejerskov, Yaeger & Thylstrup 1979; Larsen, Richards & Fejerskov 1981) and pig studies in subsequent years and for our human studies on dental fluorosis.
In the early stages of my career I also developed an in situ experimental human fissure-caries model (Fejerskov, Silness, Karring & Löe 1976; Theilade, et al. 1974, 1977, 1978 and 1982; Theilade, Fejerskov & Horsted 1976). I presented these findings during meetings at ORCA where I received critique as well as support from Klaus König, Hans Mühleman, Bernie Guggenheim (all of whom I was introduced to by Hubert Schroeder) and, Robert Frank, John Weatherell, Geff Ingram and Yngve Ericsson. I established a close friendship with some of these ‘giants’, especially with Bernie who involved me for almost 20 years in his ‘European Research Group of Oral Biology’ as its secretary. It was stimulating and challenging because of Bernie’s intellect and strong personality. Twice a year we invited 12 people for a weekend addressing recent, often unpublished research results covering the whole spectrum of Oral Biology – for me a unique opportunity for being updated on the most recent scientific achievements.
In an attempt to move from the laboratory and rat experiments on dental fluorosis into a human clinical setting of high relevance Thylstrup and I raised money to perform studies in Tanzania on populations exposed to various fluoride concentrations in the environment. As a result we developed a more detailed and specific classification of dental fluorosis — the TF-index (Thylstrup & Fejerskov 1978). The index was based on associating the pathological changes in enamel as seen under microscopes with clinical signs of dental fluorosis. It is a natural extension of Dean’s classification, but more precise and more easily reproducible. Our studies raised the need to further develop our basic studies in the laboratories and in animal studies. We established an experimental pig model in which we were able to carry out longitudinal studies and combine clinical/histological studies, chemistry measurements, bone metabolism studies, dose-response studies and pharmacological clearance studies. A young English colleague from the London Hospital, Alan Richards, was recruited and became responsible for the fluoride-pig experiments (Richards, Fejerskov & Ekstrand 1982; Kragstrup, Richards & Fejerskov 1984, 1989; Andersen, et al. 1986; Richards, et al. 1986). At the same time we turned to the rat model to better understand the complex events that occurred at cellular level during enamel maturation (Josephsen & Fejerskov 1978; Warshawsky, et al. 1981). We compared these findings with those conducted on materials from full-born human fetuses (Thylstrup, et al. 1977).
Anders became professor in Copenhagen by the start of the 1980s and proceeded to establish his own research group. So, I was in acute need of a strong epidemiologist and biostatistician within the group. As a by-product of our research in African populations, our results suggested that the pathogenesis of periodontal breakdown and of dental caries was radically different to what we had been taught at dental school. Our hypothesis was that we would gain a greater understanding if we were to conduct epidemiological studies in populations with limited or no access to dental care. So, in addition to the different avenues we wanted to pursue in our enamel and fluoride research, I set out on a mission to create another new group in order to identify populations of adults and the elderly whom we could follow longitudinally. This would allow us to combine clinical recordings with microbiological sampling in the same individuals over time. So, we had to find an epidemiologist and a microbiologist to join our group.
When Anders left we decided to strengthen the more basic research in cariology at the department so we recruited a young clinical teacher, Bente Nyvad, to be trained in microbiology. Bente focused on basic scientific studies on streptococci. Supervised by Mogens Kilian, and together with me, she spent about 10 years looking at different aspects of root caries. The development of in situ models significantly added to our understanding of the pathogenesis of dental caries and the role of fluoride in lesion initiation and progression (Nyvad & Fejerskov 1986; 1987a; 1987b; 1989; 1990; Nyvad, ten Cate & Fejerskov 1989; 1997; Thoda, Fejerskov & Yanagisawa 1996; Fejerskov, Nyvad & Larsen 1994).
In Kenya, there was in the beginning of the 80’ies a vigorous debate on the use of fluorides in a variety of dental products because a multinational company was doing its utmost to sell products which would add to the fluoride burden in a population which already had extensive dental fluorosis because of the fluoride content of drinking waters. Working as a lecturer in community dentistry at the Nairobi dental school, Firoze Manji, together with his colleagues, organized an international symposium to discuss the fluoride situation. It was there that, after exchanges of letters, we first met. Soon after the symposium, he joined the Kenya Medical Research Institute to found and lead the first publicly-funded oral health research unit in Kenya. Firoze appeared to be the most intelligent, creative, scientifically sound and hard- working individual I have ever met. We undertook a series of studies on dental fluorosis to provide epidemiological evidence of the association between altitude and dental fluorosis (Manji, Baelum & Fejerskov 1986 a and b). Trained in the UK by Aubrey Sheiham who supervised his PhD, Firoze took on the responsibility for organizing oral health surveys in a rural population in Machakos district in Kenya that had been extensively researched demographically and medically (van Ginneken & Muller 1984), comprising about 25.000 where we could conduct the longitudinal studies. I had a young promising PhD student in epidemiology, Vibeke Baelum. She together with Firoze was responsible for design, sampling, organization and biostatistical analyses in the project. At the university of Göteborg in Sweden they had just recruited a new, young professor in microbiology, Gunnar Dahlen, to succeed Jørgen Slots who had recently moved to the USA. Jørgen suggested that Gunnar should join forces with the three of us. By chance we had established a fantastic collaborative group because we complemented each other in our approach. In addition to working hard, we developed a close friendship. Research wise it was very productive ( Baelum, Fejerskov & Manji 1988; Dahlen, et al. 1989, 1992; Manji, et al. 1989; Manji, Fejerskov & Baelum 1989; Fejerskov, et al.1989; Manji, Baelum & Fejerskov 1986a and b,1988; Baelum, Manji & Fejerskov 1986, 1990, 1991; Manji, et al. 1986; Manji & Fejerskov 1990; Manji et al. 1991; Manji, Fejerskov, Nagelkerke & Baelum 1991; Baelum, et al 1993 and 1995; Fejerskov, et al. 1994 ) and gave us a whole new way of looking at dental caries and not least periodontal breakdown based on epidemiological evidence.
