Acta Veterinaria Scandinavica 2007, 49:10 http://www.actavetscand.com/content/49/1/10 levels for demineralisation of cement, (pH < 6.7) [1] and enamel (pH ~ 5.5) [5,6]. A decrease in pH appears to cause very similar damage in human and equine enamels [7]. The subsequent removal of the tooth matrix by prote- olysis leads to the so-called cavity of decay. The equine premolar tooth differs from its human counterpart in that it expresses all three types of dental hard tissue on its occlusal surface (Fig. 1). Necrosis of infundibular cemen- tum, infundibular cemental hypoplasia, and micro frac- tures have all been suggested as factors that predispose carious lesions in equine teeth [8]. Honma et al. [9] classified tooth decay on a 5 grade scale, and the definitions of the different levels of this scale were modified by Dacre [10]when describing the severity of infundibular decay. When including all enamel, dentin and cement defects in the definition of dental caries, Honma et al. [9] reported a caries incidence of up to 97% in abattoir skulls from mainly older horses. Examining 355 abattoir skulls, Wafa [11] reported that 29% of these skulls had caries-affected teeth. When excluding infundib- ular cemental hypoplasia from the diagnosis, Brigham and Duncanson [12] found caries in 6 out of 50 abattoir sculls. However, when defining caries as a progressive demineralisation including infundibular cementum, enamel, and dentin, the malady has been found to have a prevalence of approximately 1% in the living equine pop- ulations of Germany and Sweden, [13,14] quite often sec- ondary to primary diseases such as tooth fractures and congenital dental defects. The fourth upper premolar (P4) [8] and the first upper molars (M1) [8,9,15] have been reported to be the most commonly affected teeth. In Swedish equine dental practices, the occurrence of car- ious lesions in the first permanent premolar teeth (P2) of the upper jaw as a primary disorder has empirically been found to have increased during the last 10 years. A previ- ously unknown bacterium, Streptococcus devriesei (CCUG 47155T), has recently been isolated from such carious lesions [16]. This bacterium is related to S. mutans and appears to share its capability of adhering to the tooth sur- face. When given the right substrate, it produces copious extracellular polysaccharides that provide the bacteria with a favourable environment for multiplication. Like the human mutans streptococci [1]S. devriesei produces acid when fermenting sugars such as mannitol, sorbitol, raffinose, inulin and melibiose [16]. Thus, since it is capa- ble of lowering the pH at the site of colonisation, it also shares the ability of S. mutans to dissolve the hydroxylap- atite crystals in the dental hard tissues. Prompted by the above observations, the purpose of this study was to test the hypothesis that S. devriesei is present in all carious upper P2 teeth in Swedish horses. We also determined whether horses with such lesions had this type of bacteria on the occlusive surface of healthy premolar teeth. Methods A total of 117 horses and ponies that had attended either the equine clinic at the Swedish University of Agricultural Sciences or the animal dental clinic in Söderköping, Swe- den, for an oral examination as a part of a normal health check-up or after showing symptoms of an oral disorder were included in the study. Carious lesions were defined in this study as progressive decalcification and destruction of the cementum, enamel, and dentin in the infundibu- lum of the permanent P2 in the upper jaw (Fig. 2). Using the scale of Dacre, [10] this corresponds to grade 3 infundibular caries; that is, clinically the enamel ridge of the infundibulum is completely or partly missing and the decay feels sticky when an investigation probe is inserted into it. Samples for bacteriological analyses were collected from P2 carious lesions in 27 animals between 1990 and 1999 and from 50 horses with P2 caries and 40 control animals with normal P2 occlusal surfaces after 2002. All caries lesions comprised the anterior infundibulum. All patients were examined and sampled by the same clinician (Dr. T. Lundström). All horses with caries had shown clinical signs such as unwillingness to eat and discomfort when ridden. None of the animals had been treated with any drugs or with antibiotics for 14 days and 6 months prior to sampling, respectively. Further, the controls had no diagnosis of general disease, nor had they been treated with NSAIDs or been examined or treated in the oral cav- ity for 6 months prior to sampling. The age, sex, and breed distributions of animals sampled after 2002 are shown in Fig. 3. The animals sampled between 1990 and 1999 were between 7 and 17 years old (mean, 11 years) and consisted of 10 mares, 16 geldings, and 1 stallion. Four of them were ponies, 5 were Icelandic horses, 10 were Swedish warmbloods, and 8 were stand- ardbred trotters. Sampling Each horse was given a sedative, detomidine (Domose- dan® Orion Pharma AB, Animal Health, Sollentuna, Swe- den) at 10 μg/kg body weight intravenously, and its head was rested on a support to facilitate a dental examination (Fig. 4). A Haussmann oral speculum (Globus Sport AB, Karlskrona, Sweden) was attached and the oral cavity was rinsed with tap water of drinking quality. Samples were then collected by means of a sterile dental excavator (no.2 Straumann, Basel, Switzerland) that was inserted into the anterior infundibulum of caries-affected teeth (Fig. 5). The debris caught with the excavator was transferred to a Page 2 of 9 (page number not for citation purposes)