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These may eliminate the bacterial insult and block the route of infection. Unchecked, invasion results in pulpitis and pulp necrosis, infection of the root canal system, and periapical disease. While several hundred bacterial species are known to inhabit the oral cavity, a relatively small and select group of bacteria is involved in the invasion of dentinal tubules and subsequent infection of the root canal space. Gram-positive organisms dominate the tubule microflora in both carious and non-carious dentin. The relatively high numbers of obligate anaerobes present-such as Eubacterium spp., Propionibacterium spp., Bifidobacterium spp., Peptostreptococcus micros, and Veillonella spp.-suggest that the environment favors growth of these bacteria. Gram-negative obligate anaerobic rods, e.g., Porphyromonas spp., are less frequently recovered. Streptococci are among the most commonly identified bacteria that invade dentin. Recent evidence suggests that streptococci may recognize components present within dentinal tubules, such as collagen type I, which stimulate bacterial adhesion and intra-tubular growth. Specific interactions of other oral bacteria with invading streptococci may then facilitate the invasion of dentin by select bacterial groupings. An understanding the mechanisms involved in dentinal tubule invasion by bacteria should allow for the development of new control strategies, such as inhibitory compounds incorporated into oral health care products or dental materials, which would assist in the practice of endodontics.<\/jats:p>","DOI":"10.1177\/154411130201300207","type":"journal-article","created":{"date-parts":[[2009,1,8]],"date-time":"2009-01-08T19:40:32Z","timestamp":1231443632000},"page":"171-183","source":"Crossref","is-referenced-by-count":381,"title":["I\n                    <scp>nvasion of<\/scp>\n                    D\n                    <scp>entinal<\/scp>\n                    T\n                    <scp>ubules by<\/scp>\n                    O\n                    <scp>ral<\/scp>\n                    B\n                    <scp>acteria<\/scp>"],"prefix":"10.1177","volume":"13","author":[{"given":"R.M.","family":"Love","sequence":"first","affiliation":[{"name":"Department of Stomatology, University of Otago School of Dentistry, PO Box 647, Dunedin, New Zealand;"},{"name":"Department of Oral and Dental Science, University of Bristol Dental School, Bristol BS1 2LY, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.F.","family":"Jenkinson","sequence":"additional","affiliation":[{"name":"Department of Stomatology, University of Otago School of Dentistry, PO Box 647, Dunedin, New Zealand;"},{"name":"Department of Oral and Dental Science, University of Bristol Dental School, Bristol BS1 2LY, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2002,3,1]]},"reference":[{"key":"ADRIAENS-ETAL-1987A","doi-asserted-by":"crossref","unstructured":"Adriaens PA, De Boever JA, Loesche WJ (1987a). 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