One of the more challenging observations was that despite extremely poor oral hygiene in the majority of the population, there were relatively few teeth lost with age due to periodontal disease. This was so contradictory to the ‘natural history of periodontal disease’ as derived from the studies from Sri Lanka by Löe et al. (1986), so Baelum had – when being a young scientist – difficulty in getting our first several papers accepted on the subject. One referee comment was ‘this is of limited interest because it is based only on observations in African populations’. This triggered us, and Vibeke, Gunnar and I took on the impossible: to set up longitudinal studies in rural and urban, adult and elderly, populations in China. Thanks to professor Luan Wenmin who was now director at Beijing Hospital and had been post-doc with me in Aarhus for two years, this became a reality. For more than 20 years we worked together with Wenmin. In addition, we were lucky to get a young Greek, Panos Papapanou, from Gunnar’s group involved as well. Suddenly, I realize that we were the only group that has managed to conduct such demanding clinical and microbiological longitudinal studies with the same researchers doing the meticulous clinical scoring and data collection on large adult and elderly populations in Africa and Asia. (Papapanou, et al. 1997; Baelum, et al. 1997a, b and c; Luan, et al. 2000).
Combining the results from our basic laboratory and animal studies with the data from clinical and epidemiological studies, we developed a radically different way of understanding the natural history of both dental caries and periodontal diseases in humans. At regular intervals we tried to see our results in a broader clinical perspective by writing review papers (Fejerskov, Thylstrup & Larsen 1977, 1981; Baelum, Manji & Fejerskov 1991; Fejerskov, et al. 1994; Aoba & Fejerskov 2002). Moreover, from the 1980s, we started to share our knowledge with younger generations by writing and editing international textbooks (Textbook of Cariology, Munksgaard 1986; Dental Fluorosis, Munksgaard 1988; Textbook of Clinical Cariology, Munksgaard 1994; Fluorides in Dentistry, Munksgaard 1996; Dental Caries – the disease and its clinical management Blackwell/Wiley 2003, 2008, 2015; Essentials of Dental Caries, Oxford Uni. Press 2016).
From dentistry to general health—and back to the lab
My experience from working in the broader general health and sciences’ field in the last 25+ years has influenced my perspectives on oral health. From 1993-98 I became rector of the Danish Research Academy, a governmental institution responsible for stimulating the quality of research as well as coordinating the development of PhD training programs within all faculties of Danish universities. Subsequently, from 1999-2006, I became director of the Danish National Research Foundation whose responsibility was to identify and fund the most outstanding Danish scientists by creating centers of excellence within all disciplines of Humanities and Social sciences and not least the basic Natural and Health sciences. The Foundation’s task was to enable Danish scientists to compete with the most advanced groups internationally in the respective areas of research. When I returned to Aarhus University to do basic research from 2007, I was so fortunate to become a member of one such center of excellence, The Water and Salt Center, at the Medical Faculty of Aarhus University. The director, Søren Nielsen, was a vibrant and dynamic scientist who was open-minded and allowed me to benefit from the center’s expertise on cell membrane ion-pumps and exchangers. This allowed us to better understand the complex cellular events that take place during enamel maturation. Kaj Josephsen and I found ourselves back at the bench where we started supervised by an excellent basic scientist, Sebastian Frische (Josephsen, et al. 2010; Damkier, et al. 2013; Frische, et al. 2014).
Summary of findings on dental caries, fluorides, dental fluorosis, and periodontal disease
In the following I want to summarize the findings from our laboratory studies, animal experiments in rats, pigs and humans, together with the epidemiological evidence that we have accumulated. This will allow me to reflect on the future of dentistry and to make proposals about what needs to be done to improve oral health internationally.
- Dental caries is ubiquitous. It is biofilm-induced and continues to develop and progress life-long if inappropriate oral hygiene prevails.
- Caries incidence is fairly constant in a given population depending on dietary habits and other cultural traditions.
- Dental caries should be recorded at pre-cavitated stages. Otherwise, if we only record frank cavities in children as part of national health care planning, we severely underestimate the expected occurrence of caries in adult populations.
- Active dental caries can be arrested at any stage (until the pulp is irreversibly affected). Caries can remain inactive lifelong if appropriate control measures are performed.
- Root surface caries is inversely related to number of teeth remaining at high age. If an individual reaches 60 or 70 years of age with more than an average of 9 teeth remaining, he/she is not more likely to develop new lesions despite gradual exposure of root surfaces to the oral environment.
- Tooth loss is predominantly the result of dental caries and of restorations that fail, resulting in the vicious restorative cycle where teeth are eventually extracted.
- Treatment decision should be based on a clinical assessment of caries lesion activity and past experience – combined with cosmetic wishes of the patient.
- Fluoride is a therapeutic agent which must be present in slightly elevated concentrations in the oral fluids (e.g. the biofilm fluid) to exert its cariostatic effect.
- Fluoride incorporated into the tooth mineral does not have any significant caries preventive effect.
- Fluoride gradually becomes incorporated into the surface enamel mineral underneath dental biofilms as a result of multiple pH fluctuations.
- Dental fluorosis is the result of increased porosity of enamel (hypomineralisation). The severity of hypomineralisation is dose dependent (mg F ingested/kg body weight) assuming regular daily ingestion during the period of enamel formation.
- Dental fluorosis is best recorded using the TF-index as it is reliable and the most sensitive way of classifying the degree of hypomineralisation.
- Dental fluorosis is most likely the result of interference with otherwise normal enamel maturation. The relative effect of fluoride on the stages of enamel matrix secretion is not known. The dark stained enamel pits in more severe stages of dental fluorosis is a result of mechanical damage of the fragile surface zone covering the extensive deeper parts of porous enamel. These are not to be confused with true hypoplasia.
