When was tooth decay discovered

If cavities go unaddressed, they will grow — eventually causing decay that destroys teeth. Cavities, also referred to as dental caries, have caused tooth pain for millions of years. Fossils from the Australopithecus species reveal some of the earliest dental caries from 1. Paleolithic and Mesolithic skulls also show signs of cavities. The Paleolithic period took place roughly 3. Two of the leading factors of increased dental caries were the consumption of plant-based foods containing carbohydrates and rice cultivation.

This led to the development of the first cavity treatments in Pakistan between 7, BC and 5, BC. At this time, simple dental drills were used to treat cavities. Text from the Sargonid dynasty of Assyria which lasted from BC to BC revealed that tooth inflammation was cured via tooth extraction. Ancient Egyptians, Greeks and Romans also used a broad range of cavity treatments.

In the 11th century, the appearance of sugar cane led to an increase in the number of reported cavities. Top treatments for dental caries at this time included charms and herbal remedies. Meanwhile, the Age of Enlightenment proved to be a critical period for the advancement of cavity treatments. French physician Pierre Fauchard, often considered the father of modern dentistry, was one of the first people to cite sugar as a possible cause of cavities.

In the s, W. Miller and dental pioneers G. Black and J. Williams researched plaque and investigated the causes of dental caries. In , scientist Fernando E. Rodriguez Vargas discovered several strains of lactobacilli bacteria linked to dental caries. Hamster studies performed by R. Fitzgerald and Paul Keyes in the s ultimately showed a direct correlation between bacteria and cavities.

It seems Harris, Robertson, Rognard, and others had simply failed to grasp the full meaning of the relationship of caries to fermentation. In , the theory of fermentation had been fully explained by Von Liebig—an unlikely nondental scientist whose chemistry research was first presented as an oral report to the British Association for the Advancement of Science, with their full acceptance [ 46 ].

The mechanics of fermentation had been used for centuries, but it required the genius of Professor Von Liebig to present it to the scientific world in a meaningful form. Until Von Liebig, there was no understanding of fermentation in terms of chemical processes. In that era, an acceptable theory of dental caries required something more than the simple hypothesis of chemical dissolution of enamel by an acid.

The acid theory was close to the true cause of caries, but the level of science of the preceding decades simply failed to understand the missing equation—bacteria. In retrospect, due to the absence of available fermentation science before Von Liebig, it is easy to understand that until the work of Louis Pasteur from to demonstrating the necessity of microbes in fermentation [ 47 ], just why the scientific understanding of bacterial fermentation causing caries was never completely understood.

When we project a few decades ahead in our scientific understanding of bacterial fermentation, we can see that Miller presented the chemo-parasitic nature of bacteria within the oral cavity and their importance in the initial cause of acid demineralization of enamel and invasion through the enamel-dentin junction to infect the tubule complex leading to destruction of collagen and other proteins [ 10 ].

When Tomes applied litmus paper to the cavity of a carious tooth, it always gave a strong acid reaction that demonstrated the destruction of the mineral portions of enamel and dentin. Professor Black wrote [ 49 ] that the studies of Leber and Rottenstein discussed that decay was a consequence of bacteria and their capacity to promote fermentation.

Black showed that by treating decayed human dentin with iodine solutions, the underlying tubules showed a violet color, indicative of bacterial glycogen; he concluded that the tubules were filled with bacteria [ 49 ]. In their haste to report their observations, Leber and Rottenstein indicated that the fungus Leptothrix buccalis was constant in the production of caries [ 50 ].

Their observations were important to Miller as he understood the difficulties others had to contend with, but were of little use to understand the fermentation of bacteria and the cause of caries. In the late s, Leber and Rottenstein showed the presence of bacteria in the tubules causing carious dentin, making a profound impact on the dental profession [ 50 ]. Milles and Underwood of London used the techniques of Koch, to verify the work of Leber and Rottenstein.

