Calcification and ossification of the vertebral ligaments are common phenomena, between which a clear distinction is not usually made. Their pathogenesis is disputable. Léri observed that the ligaments may calcify or ossify when they sustain increased tension, when they are torn, or when they are involved in lesions of vertebral bone or joints (9). He inferred that calcification and ossification of the ligaments are modes of healing which help to consolidate a weakened vertebral column, whereby he implied that they are consecutive to other vertebral lesions. Simmonds believed that calcification and ossification may also occur independently, as a primary “syndesmosis” (18). This view reappears in Knaggs' classification as spondylitis ossificans ligamentosa (8). Schmorl stated that increased tension upon certain fibers of the longitudinal ligaments induces the formation of osteophytes at the vertebral edges (17). Supporting this theory, Beadle assumed that vertebral osteophytes—one of the most common lesions of the spine—are, in reality, ossified fibers of the anterior longitudinal ligament (3). This would confirm Léri's view that vertebral ligaments may ossify when they are strained, although his results seem to have been unknown to Schmorl and Beadle. Calcification and ossification of undetermined origin in the posterior longitudinal (12, 14, 17), interspinal (17), and yellow ligaments (ligamenta flava) (2, 5, 9, 11, 12) have also been recorded. Clinically, it is held that in a region with calcified or ossified ligaments vertebral mobility is diminished or absent. Thus ossification of the longitudinal ligaments is believed to cause the vertebral rigidity which is typical of rhizomelic spondylosis (Strümpell-Marie disease of the American, or Bechterew disease2 of the German, nomenclature). But Fraenkel showed as early as 1903 that this syndrome is produced by, or associated with, an ankylosing inflammation of the apophyseal joints, spondylarthritis ankylopoietica, which is not necessarily accompanied by ossification of ligaments (7). Thickening and calcification of lumbosacral ligamenta flava were held responsible by Léri (9) for certain forms of enuresis, and by Brown (5) and Naffziger, Inman, and Saunders (11) for pain low in the back; but both Léri himself (9) and Bakke (1) reported that this lesion may also occur in the absence of any clinical manifestations. These differences of opinion seem to arise from two main sources. First, no control series has as yet been published to substantiate the various theories. Second, most views are based upon postmortem findings. There would seem, however, to be few hypotheses that could not be supported by an analysis of vertebral specimens, since the reactions which occur in the vertebrae in the course of a chronic lesion are uncharacteristic, variable, and in most cases overlapping.