Thomas Bell first observed the pink teeth phenomenon in 1829 (Fig. 18.1). He illustrated that a pink coloration in teeth had appeared in drowned or strangled bodies. It was the consequence of an increased intrapulpal pressure, which caused the formation of pink teeth (Bell 1829). Miles et al. (1953) stressed the occurrence of this phenomenon in cases of strangulation and carbon monoxide intoxication in connection with the Christie murder case. On examination of the tooth’s anatomical features, including alveolar bone, periodontal ligament, and the pulp, marked hyperemia was observed more specifically in root dentin than in coronal dentin. Van Wyk (1987) described that a red-pink coloration was observed in the root of the teeth, which, on reaching predominantly deeper areas toward the cementoenamel junction, usually fades off, but the pink color was still visible beneath the enamel. The pulp area in fractured and sectioned teeth was depicted as being filled with a deep red or pink gelatinous material that extended into the dentin, waning in intensity toward the enamel or cementum. In addition, he also commented upon the variability between even adjacent teeth within the same jaws, where some of them displayed a marked “pinkness,” while others were relatively unaffected. Van Wyk also performed a histological identification for the causative pigment and recommended that the tubules played a vital role in pigmentation formation, as the “larger their diameter, the greater is the chance of pigmentation of the dentin” (van Wyk 1987, p. 13). He found that the heme group is accountable for the presence of colored pigments that show the phenomenon of postmortem pink teeth; this heme group is present in hemoglobin, the porphyrins, hemosiderins, bile, and its related pigments. Of these, the most important is hemoglobin. Hemosiderin is composed of a protein framework combined with ferric acid and is a breakdown product of hemoglobin, but it only crops up when breakdown is due to macrophages. Hemoglobin was found to be the most likely pigment responsible for the postmortem pink staining. It occurs naturally after death in many forms, i.e., oxyhemoglobin, reduced hemoglobin, meth-hemoglobin, hematin, and hemochromogen (van Wyk et al. 1987; van Wyk 1987, 1988a, b, 1989). Strangling, suffocation, and hanging positions of the body markedly increase the prevalence of pink teeth formation. If there had been an increase in hemosiderin levels soon after death, it possibly would be due to autolysis in the tissues and observation of marked congestion in the head region, which would bring about further congestion within the pulp, followed by hemorrhage and diffusion of blood into the pulp chamber (van Wyk et al. 1987). Miller (1957) found that this phenomenon could also occur in living subjects most frequently associated with infectious disease (e.g., typhoid fever). However, the causes are different from those of postmortem pink teeth. Camps (1953) reported that the formation of carbon monoxide complexes with the heme group occurs as a result of blood vasodilatation, and this would penetrate the pulpal tissues, creating the prerequisites for the pink teeth. An ample amount of blood must be present in the pulp chamber in order to release enough hemoglobin or hemoglobin derivatives from hemolysis to penetrate into the dental hard tissues. Kirkham et al. (1977