A series of sterile flask experiments showed that tooth demineralization was due to acids secreted by bacteria. However, they could not accept the chemical theory of caries from acid demineralization of dentin under aseptic situations, as they placed a tooth in a closed flask with malic and butyric acid with human saliva in a meat suspension under aseptic conditions and no caries developed, finding uniform demineralization on all tooth surfaces, which did not resemble naturally occurring human caries, which was known to be more localized [ 51 ].

In his small Berlin laboratory that he shared with Robert Koch, Miller observed certain bacteria could convert starch by ptyalin amylase to form sugar that was fermented to lactic acid [ 10 ]. Miller cited the work of Milles and Underwood who wrote that caries most likely caused decalcification as a consequence of acids secreted by oral bacteria [ 51 ].

Miller's experiments supported studies that implicated caries due to the corrosive action of lactic acid from bacteria that demineralized the mineral of enamel and dentin [ 10 ].

In hindsight, it seems that Miller's failure to recognize the true relationship of plaque bacteria to localized dental caries may have been due to his lack of clinical experience compared to that of Black [ 5 ].

Until that time, Miller's observations of fermentation had been mainly to study the digested agent dentin by lactic acid [ 10 ]. It now seems that Black was able to piece together the complex puzzle of the cause of human caries by his own and other colleague's research data. The deeper zone, located towards the pulp, was called affected dentin, often referred to as secondary caries, being composed of fewer bacteria and demineralized dentin [ 53 ].

Black's use of references is an indication of his erudite nature It was obvious his depth of reading, understanding, knowledge, and forward thinking about the cause of caries for that era surpassed many others [ 67 ]. He understood that caries disintegration always begins on the enamel surface of the tooth in some pit or irregularity and that acid was formed at the very spot where caries begins. His clinical experience showed him that certain foods were associated with higher levels of caries.

He grasped the importance of bacteria feeding upon lodged food particles and fermenting them to organic acids. Black had made certain personal histological observations.

Black also observed that in the initial carious invasion, the internal diameter of the tubules became enlarged and using an aniline dye stain, he demonstrated the tubules were occupied with bacteria. Regarding enamel caries, Black's laboratory studies demonstrated that enamel rods fell apart at the periphery and not in the rod center. Leon Williams, a colleague of G. Using various microscopic techniques, Furrier illustrated six-zones of carious dentin: bacteria-rich, bacteria-few, pioneer-bacteria, turbid-layer, transparent and a vital reaction layer.

However, from a clinical point of view, tactile discrimination of caries varied from clinician to clinician due to its softness [ 69 ]. The issue of caries discrimination was solved by Professor Fusayama and Terachima, using an in vivo stain.

They demonstrated that softened carious dentin is composed of two layers [ 57 ]. Their research demonstrated an outer infected carious zone just below the enamel-dentin junction densely populated with facultative and anaerobic bacteria that secrete 1 organic acids capable of dissolving hydroxyapatite crystals, and 2 proteases that degrade collagen and other proteins causing detachment of apatite crystals leaving the once solid substrate to simply collapse on itself.

This outer infected caries is completely dead, with no capacity to register any sensitivity to tactile or thermal stimuli and is not physiologically capable of remineralization. This fact makes its removal clinically painless as no anesthesia is necessary.

It is somewhat softened due to organic acids dissolving the mineral rich crystals without proteases damaging the organic proteins [ 57 ]. This deeper carious zone is vital with a sensory capacity to respond to various stimuli. Once the clinician reaches this vital layer with minimally invasive instrumentation, they realize when to stop instrumentation as the underlying affected tubule complex is physiologically capable of remineralization with crystals that fill the lumen of dentinal tubules to become sclerotic [ 59 , 65 ].

This expression from Benjamin Franklin — means it is better to avoid problems in the first place, rather than trying to fix them once they arise. In a lecture to students, G. We wonder what Black would think if he realized that most of today's dental schools throughout the world still teach a restorative focused curriculum; rather than a series of preventive courses?

Since the s, our profession has witnessed the introduction of caries detectors, acid etchants, glass ionomers and composites that seem more suited to minimal intervention than Black's extension for prevention concepts of amalgam placement.