- If fluoride is ingested from birth the rapidly growing skeleton takes up most of the fluoride and acts as a reservoir for slow release into the plasma as the bone undergoes constant remodeling. Plasma levels of fluoride steadily increase with age if persons remain exposed to the same background level.
- There is no level of water fluoride concentration below which dental fluorosis may not occur. Therefore such a claim as ‘optimal fluoride dose’ is a misnomer.
- The prevalence and severity of fluorosis is dependent on altitude assuming a constant fluoride exposure.
- The relative severity of dental fluorosis within the dentition, assuming a stable fluoride exposure for 10-20 years, varies, with the most severely affected teeth being those which develop and erupt latest. Estimations of exposure to fluoride and severity of dental fluorosis in a population can best be assessed from 12 years of age.
- In populations with bad oral hygiene, loss of periodontal attachment gradually progresses with age accompanied by a gradual recession of the gingival margin
- Bad oral hygiene does not in and of itself result in rapid loss of attachment and enhanced tooth loss.
- There is no correlation between neither the amount of dental plaque nor specific microorganisms in the gingival pocket and rate of loss of attachment.
- Is periodontal disease to be considered an infectious disease in a classical sense?
If these observations and conclusions are kept in mind, a few additional statements may indirectly follow:
- A certain amount of dental fluorosis in a population is not an unavoidable condition in order to obtain a maximum caries reduction because fluorides do not need to be ingested to obtain maximum caries control.
- The concept of ‘caries prevention’ should be replaced by the concept of ‘caries control’
- Dental caries is not to be considered ‘an infectious and transmittable disease’. It is a result of fluctuating pH in the dental biofilm in the local eco-niches intraorally. The dental biofilm is composed of a commensal microflora the composition of which is dependent on the local environmental conditions (e.g. pH).
The dental profession and the global oral health situation in 2017
Of course the dental profession deals with more than just caries. The reality, however, is that in most private dental clinics in most countries, more than 85% of the ‘treatment’ is for cosmetic reasons, sore or bleeding gums, removal of periodontal pockets, scaling and polishing, and mechanical repair of those teeth destroyed by caries and /or by previous restorations. Partial dentures and crown and bridge work is still common, but in the Nordic countries, and for those who can afford it around the world, there is growing use of dental implants to replace teeth lost due to caries or to repetitive restorative repair. (The remaining 15 % of work undertaken by dentists is devoted to TMJ problems, minor oral surgery, occlusal adjustments, orthodontics, etc.) It is remarkable that most of these activities are mainly directed at those cohorts who are from the era when the young had large numbers of dental cavities, enough to keep most dentists occupied with the ‘restorative cycle’ in their practices. However, as I have shown from the Danish experience, it is possible in 2017 to have most 20-year-olds almost free from cavities and fillings by providing very simple, non-invasive, caries control measures. Such a cavity- or filling-free status can be maintained life-long if the oral health workforce were willing to perform cost-effective control measures. But traditional restorative dentists can only make a living under conditions where they are primarily paid on the basis of ‘fees-for- restorative-work’.
The global burden of oral diseases is huge and not declining (Marcenes, et al. 2013). Despite some improvements in oral health outcomes in some high-income countries we are at a global stage facing a ‘dental crisis’ .In many parts of the world there is almost an explosion in the number of dental schools producing the classical restorative dentists. Colombia is an example of a country with some of the largest socio-economic disparities, a large almost unchanged burden of oral diseases (the national oral health situation as described in MoH reports and data 2016) and yet, by year 2020, the dental schools will have produced a ratio of one dentist to 750 inhabitants, all trained as traditional dentists with restorative care as their primary focus. It is striking that there appears around the world to be no relationship between the number of dentists trained and available and the oral health burden in the populations they are serving.
One might argue that variations in global socio-economic and cultural conditions makes it impossible to propose a solution which may be applicable to all societies. However, based on my experiences from Europe, Africa and Asia there are common features in the way oral diseases are coped with and the same mistakes which we in Europe made in the last 50 years are now repeated around the world.
In recent years several international organizations have addressed the challenges which the dental profession is facing (FDI 1982; Hobdell, et al. 2003) and formulated goals to be achieved. Most of these ‘vision papers’ have addressed and identified the obvious problems we are facing. But when it comes to proposing solutions, all we hear is the same mantra which, in my opinion, will make it almost impossible to produce better oral health for all in a cost-effective manner. The ethos and philosophy of dentistry is focused on a downstream, patient-centered, curative and rehabilitative approach to cope with oral diseases (Baelum 2011). Naturally, the dental profession can only imagine that it should be the classically trained dentists who in the future should be the leaders of dental teams that can ensure appropriate prevention, control and treatment of oral diseases.
In our view the classically trained dentist is predominantly shaped in a mechanically and technically focused dental curriculum. Therefore, they are not the appropriate cadre for leading teams of oral health care personnel that could be responsible for a population’s oral health, diagnosis, control and prevention of disease, and making of suitable treatment decisions (Fejerskov et al. 2013).
Oral diseases share social determinants (Watt 2012), biological pathways and risk factors (Sheiham & Watt 2000) with the other non-communicable diseases and oral health must be totally integrated into the broader medical care infrastructure. The current training of dental personnel and the service provision as well as the distribution of oral health care teams in most countries do not address the needs of most populations.
Many argue that dentistry should have many more specialists in various sub-disciplines. There is a big global market for postgraduate masters programs. Such developments only result in little interdisciplinary communication. Often, such sub-disciplines become isolated silos having loose connection with the development of sciences and general health, and tend to become narrow-minded with tunnel vision (DePaola & Slavkin 2004).
The role of dental research and industrial influence on caries research
Most dental schools do not have a significant backbone of ongoing high quality research because biomedical research related to oral diseases has become complex and multidisciplinary. There is neither funding, nor availability of advanced equipment, nor the presence of research groups of sufficient size. Many schools have limited or no research trained clinical staff and limited research being undertaken at all. To-day, oral health addressing basic science questions can only be conducted with the close collaboration of researchers experienced in the general basic sciences, preferably integrated into strong research groups in the natural and medical sciences. So the gap between students entering dental clinical disciplines and understanding of basic sciences and scientific reasoning is widening. Clinical departments are mostly staffed with clinical dentists who have limited or no training in evaluating research publications, so the teaching is based on what the teachers learnt themselves when they were training at dental school.
