The photo catalogue gives a visual impression as to how tooth diagenesis may compare to what is known of bone diagenesis. In contrast to what can be observed in bone (compare for example with Jans (2005) and Hedges et al. (1995), none of the analysed teeth has suffered complete destruction of the microstructure and all display histological indexes greater than 1. In other words, all of the teeth contained histologically pristine areas making up at least more than 15% of the total section surface studied. For bone, Hedges et al. (1995) observed a bimodal distribution in terms of histological integrity; the material preserves either very well or very poorly when considering microbial attack. If bioerosion happens in bone, it tends to go to 'completion'. Approximately 20% out of a large bone assemblage analysed (n = 139) displayed OHI of 0 or 1 (Hedges et al. 1995). The Eindhoven bone samples display the same pattern. For the teeth, we observe a similar bimodal distribution, but between 'medium' and 'excellent' in terms of the bioerosion index (Figure 71). If this is a representative pattern, it may be support for the idea that skeletal elements further from the abdomen preserve better (Jans et al. 2004; Child 1995) as teeth are further away than femora, on the premise that endogenous gut bacteria are involved in eroding the skeleton (see discussion further below). Consequently, teeth contain larger areas of well-preserved tissue once environmental conditions have been established that inhibit further microbial activity. Alternatively/additionally, the difference in the microstructure, including the lower number of cell cavities, the lack of connection via canaliculi and the layer of Tomes at the cemento-dentinal junction, may slow down progress into the tissue. Finally, the enamel and the surrounding bone will protect the cementum/dentine from attack by soil microorganisms. Sognnaes (1950) found that the teeth he studied were increasingly affected by bioerosion with increase in post-mortem age, testifying to the role of aerobic soil-bacteria in post-mortem decay. Turner-Walker (2008) similarly considers aerobic soil bacteria the cause of most tunnelling seen in bone and teeth. However, it has also been suggested that extensive bone bioerosion may occur early post-mortem as part of putrefactive processes while soft tissues are still present (Yoshino et al. 1991; Bell et al. 1991; Jans 2005), making gut bacteria the potential 'perpetrators. Internal invasion by bacteria suggests the action of microbes travelling by the inter-connected vascular system. We also observed internal invasion in some of the teeth where bacteria mainly enter via the apex and the pulp cavity (Figures 8 and 9). It is not yet clear, however, if such a pattern can be assigned to endogenous bacteria. Soil bacteria may also be able to enter deep into the bone and teeth via the groundwater, while an inhibiting environment at the outer surfaces of the skeletal elements prevents them from utilising the areas close to the outer surfaces. Furthermore, the cementum does not contain pores connected to the surface as the pulp cavity surface does and the latter may thus be the route of least resistance. However, tunnelling from the cementum surface was also observed (Figure 9, Figure 10 and Figure 14). Another interesting observation is that the only clear fungal tunnelling observed (Wedl type tunnels) was in one of the cattle teeth. Although it is a single observation, it corroborates the findings of Jans et al. (2004) where fungal tunnelling was the dominant type in bones of slaughtered animals and was not observed as frequently in human bones. The authors suggested several explanations including differences in structure and porosity in human and animal bones, as well as differences in burial contexts and pre-excavation treatments such as slaughtering (thus removing the gut, the source of putrefactive bacteria).
Little is known of the species involved in bioerosion of skeletal material and the processes by which the organisms alter the material. It is furthermore not clear what the different morphological categories of MFD represent; different species, or different stages of tunnelling. In less severely attacked teeth, where individual tunnels can be more easily studied, a range of shapes are apparent that seem to relate to the type of tissue and the orientation of the mineralised collagen, but also stages of progression of bacteria into the tissue. For example, enlarged cementocyte canaliculi and tubuli and narrower canals, can be seen to expand into wider, more globular shapes. Another shape frequently observed consisted of connected, oblong shapes (Figure 11), again suggesting the progressive invasion of bacterial colonies. A further shape that may be linked to bacterial decay relates to the enlarged canaliculi, sometimes expanding into longer, 'bloated' branches of a cementocyte lacunae, as observed in Figure 13 and possibly in Figure 66. In Figure 18, Figure 19 and Figure 20, features can be seen that are similar to budded tunnels observed in bone. The focal destructions in the teeth show the same features with 1 micron-sized cavities in a demineralised zone surrounded by a hypermineralised border, as observed in bone MFD (Jackes et al. 2001). Hackett (1981) described budded tunnels in bone to be around 30 micron in diameter, whereas these MFD are much larger, up to roughly 300 micron. The size may relate to the difference in microstructure in bone and dentine as the osteonal system may provide a restriction in MFD size in bone. Contrary to what Turner-Walker (2008) observed, both globular and elongated shapes are found in the dentine, as seen in Figure 11. There is in sum a large variety of morphologies of MFD observed, from branching tree- or bush-like shapes, enlarged canaliculi and tubuli, sometimes with a small bulb at the end and demineralised zones with borders and cavities, of various shapes and sizes.
An advantage of teeth in the investigation of post-mortem bacterial destruction is that examples of similar processes can be found in the literature on dental pathologies. An experimental study by Nyvad and Fejerskov (1990) demonstrated that actively progressing cementum caries lesions show a gradient of demineralisation and are invaded by bacteria. They observed that the bacterial activity mainly occurred between groups of relatively well-mineralised extrinsic collagen fibres. The cemento-dentinal junction furthermore seemed to form a barrier to bacterial penetration into the dentine which could be explained by the presence of a narrow hypermineralised zone and/or the abrupt change in collagen fibre orientation at the junction (Nyvad and Fejerskov 1990). The cemento-dentinal junction has recently been described as an enamel-like, hypermineralised zone containing little organics (Cherian 2011). Nyvad and Fejerskov (1990) found that in a few cases, bacteria would penetrate into the dentine, keeping to the dentinal tubuli and their lateral branches. In-vivo, this process is inhibited, as a bacterial presence in the tubuli will cause a cellular response that closes the tubuli to protect the dental pulp (Broncker pers. comm.). That fibre orientation plays a role also for post-mortem bacterial attack in teeth is clear from the patterns found in the present study. However, bacterial tunnels are also observed crossing the cemento-dentinal junction (Figure 10). Additionally, some features could be interpreted as microbial tunnelling extending into the enamel (Figures 54, 55, 56, 57 and 58), further discussed below. In addition to the microbial tunnels, the unknown insect and fungal-like inclusions observed (Figures 62, 63, 64, 65, 66, 67 and 68) serves as an illustration of the complex set of organisms probably colonising the material at several different stages throughout the post-mortem history of the material. When these processes are better understood, teeth and bone will constitute an even richer archive of taphonomic and environmental information.