Review Article

The Caries Phenomenon: A Timeline from Witchcraft and Superstition to Opinions of the 1500s to Today's Science

Table 1

The caries phenomenon timeline.

DateClinical/ScientistObservations

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 BCDecay 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 BCClay 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 BCOracle bones of the Shang Dynasty of China showed characters that mentioned a tooth worm that invaded the mouth and teeth [21].
460–377 BCHippocratesGreek 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 BCAristotleGreek 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 BCAgatharchidasPeople of the Red Sea suffered and died from small worms that gnawed away on many body tissues [30].
62 ADPliny the ElderWrote that his friend Pherercydes of Syros died from creepers that crawled from his mouth and body [30].
129–200/217 ADGalen of PergamumA Greek physician who believed that poor nutrition caused weak, thin, and brittle teeth; accumulation of internal corroding humors caused caries [14, 27].
1300–1368 ADGuy de ChauliacBelieved 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 ADAmbroise ParéInternal life forces from within the body and teeth caused decay. He discredited the tooth worm idea [34].
1684 ADAntonie van LeeuwenhoekObserved many small spinning microorganisms from mouth spittle,which he called animalcules [47].
1700 ADBondette and JourdainThey called caries a dental gangrene that was caused by tissue inflammation and death of the bone around the tooth neck [20].
1700 ADAntonie van LeeuwenhoekWrote 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 ADPierre FauchardConsidered 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 ADJohn HunterPreferred 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 ADT. Charles HopeHe believed caries was due to external forces, and dismissed the internal tooth inflammation theory [42].
1806 ADJoseph FoxPreferred the term caries. He believed tooth inflammation was due to internal injury of the lining membrane along the pulp-dentin wall [37].
1831 ADThomas BellBelieved that caries had a hereditary component [38].
1835 ADWilliam RobertsonCaries was due to the chemical disintegration on the outside of the tooth. He denounced internal factors [41].
1838 ADM. RognardBelieved that caries began in pits and fissures of the crown on the outside of the tooth [44].
1841 ADM. A. DèsirabodeDesignated seven stages of tooth decay [45].
1841 ADLevi Spear ParmlyThe first advocate of oral hygiene for the patient [52].
1842 ADLeonard KöeckerBelieved that tooth caries was due to internal inflammation from rapid temperature changes [39].
1843 ADA. Wescott and J. W. DalyrympleEnglish clinicians who believed tooth decay was caused by external forces of the oral environment [43].
1847 ADJustis von LiebigDescribed fermentation as a chemical process [46].
1848 ADJohn TomesBelieved that incipient caries caused mineral disintegration that led to tooth hypersensitivity [48].
1855 ADChapin A. HarrisEarly American educator who believed that caries was due to external factors of the oral environment [40].
1861 ADLouis PasteurDemonstrated that fermentations are “vital processes” requiring microorganisms [47].
1878 ADT. Leber and J. W. RottensteinBelieved 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 ADFrank AbbottBelieved that caries was due to a chemical process that dissolved tooth minerals, followed by the formation and organization of a protoplasmic gelatinous mass [24].
1881 ADG. A. Milles and A. S. UnderwoodCaries was most likely due to demineralization by organic acids produced by bacteria [51].
1884 ADGreene Vardiman BlackFirst to assemble the caries puzzle that involved food debris, gelatinous debris, and acids, which caused demineralization leading to the initial caries lesion [5].
1890 ADWilloughby D. MillerCaries was due to corrosive actions of lactic acid from bacteria that caused enamel lesions [10].
1897 ADJohn Leon WilliamsDecayed human teeth showed a dense felt-like mass of acid-forming microorganisms, dental plaque, that exerted its chemical influence upon calcified tissues [68].
1923 ADW. Clyde DavisIdentified a soft superficial carious zone with many bacteria and deeper caries zone with fewer bacteria and some demineralization [53].
1940 ADR. M. StephanIn situ changes in dental plaque biofilm pH in the presence of sugar [54].
1954 ADB. E. GustafssonFrequency of sugar consumption in institutionalized children (Vipeholm) related to caries experience [55].
1955 ADFrank J. OrlandDemonstrated that caries did not develop in germ-free rats [15].
1960 ADRon Fitzgerald and Paul KeyesThey demonstrated the etiological role of specific streptococci in the caries process making it an infectious and transmissible disease [15].
1965 ADSam KakehashiDemonstrated bacteria are necessary for pulpal inflammation or necrosis using germ-free animals [56].
1972 ADTakao Fusayama and S. TerachimaShowed clinical discrimination of two layers of carious dentin with a biological stain that provided distinct visual differentiation of infected and affected layers [57].
1975 ADA. Scheinin and K. K. MakinenTurku study indicated that replacement of sugar with xylitol decreased caries experience [58].
1978 ADMaury MasslerShowed the clinical importance for the dentist to differentiate the outer infected active carious dentin from the deeper arrested carious dentin [59].
1980 ADTheodore KoulouridesLesion consolidation with remineralization and rehardening of enamel in calcifying solutions containing fluoride [60].
1981 ADMartin BrännströmBacterial microleakage into dentin and pulp causes recurrent decay, pulp inflammation and necrosis [61].
1986 ADWalter J. LoescheDeveloped the “specific plaque hypothesis” that stated caries was an acidogenic bacterial infection caused by mutans streptococci and lactobacilli species [62].
1994 ADPhilip D. MarshDeveloped 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 ADEva. 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 ADEdwina A. M. KiddMetabolic 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 ADEric C. ReynoldsConcluded that calcium phosphate-based remineralization technologies showed promising adjunctive treatments to fluoride therapy in early caries management [66].