Moreover, in many countries it is becoming increasingly more difficult to rise funding for clinical dental research. As a consequence, many dental schools have turned towards industry and multinational corporations for funding their research work. They even allow in some countries such companies to fund departments partly staffed by dentists paid by the corporations. While they appear to be university research units, and having thereby the ethos of ‘independence’, in practice the research they do is heavily influenced by the commercial interests of the sponsoring corporation.
The pharmaceutical industry’s role in general medicine, for example, has been exposed recently (Gøtzsche, Smith & Rennie: Deadly medicines and organised crime; how big pharma has corrupted healthcare 2013 by Radcliffe Publishing; Gøtzsche: Deadly Psychiatry and Organised Denial 2015 by People’s Press). Two examples from dentistry should be presented because they both exemplify what the dental profession – and the public – are faced with in the future when trying to develop better oral health for all.
Sugar is the key dietary component most responsible for caries development (Sheiham & James 2014) and yet there has been very little research trying to understand how to restrict sugar intake since that would substantially reduce the burden of caries in the population. Kearns, Glantz and Schmidt published in 2015 documentation on how the sugar industry managed to influence the scientific agenda of the 1971 National Caries Program (NCP) of the US National Institute of Dental Research (NIDR). Based on an analysis of internal documents, they showed how the sugar industry managed to infiltrate the NCP so as to ensure an alignment of the research agendas of the NIDR with the interests of the sugar industry. Thus, the NCP ignored all strategies to limit sugar consumption. Instead they focused their work on fluoride delivery; on stimulating research on how to reduce the virulence of some commensal oral bacteria which, at the time, some proposed were responsible for causing caries – even focusing attention on research promoting a S. Mutans vaccine against tooth decay; on stimulating research on enzymes that might break up dental plaque; and research on how to modify food products with additives to reduce sugar’s harmful effects. No surprise that NCP failed to significantly reduce the burden of dental caries.
Europe, and not least the Royal College of Surgeons of England, looked to and followed what the US was doing. Many of the key researchers from NCP played key roles in the debates and research agendas proposed at scientific conferences, even at ORCA. This severely set back and skewed research on dental caries for decades. The sugar industry protected itself from potentially damaging research by stimulating and indirectly funding caries research in many other directions. They thereby, with the collusion of many dental research scientists, succeeded in interfering with efforts to improve public dental health. The parallels with the role of the tobacco industry in the development of lung cancer is, of course, obvious. Likewise concerning the likely role of sugar in the global epidemic of obesity and diabetes 2 (Taubes: The Case Against Sugar 2016 by Penguin Random House)
Another equally sophisticated way of influencing the research agenda is seen when multinational companies constantly promote new products simply to increase their market share. This may be by recommending the use of toothpastes with different fluoride concentrations specifically designed, allegedly, for use by children or the elderly. In other cases, products are developed that may reduce the rate of caries lesion developments in controlled clinical trials, but which are simply not cost-effective measures for public health use if they require that the treatment is given by a dentist. Many dental schools benefit from conducting such clinical trials but may not be able to analyze the data themselves, even if staff members are co-authors of the publications. Shaw, Naimi-Akbar & Astvaldsdottir (2015) have recently pointed at a case of interest for this debate in a short paper in the BMJ. A multinational toothpaste company has tested the effect of a fluoride toothpaste also containing arginine on populations in Thailand and China. The publications arising from the studies they supported claimed a positive effect, and the company promoted the use of this paste claimed to be better than conventional fluoride toothpastes. After careful scrutiny of the 4 publications, Shaw and colleagues conclude that:
‘the studies which supposedly establish the efficacy of arginine toothpaste are ethically and methodologically flawed, in addition to concerns about research integrity which also tarnish the studies. As well as the unethical use of an unnecessary placebo arm and failure to report the effects on placebo participants, the studies do not seem to have been properly blinded, the quality of randomization is unclear, no protocols were published before the studies were conducted, and many of the authors had serious conflicts of interest which were not disclosed in all published articles’.
Shaw, Naimi-Akbar & Astvaldsdottir further point out that arginine toothpaste is substantially more expensive than normal fluoride toothpaste. This means anyone who accepts the claims concerning its efficacy is likely to spend more money on toothpaste, may be to no added benefit. And in any situation where arginine toothpaste is provided for free by public health authorities, public money might be better spent on ordinary fluoride toothpaste.
To sum up my experience so far: Some high-income countries have seen some improvements in oral health outcomes, but the profession has not adapted to the prevailing oral health situation and is facing a crisis ( report from the U.S. Senate Committee on Health, Education, Labor and Pensions 2012 entitled ‘Dental crisis report’). In low and middle income countries oral diseases are ubiquitous (Abid, et al. 2015) and oral and dental diseases afflict almost everyone worldwide (Marcenes, et al. 2013). Open carious cavities in the permanent dentition rank as the most prevalent of all health conditions surveyed in the latter paper. Dental caries causes pain and discomfort in children, it affects learning at school and in adults and elderly dental caries/pain restricts dietary intake and social function (Tsakos, et al. 2012) and results in extensive tooth loss (Fejerskov et al. 2013). This is appreciated by international bodies such as FDI (da Silva & Glick 2012; Glick, et al 2012), but when it comes to suggesting solutions they fall back on old formulae, failing to realize the urgent need for rethinking our approach, especially whether we are producing the right workforce and structure of the profession to serve the need of populations. We know today how to control dental caries cost-effectively (Fejerskov, Nyvad & Kidd, eds. Textbook on Dental Caries 2015; Kidd & Fejerskov, Essentials of Dental Caries 2016)
Proposal for training the future oral health personnel and organize oral health care integrated within the general health sector
Many before us have reflected in depth on the need for action from dental educators and academic leaders on the different components of oral healthcare provision. While most have discussed a need for adjustments of the dental curriculum in response to rapidly changing oral disease patterns or a perceived need for expansion of dental specialist training, few have given much attention to considering how the current structure and organization of the oral healthcare system acts as a major obstacle for achieving a functional natural dentition for life for all. Tomar and Cohen (2010) emphasized the urgent need to integrate oral health care into general health care, and we think that their ‘diagnosis’ of the problem in the USA is of relevance beyond there. They stated that:
‘in the coming decades, the US population will continue to shift toward an older age distribution and an increasing number of Americans will reach their golden years with relatively intact dentitions, chronic disease, and multiple medications. […..] Because of the tremendous overlap of risk factors that threaten oral health and those that increase the risk for other chronic diseases, an integrated system may be able to reap broader benefits from health promotion and disease prevention’.
