Interpretations of general problems 

 in amelogenesis 



Albert A. Dahlberg 



1 he microscopic and gross morphological details of tooth 

 parts have been recognized by paleontologists and biologists 

 for a long time and have been used as differentiation markers 

 in classification; many of them have been the significant 

 points of taxonomical considerations. However, these same 

 important properties of tooth part details are a frequent 

 source of confusion because of the complexities of the ame- 

 logenesis and calcification process. 



The simplest forms of enamel hypoplasias are those that 

 are the result of nutritional deficiencies or pathological con- 

 ditions accompanied by high fevers or infections, and are 

 easily recognized by the matching occurrence of a circle or 

 ring of pits and adjacent defects on the enamel. This dys- 

 crasia occurs at the level of calcification that was in progress 

 at the time of the insult, differing in position from tooth to 

 tooth as they were developing. The key to this category of 

 enamel developmental display is the timing-location factor. 

 Chemical hypoplasia from high fluorosis or circumstances 

 such as phosphate deficiencies may be similarly expressed. 

 Other individual or combined effects involving enamel for- 

 mation, rate of growth, and variations in morphological size 

 and proportions have been recorded in the literature. Crenu- 

 lated enamel surfaces on some of the fossils and similarly 

 disturbed surfaces of later forms having disorganized pat- 

 terns of enamel have, at times, invited erroneous diagnoses. 

 This is particularly true in regard to some of the mulberry 

 molars of the congenital syphilis triad (Bradlaw 1953). 



The biochemical control of the phylogenetic architecture 

 of occlusal cusp patterns is sometimes disturbed to the extent 

 of losing almost all the identity of the surface. A long list of 

 authors hold differing views and explanations of these occur- 

 rences (Weidenreich 1937; Samat and Schour 1941-1942; 

 Dahlberg I960; Taylor 1978; White 1978; Goodman and 

 Armelagos 1980; White and Johanson 1982; Pindborg 1982; 

 Mayhall and Saunders 1 986; Cook and Buikstra 1 979; Tobias 

 1986) and present a variety of perspectives in many direc- 

 tions. 



Explanations of ontogenetic and genetic interactions have 

 been useful in explaining some of the literature reports. Evo- 

 cative interpretations can be made from observations of the 

 terminal growth of such structures as the deflecting wrinkle 

 of the metaconid ridge of the lower molar occlusal surfaces, 

 the enamel extensions between the roots of the lower molars, 

 enamel occlusal pearls, enamel molar cusp bulges (Kir- 

 veskari et al. 1972), and the structural relationship of the 

 outer crown patterns compared to the endocast topography of 

 those same teeth (Korenhof 1960,1982). Both Korenhof 

 ( 1960) and Tobias (1986) discussed the crests, wrinkles and 

 crenulations of the outer crown surface and the relationship 

 to the dentin endocast, some of which perhaps may be due to 

 the developmental events of the enamel growth and direction 

 taken within the enamel organ itself. Similar comments can 

 be made relating to the enamel bulges of the buccal cusps 

 described by Kirveskari et al. (1972). Events in the growth 

 processes are vulnerable to environmental input and interact 

 with the sequence and nature of induction responses (Kollar 

 1975). 



Growth of enamel occurs in directions away from the first 

 initiated ameloblasts, a site which becomes known as the tips 

 of the cusps, with the mitotic divisions favoring the direction 

 of the adjacent cusps. The mitotic divisions follow the same 

 pattern of succession in all the lower teeth: from the pro- 

 toconid to metaconid, to hypoconid, to entoconid, to hypo- 

 conulid. and lastly to the accessory sixth, seventh and other 

 peripheral cusplets. A similar succession of initiation, divi- 

 sion, further division, and calcification occurs in the maxil- 

 lary teeth from paracone to protocone, to metacone, to hypo- 

 cone, to Carabelli's cusp, and so on. In all the teeth the 

 ameloblast activity changes course to conform with the tooth 

 architecture as the growth activity approaches the line angle 

 limits of the buccal, lingual, mesial, or distal outer surfaces. 

 How this occurs is assumed to be a biochemical problem such 

 as Kollar (I97S) and others have discussed in tissue culture 

 demonstrations. 



Zagreb Paleopathology Symp. 1988 



269 