The addition of fluoride to public water has proved effective to reduce caries in human dentitions [ 80 ]; postdevelopmental use of fluoride is known to cause a significant reduction in caries through topical interaction with surface enamel and dentin throughout life [ 60 , 66 , 81 ].

Other measures have shown that an alteration or reduction of dietary sugars also results in a major decrease of caries in experimental animal models [ 82 , 83 ] and humans [ 55 , 58 ]. It is interesting to pause and reflect on dental research since mid Once caries was known to begin on the external tooth surface and proceed inwards, the dental profession gained recognition amongst the worldwide populace. As the science of caries prevailed, the tooth worm faded into oblivion.

New devices and technologies emerged in parallel fashion and became used in the laboratories of clinicians who were searching for answers to the biology of the tooth and caries.

North American notables such as Harris — , Black — , Webb — , Williams — , and Miller — all shared very common childhood experiences [ 5 , 9 , 10 , 40 ]. They were not born of nobility or gentry, but grew up in humble rural surroundings and learned of life by spending long hours in the pursuit of Nature. American cultural history records that almost every home contained the popular textbook of the day of Comstock's Philosophy for family reading and group discussions after dinner time in the evening [ 84 ].

Each of these individuals had a similar introduction to dentistry and study, they used their own personal finances; no governmental agency dispensed research funds for their research. They pursued answers to questions that had evaded other colleagues and published their findings because they wanted to make sure new knowledge was available to colleagues worldwide. There was no academic pressure to publish or perish. Where should we go from here?

It seems that much of the above information, although still available in the dental literature, remains somewhat lost in the academic teaching of caries for today's dental students. A fundamental knowledge of dental caries and the pulpal response to this bacterial insult remains illusive to many of today's clinicians and educators.

Since the s, we have learned that bacteria are the cause of caries [ 15 ] as a dynamic biofilm dental plaque [ 62 , 63 ], and that bacteria are essential for pulpal disease [ 56 ]. Restorative procedures and devices have been developed to identify and remove caries. Has our current cosmetic-restorative era failed us? Are today's dental students integrating the appropriate clinical and scientific information for caries risk assessment, minimal intervention in caries removal, preservation of the vital pulp, and total prevention of dental decay within the human dentition?

Thanks to the personal curiosity and initial research efforts of Harris, Webb, Black, Williams, Miller, and other colleagues of the late s, our dental community now recognizes the cause of caries. The authors, again, remind the readers of Professor G. The time is Now as we travel along this timeline from the past to the future. Our scientific community has made enormous advances in molecular biology to further our understanding of dental caries as a biological phenomenon [ 85 — 87 ].

We must integrate our current discoveries and past knowledge base into clinical practice. Let us not only prevent dental caries at all levels, but also preserve the vital dental pulp. The authors thank Mr. Jeffrey S.

Cox of Phoenix Dental Inc. Tokyo, Japan for their support of resources for development and funding of this paper for publication. National Center for Biotechnology Information , U. Journal List Int J Dent v. Int J Dent. Published online Jul John D. Charles F. Author information Article notes Copyright and License information Disclaimer. Ruby: ude. Received Oct 23; Accepted May Ruby et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC. Abstract This historical treatise follows the documented timeline of tooth decay into today's understanding, treatment, and teaching of caries biology. The Human Tooth The human tooth is a unique tissue composite of soft and mineralized tissues. Table 1 The caries phenomenon timeline. He discredited disease being caused by magic or mythology [ 21 , 24 ]. He suggested fumigation with leek, onion, and Henbane to cure the persons tooth pain [ 29 ].

He discredited the tooth worm idea [ 34 ]. Charles Hope He believed caries was due to external forces, and dismissed the internal tooth inflammation theory [ 42 ]. He believed tooth inflammation was due to internal injury of the lining membrane along the pulp-dentin wall [ 37 ]. He denounced internal factors [ 41 ]. Rognard Believed that caries began in pits and fissures of the crown on the outside of the tooth [ 44 ]. Wescott and J.