The current practice-based approach to dental treatment and rehabilitation of individuals represents a cul-de-sac from a social, ethical and cost-effectiveness point of view. Improved oral health care systems cannot be achieved through minor adjustments neither of the dental curriculum, nor of the number of dental specialties, nor of the payment systems, nor of the solo-practice-based delivery system. In our view, it necessitates a more profound break with long-standing traditional thinking in dental education and in the organization oral health care delivery.
We cannot expect that any society should spend more money on oral health as general health is meeting increasingly great challenges and expenditures. Even if it was possible it would not be justifiable as we have had only a minor effect on the oral health situation globally so far. The ‘traditional dentist’ is not the answer to how to provide oral disease control to everyone so that a functional dentition can be maintained lifelong.
Time has come to realize that the current dental workforce should be replaced by two new types of dental professionals: the ‘oral health care provider (OHCP), who will comprise the vast majority of the group of dental professionals, and the ‘oral clinical specialist’ (OCS).
The Oral Health Care Professional (OHCP) should be at the centre of health services to meet the needs of most individuals, families and communities. They would be responsible for addressing the health care needs of all age groups, with their principle focus being on evidence-based diagnosis and oral disease control. The OHCP would be a cost-effective health professional who has a profound understanding of oral disease control and oral health as part of general health and well-being and who is willing to cope with social needs in a critical, creative and pertinent way. The OHCP should be competent and skilled not only in the diagnosis and control of oral diseases, but importantly also in public health, basic health economy, management and communication. A major role of the OHCP would be to lead teams of oral health personnel, which may include auxiliaries/dental assistants/hygienists/therapists according to the particular fabric for each country, at community level, and to plan health care and set priorities at community level involving all age groups, including all the currently un- or under-served groups in the community. Their activities should be integrated into the general health care services. The OHCPs and their staff will be able to cater for the oral health care needs of the large majority of the population. The OHCPs and their staff should therefore be the gatekeepers with respect to advanced oral health care needs, just as their services should be integrated into the general health care system. The OHCPs will also when needed be able to perform simple restorative treatments.
The Oral Clinical Specialist (OCS): There will always in future populations be a number of individual patients who are in need of more oral advanced care including complex rehabilitation. These patients are in particular likely to belong to the growing fraction of older people with chronic diseases and multiple medications. We need a new cadre, the OCS, to cater for their needs. To ensure that complex oral care for individuals with chronic diseases and multiple medications becomes integrated with general health care, we suggest that the OCS is a medically trained person who has a comprehensive 2-3 years postgraduate training in one of three different clinical specialties: Oral Rehabilitation, Oral Surgery and Medicine, or Orthodontics. The OCS will be part of larger general health care clinics comprising also ENT doctors, Ophtalmologists, endoscopic diagnostic facilities, X-ray facilities, etc. Such clinics will typically be scattered at regional level and in addition the OCS will also be integrated in regional and central hospitals. Patients are referred to these clinics/hospitals by the OHCPs operating at rural and urban community level.
Many of the arguments developed here may, at a first glance, seem to apply primarily to the industrialized countries with a well-developed health care system. However, our experiences from Africa, South-East Asia, China and South America have convinced me that one of the worst things that could happen in many of these countries would be the uncritical attempt to replicate the oral health care systems prevailing in Europe and North America. In this context, I would like to cite extensively from a previous publication (Baelum, van Palenstein, Hugoson, Yee & Fejerskov 2007):
‘Broadly speaking, the oral disease profile of populations in low-income countries in Africa, China, Southeast Asia and South America are typically characterized by a relatively low occurrence of caries, poor oral hygiene conditions, widespread and severe gingivitis, and considerable periodontal breakdown, which, however, does not result in major tooth loss endangering a functional dentition, except for a sub-fraction of the population. The existing oral health care services are often rudimentary, and the challenge for such countries is to avoid the implementation of dental services based on the high-technology clinical approach well known from the Western high-income countries. Unless regulatory steps are taken it is easy to foresee that private initiatives in case of socio-economic growth will result in such services. In the early phase such private enterprises will serve only the relatively small, but affluent, subgroup of the population that can pay. Gradually, the next phase is entered where the existing services are too limited and the economic means of the general population too small to be compatible with dental treatment and the disease affected teeth are therefore extracted. Provided economic growth continues, the third phase is characterized by the dental services gradually approaching the contents and extent well known from the high-income countries in the hey-days of restorative dentistry. Increasing availability and access to classic dentists as they are known from Europe and North America would thus have deleterious consequences’.
As classic dentistry will not give priority to disease control based on biologically sound principles, we surmise that our proposal for OHCPs and OCS apply equally to countries presently developing their services. It is our view that only by thoroughly reconsidering the oral health care workforce can we continue the stride towards the ideal oral health care system, which has the attributes of being integrated, health promotional and prevention oriented, monitoring, evidence based, cost-effective, sustainable, equitable, universal, comprehensive, ethical, quality assuring, culturally competent and empowering (Fejerskov et al. 2013).
