Table 1.

The caries phenomenon timeline.

Date	Clinical/Scientist	Observations
40.000–25,000 BC		Decay and alveolar bone loss is evident in the jaws of Neanderthal skulls from the Paleolithic Era [20].
22,000 BC		Decay of teeth and bone loss on Cro-Magnon jaws from the Paleolithic Period showed most lesions were located at or along the cement-enamel junction [20].
2,100 BC		Clay tablets from Assyria asked the goddess Ea to place the tooth worm between the teeth and jaw bone to destroy the blood and strength of the teeth [21, 23].
1,500 BC		Oracle bones of the Shang Dynasty of China showed characters that mentioned a tooth worm that invaded the mouth and teeth [21].
460–377 BC	Hippocrates	Greek Father of Medicine whose doctrine of disease was based on humoral pathology: stagnation of depraved juices in teeth caused pain. He discredited disease being caused by magic or mythology [21, 24].
384-322 BC	Aristotle	Greek philosopher who observed that sweet foods such as soft figs and dates caused a sticky film on the tooth that led to putrification and tooth decay [26].
200 BC	Agatharchidas	People of the Red Sea suffered and died from small worms that gnawed away on many body tissues [30].
62 AD	Pliny the Elder	Wrote that his friend Pherercydes of Syros died from creepers that crawled from his mouth and body [30].
129–200/217 AD	Galen of Pergamum	A Greek physician who believed that poor nutrition caused weak, thin, and brittle teeth; accumulation of internal corroding humors caused caries [14, 27].
1300–1368 AD	Guy de Chauliac	Believed the tooth worm existed and was responsible for tooth decay. He suggested fumigation with leek, onion, and Henbane to cure the persons tooth pain [29].
1525 AD	Ambroise Paré	Internal life forces from within the body and teeth caused decay. He discredited the tooth worm idea [34].
1684 AD	Antonie van Leeuwenhoek	Observed many small spinning microorganisms from mouth spittle,which he called animalcules [47].
1700 AD	Bondette and Jourdain	They called caries a dental gangrene that was caused by tissue inflammation and death of the bone around the tooth neck [20].
1700 AD	Antonie van Leeuwenhoek	Wrote to the Royal London Society that he took live tooth worms from corrupt teeth of his wife, noting they were the same as living cheese-worms that were found from a cheese shop [32].
1728 AD	Pierre Fauchard	Considered to be The Father of Modern Dentistry, discredited the tooth worm theory, and thought dental caries was caused by a tumor of osseous fibers [20, 35].
1780 AD	John Hunter	Preferred the term mortification to caries, and believed the source of decay was due to an imbalance of internal forces that caused inflamation and pulp disease [36].
1798 AD	T. Charles Hope	He believed caries was due to external forces, and dismissed the internal tooth inflammation theory [42].
1806 AD	Joseph Fox	Preferred the term caries. He believed tooth inflammation was due to internal injury of the lining membrane along the pulp-dentin wall [37].
1831 AD	Thomas Bell	Believed that caries had a hereditary component [38].
1835 AD	William Robertson	Caries was due to the chemical disintegration on the outside of the tooth. He denounced internal factors [41].
1838 AD	M. Rognard	Believed that caries began in pits and fissures of the crown on the outside of the tooth [44].
1841 AD	M. A. Dèsirabode	Designated seven stages of tooth decay [45].
1841 AD	Levi Spear Parmly	The first advocate of oral hygiene for the patient [52].
1842 AD	Leonard Köecker	Believed that tooth caries was due to internal inflammation from rapid temperature changes [39].
1843 AD	A. Wescott and J. W. Dalyrymple	English clinicians who believed tooth decay was caused by external forces of the oral environment [43].
1847 AD	Justis von Liebig	Described fermentation as a chemical process [46].
1848 AD	John Tomes	Believed that incipient caries caused mineral disintegration that led to tooth hypersensitivity [48].
1855 AD	Chapin A. Harris	Early American educator who believed that caries was due to external factors of the oral environment [40].
1861 AD	Louis Pasteur	Demonstrated that fermentations are “vital processes” requiring microorganisms [47].
1878 AD	T. Leber and J. W. 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].
1879 AD	Frank Abbott	Believed that caries was due to a chemical process that dissolved tooth minerals, followed by the formation and organization of a protoplasmic gelatinous mass [2–4].
1881 AD	G. A. Milles and A. S. Underwood	Caries was most likely due to demineralization by organic acids produced by bacteria [51].
1884 AD	Greene Vardiman Black	First to assemble the caries puzzle that involved food debris, gelatinous debris, and acids, which caused demineralization leading to the initial caries lesion [5].
1890 AD	Willoughby D. Miller	Caries was due to corrosive actions of lactic acid from bacteria that caused enamel lesions [10].
1897 AD	John Leon Williams	Decayed human teeth showed a dense felt-like mass of acid-forming microorganisms, dental plaque, that exerted its chemical influence upon calcified tissues [6–8].
1923 AD	W. Clyde Davis	Identified a soft superficial carious zone with many bacteria and deeper caries zone with fewer bacteria and some demineralization [53].
1940 AD	R. M. Stephan	In situ changes in dental plaque biofilm pH in the presence of sugar [54].
1954 AD	B. E. Gustafsson	Frequency of sugar consumption in institutionalized children (Vipeholm) related to caries experience [55].
1955 AD	Frank J. Orland	Demonstrated that caries did not develop in germ-free rats [15].
1960 AD	Ron Fitzgerald and Paul Keyes	They demonstrated the etiological role of specific streptococci in the caries process making it an infectious and transmissible disease [15].
1965 AD	Sam Kakehashi	Demonstrated bacteria are necessary for pulpal inflammation or necrosis using germ-free animals [56].
1972 AD	Takao Fusayama and S. 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].
1975 AD	A. Scheinin and K. K. Makinen	Turku study indicated that replacement of sugar with xylitol decreased caries experience [58].
1978 AD	Maury Massler	Showed the clinical importance for the dentist to differentiate the outer infected active carious dentin from the deeper arrested carious dentin [59].
1980 AD	Theodore Koulourides	Lesion consolidation with remineralization and rehardening of enamel in calcifying solutions containing fluoride [60].
1981 AD	Martin Brännström	Bacterial microleakage into dentin and pulp causes recurrent decay, pulp inflammation and necrosis [61].
1986 AD	Walter J. Loesche	Developed the “specific plaque hypothesis” that stated caries was an acidogenic bacterial infection caused by mutans streptococci and lactobacilli species [62].
1994 AD	Philip D. Marsh	Developed the “ecological plaque hypothesis” to describe the dynamic relationship within plaque biofilm consortiums where low pH selects for the growth of cariogenic microorganisms [63].
1998 AD	Eva. J. 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].
2004 AD	Edwina A. M. 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].
2009 AD	Eric C. Reynolds	Concluded that calcium phosphate-based remineralization technologies showed promising adjunctive treatments to fluoride therapy in early caries management [66].