Dalyrymple English clinicians who believed tooth decay was caused by external forces of the oral environment [ 43 ]. Harris Early American educator who believed that caries was due to external factors of the oral environment [ 40 ]. Leber and J. Rottenstein Believed that caries was due to bacterial fermentation of food debris, and oral fluids that led to the presence of bacteria in dentin tubules [ 50 ].

Milles and A. Underwood Caries was most likely due to demineralization by organic acids produced by bacteria [ 51 ]. Miller Caries was due to corrosive actions of lactic acid from bacteria that caused enamel lesions [ 10 ]. Clyde Davis Identified a soft superficial carious zone with many bacteria and deeper caries zone with fewer bacteria and some demineralization [ 53 ].

Stephan In situ changes in dental plaque biofilm pH in the presence of sugar [ 54 ]. Gustafsson Frequency of sugar consumption in institutionalized children Vipeholm related to caries experience [ 55 ]. Orland Demonstrated that caries did not develop in germ-free rats [ 15 ]. Terachima Showed clinical discrimination of two layers of carious dentin with a biological stain that provided distinct visual differentiation of infected and affected layers [ 57 ].

Scheinin and K. Makinen Turku study indicated that replacement of sugar with xylitol decreased caries experience [ 58 ]. Mertz-Fairhurst et al.

Ten-year clinical outcome study of carious lesions with sealed dentin showed arrested lesion progression with no more clinical pulp failures when compared to the control group with conventional caries removal [ 64 ]. Kidd Metabolic activity in the human plaque biofilm is the all-important driving force behind any loss of mineral from the tooth or cavity surface and resultant pulp inflammation [ 65 ]. Reynolds Concluded that calcium phosphate-based remineralization technologies showed promising adjunctive treatments to fluoride therapy in early caries management [ 66 ].

Open in a separate window. The Antiquity of Tooth Decay Skeletal remains are an excellent historical kymograph of human conditions. The External Chemical Theory of Caries Replaces the Internal Inflammation Theory In the late s into the early s, a number of colleagues from different counties—using histological preparation and stain technologies—made parallel observations that caries was caused by external chemical agents.

Answers Arrive from an Unlikely Source: Agricultural Chemistry In , the theory of fermentation had been fully explained by Von Liebig—an unlikely nondental scientist whose chemistry research was first presented as an oral report to the British Association for the Advancement of Science, with their full acceptance [ 46 ]. Science Prevails: Caries Is No Longer an Enigma In his small Berlin laboratory that he shared with Robert Koch, Miller observed certain bacteria could convert starch by ptyalin amylase to form sugar that was fermented to lactic acid [ 10 ].

A Complex Dimensional Disease: Several Layers of Carious Dentin Using various microscopic techniques, Furrier illustrated six-zones of carious dentin: bacteria-rich, bacteria-few, pioneer-bacteria, turbid-layer, transparent and a vital reaction layer.

Remaining Challenges Where should we go from here? Acknowledgments The authors thank Mr. References 1. Ten Cate AR. Oral Histology, Development, Structure, and Function.

Abbott F. Caries of human teeth. Dental Cosmos. Black GV. Williams JL. A contribution to the study of pathology of enamel. Webb MH. Such foods can lead to serious decay, especially if the cave residents were snacking all day long, as Humphrey suspects.

There's some evidence that the Grotte people used toothpicks, but that obviously didn't help much. The new study, published in this week's Proceedings of the National Academy of Sciences , shows decay-causing bacteria have been hanging around humans since before the dawn of agriculture, Humphrey says. Other scientists say the study shows bad teeth can't always be blamed on farming.

The finding "highlights that an agricultural diet is not the only type of diet which can cause decay," says dental science researcher Christina Adler of the University of Sydney via e-mail. But she cautions that the troubles of the Grotte people were isolated, rather than the beginning of humanity's global battle against cavities. That battle, she says, probably began in earnest with agriculture.

The battle continues, thanks to the wide availability of sugar. If it weren't for modern dental treatments, Humphrey says, our teeth, rather than being better than the Grotte people's, "would probably be worse.

Facebook Twitter Email. Tooth decay first ravaged human society 15, years ago.