Through my lens, we need to – in my broken Danish translation – “put the mouth back into the rest of the body.” This means that our universities/dental schools need to be reconfigured. We need to avoid subspecialist silos and create interdisciplinary learning environments. In my view we need to spark groundbreaking reforms of the structure of the dental profession and the training of oral health care personnel. We must broaden our horizons, form coalitions and not tolerate conservative and often static organizations.
This is not going to happen overnight – I know – but in responsible countries various test models ought to be designed so that valid conclusions about the effectiveness of different ways of controlling oral health in all age groups could be tried out. Can this be done without attempts from professional organizations, industrial interests, etc. to influence the outcome? It is due time that the dental profession takes such initiatives before politicians inspired by other professions and insurance companies suddenly conclude that others should fill out the gap in oral health/physiology/medicine created because unless it somehow has a spinning instrument associated with it dentists will not be the solution!
Ole Fejerskov, DDS, PhD, Dr Odont, is Emeritus Professor, Aarhus University, Denmark
Abid A, Maatouk F, Berrezouga L, Azoda C, Uti O, El-Shamy H, Oginni A. Prevalence and severity of oral diseases in African and Middle Eastern Region. Adv Dent Res 2015;27:10-17.
Andersen L, Richards A, Care AD, Kerzel Andersen HM, Kragstrup J, Fejerskov O. Parathyroid glands, calcium, and vitamin D in experimental fluorosis in pigs. Calcif Tissue Int 1986;38:222-6.
Aoba T, Fejerskov O. Dental fluorosis: Chemistry and biology, Critical Reviews in Oral Biology and Medicine 2002;13:155-170.
Backer-Dirks O. The relationship between the fluoridation of water and dental caries experience. Int Dent J 1967;17:582-605.
Baelum V, Chen X, Manji F, Luan W-M, Fejerskov O. Profiles of destructive periodontal disease in different populations. J Periodontol Res. 1996;31:17-26.
Baelum V, Fejerskov O, Manji F. Periodontal diseases in adult Kenyans. J Clin Periodontol 1988;15:445-52.
Baelum V, Fejerskov O. Tooth loss as related to dental caries and periodontal breakdown in adult Tanzanians. Community Dent Oral Epidemiol 1986;14:353-7.
Baelum V, Luan W-M, Chen X, Fejerskov O. A 10-year study of the progression of destructive periodontal disease in adult and elderly Chinese. J Periodontol 1997;68:1033-42.
Baelum V, Luan W-M, Chen X, Fejerskov O. Predictors of destructive periodontal disease incidence and progression in adult and elderly Chinese. Community Dent Oral Epidemiol 1997;25:265-72.
Baelum V, Luan W-M, Chen X, Fejerskov O. Predictors of tooth loss over 10-years in adult and elderly Chinese. Community Dent Oral Epidemiol 1997;25:204-10.
Baelum V, Luan W-M, Dahlen G, Fejerskov O, Chen X. Six-year progression of destructive periodontal disease in 2 subgroups of elderly Chinese. J Periodontol 1993;64:891-9.
Baelum V, Luan W-M, Fejerskov O, Chen X. Tooth mortality and periodontal conditions in 60-80 year-old Chinese. Scand J Dent Res 1988;96:99-107.
Baelum V, Manji F, Fejerskov O. A new approach to investigating associations in periodontal disease data. Community Dent Oral Epidemiol. 1990;18:177-83.
Baelum V, Manji F, Fejerskov O. Posteruptive tooth age and severity of dental fluorosis in Kenya. Scand J Dent Res 1986;94:405-10.
Baelum V, Manji F, Fejerskov O. The distribution of periodontal destruction in populations in non-industrialized countries: evidence for the existence of high risk groups and individuals. In: Johnson NW, ed. Risk markers for oral diseases. Vol. 3. Periodontal diseases. Markers of disease susceptibility and activity. Cambridge: Cambridge University Press, 1991;27-74.
Baelum V, van Palenstein Helderman W, Hugoson A, Yee R, Fejerskov O. A global perspective on changes in the burden of caries and periodontitis: implications for dentistry. J Oral Rehabil 2007;34:872-906
Baelum V. dentistry and population approaches for preventing dental diseases J Dent 2011;39 (Suppl.2):S9-S19.
Bjarnason S, Finnbogason SY, Holbrook P, Köhler B. Caries experience in Islandic 12-years-old urban children between 1984 and 1991. Community Dent Oral Epidemiol 1993;21:194-197.
da Silva OM, Glick M. FDI vision 2020: a blueprint for the profession. Int Dent J. 2012;62:277
Dahlén G, Manji F, Baelum V, Fejerskov O. Putative periodontopathogens in “diseased” and “nondiseased” persons exhibiting poor oral hygiene. J Clin Periodontol 1992;19:35-42.
Dahlén GG, Luan W-M, Baelum V, Fejerskov O, Chen X. Periodontopathogens in elderly Chinese with different periodontal disease experience. J Clin Periodontol 1995;22:188-200.
Damkier HH, Josephsen K, Takano Y, Zahn D, Fejerskov O, Sebastian F. Fluctuations in surface pH of maturing rat incisor enamel are a result of cycles of H(+)-secretion by ameloblasts and variations in enamel buffer characteristics. BONE 2013.
DePaola DP, Slavkin HC. Reforming dental health professions education: a white paper. J Dent Educ. 2004;68:1139-1150.
FDI Global goals for oral health in the year 2000. Int Dent J. 1982;32:74-77.
Fejerskov O, Antoft P, Gadegaard E. Decrease in caries experience in Danish children and young adults in the 1970-ties. Proceedings: First International Conference on the Declining Prevalence of Dental Caries, Boston 1982. J Dent Res 1982;61:spec iss 1305-10.
Fejerskov O, Baelum V, Richards A. Dose-response and dental fluorosis. In: Fejerskov O, Ekstrand J, Burt BA, eds. Fluoride in dentistry. 2nd ed. Copenhagen: Munksgaard, 1996;153-66.
