|
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]. |
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