Fejerskov O, Escobar G, Jossing M, Baelum V. A functional natural dentition for all – and for life? The oral health care system needs revision. J Oral Rehabil 2013;40:707-722.
Fejerskov O, Johnson NW, Silverstone LM. The ultrastructure of fluorosed human dental enamel. Scand J Dent Res 1974;82:357-72
Fejerskov O, Joost Larsen M, Josephsen K, Thylstrup A. Effect of long-term administration of fluoride on plasma fluoride and calcium in relation to forming enamel and dentin in rats. Scand J Dent Res 1979;87:98-104.
Fejerskov O, Larsen MJ, Richards A, Baelum V. Dental tissue effects of fluoride. Adv Dent Res. 1994;8:15-31.
Fejerskov O, Manji F, Baelum V. The nature and mechanism of dental fluorosis in man. J Dent Res 1990;69: sp iss 692-700.
Fejerskov O, Nyvad B, Larsen MJ. Human experimental caries models: Intra-oral environmental variability. Adv Dent Res 1994;8:134-43.
Fejerskov O, Scheie A Aa, Manji F. The effect of sucrose on plaque pH in the primary and permanent dentition of caries- inactive and -active Kenyan children. J Dent Res 1992;71:25-31.
Fejerskov O, Silness J, Karring T, Löe H. The occlusal fissure of unerupted third molars as an experimental caries model in man. Scand J Dent Res 1976;84:142-9.
Fejerskov O, Silverstone LM, Melsen B, Møller IJ. Histological features of fluorosed human dental enamel. Caries Res 1975;9:190-210.
Fejerskov O, Thylstrup A, Joost Larsen M. Clinical and structural features and possible pathogenic mechanisms of dental fluorosis. Scand J Dent Res 1977;85:510-34.
Fejerskov O, Thylstrup A, Joost Larsen M. Rational use of fluoride in caries prevention. A concept based on possible cariostatic mechanisms. Acta Odontol Scand 1981;39: 241-9.
Fejerskov O, Yaeger JA, Thylstrup A. Microradiography of the effect of acute and chronic administration of fluoride on human and rat dentine and enamel. Arch Oral Biol 1979;24:123-30.
Fejerskov O. Concepts of dental caries and their consequences for under-standing the disease. Community Dent Oral Epidemiol 1997;25:5-12.
Frische S, Damkier HH, Josephsen K, Praetorius J, Takano Y, Fejerskov O. The role of ameloblast H+ secretion and enamel buffering for pH fluctuations during rat enamel maturation. BONE 2014;60:227-234
Glick M, Monteiro da Silva O, Seeberger GK, Xu T, Pucca G, Williams DM, et al. FDI vision 2020: shaping the future of oral health. Int Den J. 2012;62:278-291.
Heidmann J, Poulsen S, Arnbjerg D, Kirkegaard E, Laurberg L. Caries development after termination of a fluoride rinsing program. Community Dent Oral Epidemiol 1992;20:118-121.
Hobdell M, Petersen PE, Clarkson J, Johnson NW. Global goals for oral health 2020. Int Dent J. 2003;53:285-288.
Hugoson A, Koch G, Slotte C, Bergendal T, Thorstensson B, Thorstensson H. Caries prevalence and distribution in 20-80-years-olds in Jönköbing, Sweden, in 1973,1983 and 1993. Community Dent Oral Epidemiol 2000;28:90-96.
Hugoson A, Koch G. Thirty year trends in the prevalence and distribution of dental caries in Swedish adults(1973-2003). Swed Dent J 2008;32:57-67.
Joost Larsen M, Fejerskov O, Jensen SJ. Effects of fluoride, calcium and phosphate administration on mineralization in rats. Calcif Tiss Int 1980;31:225-30.
Joost Larsen M, Richards A, Fejerskov O. Effect of intraperiotoneally injected fluoride on plasma calcium in suckling and adult rats. Calcif Tiss Int 1981;33:541-4.
Josephsen K, Fejerskov O. Ameloblast modulation in the maturation zone of the rat incisor enamel organ. A light and electron microscopical study. J Anat (London) 1977;124:45-70.
Josephsen K, TakanoY, Frische S, Praetorius J, Nielsen S, Aoba T, Fejerskov O. Ion transporters in secretory and cyclically modulating ameloblasts: a new hypothesis for cellular control of preeruptive enamel maturation. Am J Physiol Cell Physiol 2010;299:1299-1307.
Kearns CE, Glantz SA, Schmidt LA. Sugar Industry Influence on the Scientific Agenda of the National Institute of Dental Research’s 1971 National Caries Program: A Historical Analysis of Internal Documents. PLoS Med 2015 12(3):e1001798. Doi:101371/journal.pmed.1001798.
Kragstrup J, Richards A, Fejerskov O. Effects of fluoride on cortical bone remodeling in the growing domestic pig. Bone 1989;10:421-4.
Larsen MJ. Enamel solubility, caries and erosions. Thesis 1975 Royal dental College Aarhus, Denmark
Löe H, Ånerud A, Boysen H, Morrison E. Natural history of periodontal disease in man. Rapid, moderate and no loss of attachment in Sri Lankan laborers 14 to 46 years of age. J Clin Periodontol 1986;13:431-440.
Luan W-M, Baelum V, Chen X, Fejerskov O. Dental caries in adult and elderly Chinese. J Dent Res 1989;68:1771-6.
Luan W-M, Baelum V, Chen X, Fejerskov O. Tooth mortality and prosthetic treatment patterns in urban and rural Chinese aged 20-80 years. Community Dent Oral Epidemiol 1989;17:221-6.
Luan W-M, Baelum V, Fejerskov O, Chen X. Ten-year incidence of dental caries in adult and elderly Chinese. Caries Res 2000;34:205-13.
Manji F, Baelum V, Fejerskov O, Gemert W. Enamel changes in two low-fluoride areas of Kenya. Caries Res l986;20:371-80.
Manji F, Baelum V, Fejerskov O. Dental fluorosis in an area of Kenya with 2 ppm fluoride in the drinking water. J Dent Res 1986;65:659-62.
Manji F, Baelum V, Fejerskov O. Fluoride, altitude and dental fluorosis. Caries Res 1986;20:473-80.
Manji F, Bælum V, Fejerskov O. Tooth mortality in an adult rural population in Kenya. J Dent Res 1988;67:496-500.
Manji F, Fejerskov O, Baelum V, Luan W-M, Chen X. The epidemiological features of dental caries in African and Chinese populations: Implications for risk assessment. In: Johnson NW, ed. Risk markers for oral diseases. Vol. 1. Dental caries. Markers of high and low risk groups and individuals. Cambridge: Cambridge University Press, 1991;62-99.
Manji F, Fejerskov O, Baelum V. Pattern of dental caries in an adult rural population. Caries Res 1989;23:55-62.
Manji F, Fejerskov O, Nagelkerke NJD, Baelum V. A random effects model for some epidemiological features of dental caries. Community Dent Oral Epidemiol 1991;19:324-8.
Manji F, Fejerskov O. Dental caries in developing countries in relation to the appropriate use of fluoride. J Dent Res 1990;69 sp iss 733-41.
Marcenes W, Kassebaum NJ, Bernabé E, Flaxman A, Naghavi M, Lopez A, MurrayCJ. Global burden of oral conditions in 1990-2010: a systematic analysis. J Dent Res 2013;92:592-597.
Nyvad B, Fejerskov O. Active root surface caries converted into inactive caries as a response to oral hygiene. Scand J Dent Res 1986
Nyvad B, Fejerskov O. An ultrastructural study of bacterial invasion and tissue breakdown in human experimental root- surface caries. J Dent Res 1990;69:1118-25.
Nyvad B, Fejerskov O. Assessing the stage of caries lesion activity on the basis of clinical and microbiological examination. Community Dent Oral Epidemiol 1997;25:69-75.
Nyvad B, Fejerskov O. Structure of dental plaque and the plaque-enamel interface in human experimental caries. Caries Res 1989;23:151-8.
Nyvad B, ten Cate JM, Fejerskov O. Arrest of root surface caries in situ. J Dent Res 1997;76:1845-53.
Nyvad B, ten Cate JM, Fejerskov O. Microradiography of experimental root surface caries in man. Caries Res 1989;23:218-24.
Papapanou, PN, Baelum V, Luan W-M, Madianos PN, Chen, X, Fejerskov O, Dahlén G. Subgingival microbiota in adult Chinese: Prevalence and relation to periodontal disease progression. J Periodontol 1997;68:651-66.
Richards A, Fejerskov O, Ekstrand J. Fluoride pharmacokinetics in the domestic pig. J Dent Res 1982;61:1099-102.
Richards A, Joost Larsen M, Fejerskov O, Thylstrup A. Fluoride content of buccal surface enamel and its relation to caries in children. Arch Oral Biol 1977;22:425-8.
Richards A, Kragstrup J, Josephsen K, Fejerskov O. Dental fluorosis developed in post-secretory enamel. J Dent Res l986;65:1406-9.
Sabbah E, Tsakos G, Chandola T, Sheiham A, Watt RG. Social gradients in oral and general health. J Dent Res 2007;86:992-996.
Sheiham A, James WPT. A new understanding of the relationship between sugars, dental caries and fluoride use: implications for limits on sugar consumption. Public Health Nutrition 2014;1-9
Sheiham A, Watt RG. The common risk factor approach: a rational basis for promoting oral health. Community Dent Oral Epidemiol 2000;28: 399-406.
Theilade E, Fejerskov O, Karring T, Theilade J. A microbiologic study of old plaque in occlusal fissures of human teeth. Caries Res 1978;12:313-9.
Theilade E, Fejerskov O, Karring T, Theilade J. Predominant cultivable microflora of human dental fissure plaque. Infect Immun 1982;36:977-82.
Theilade E, Fejerskov O, Migasena K, Prachyabrued W. Effect of sealing on the microflora of natural fissures implanted in human teeth. Arch Oral Biol 1977;22:251-9.
Theilade E, Fejerskov O, Prachyabrued W, Kilian M. Microbiological study on developing plaque in human fissures. Scand J Dent Res 1974;82:420-7.
Theilade J, Fejerskov O, Hørsted M. Transmission electron microscopy of 7-day old bacterial plaque in human dental fissures. Arch Oral Biol 1976;21:587-98.
Thylstrup A, Fejerskov O, Bruun C, Kann J. Enamel changes and dental caries in 7 year old children given fluoride tablets from shortly after birth. Caries Res 1979;13:265-76.
Thylstrup A, Fejerskov O. Clinical appearance of dental fluorosis in permanent teeth in relation to histological changes. Community Dent Oral Epidemiol 1978;6:315-28.
Tohda H, Fejerskov O, Yanagisawa T. Transmission electron microscopy of cementum crystals correlated with Ca and F distribution in normal and carious human root surfaces. J Dent Res 1996;75:949-54.
Tomar SL, Cohen LK. Attributes of an ideal oral health care system. J Public Health Dent 2010;70(Suppl.1):S6-S14.
Tsakos G, Allen PF, Steele JG,Locker D. Interpreting oral health-related quality of life data. Community Dent Oral Epidemiol 2012;40:193-200
van Ginneken JK, Muller AS. Maternal and child health in rural Kenya: an epidemiological study. Croom Helm Publ., London 1984.
Warshawsky H, Josephsen K, Thylstrup A, Fejerskov O.: The development of enamel structure in rat incisors as compared to the teeth of monkey and man. Anat Rec 1981;200:371-99.
Watt RG. Social determinants of oral health inequalities: implications for action. Community Dent Oral Epidemiol 2012;40:44-48.
Yanagisawa T, Takuma S, Fejerskov O. Ultrastructure and composition of enamel in human dental fluorosis. Adv Dent Res 1989;3:203-10.