Spinal stiffness disorders include obligatory spondylitis (AS) and diffuse idiopathic bone hypertrophy (DISH), with the common feature of progressive spinal stiffness. Ankylosing spondylitis is an HLA B-27 gene-related inflammatory disease that results in spinal stiffness due to chronic inflammation of the sacroiliac joints, intervertebral discs, and small articular processes, with a prevalence of 0.1-1.4% and a high risk of fracture and neurological damage. Clinicians are poorly aware of diffuse idiopathic bone hypertrophy, whose etiology is unknown and whose main feature is ossification of ligaments and attachment points, evident in the spine. It is associated with age over 50 years, obesity and type II diabetes mellitus. Because ankylosing spondylitis and diffuse idiopathic bone hypertrophy themselves have varying degrees of back pain, combined with often mild trauma, their fractures are more difficult to diagnose, nerve damage may be delayed, and complications and mortality are high. However, the exact reasons for the poor prognosis of this group of patients are not clear. Scholars from the Department of Orthopaedics, Utrecht University Medical Center, The Netherlands, conducted a retrospective cohort study suggesting that complications and mortality after spinal fracture are higher in patients with ankylosing spondylitis and diffuse idiopathic bone hypertrophy than in normal fracture cases, and the article was published in Spine J in May 2014. The retrospective cohort study included 165 cases of traumatic spinal fractures over 50 years of age (Table 1), including 14 cases (8.5%) of ankylosing spondylitis, 40 cases (24.2%) of diffuse idiopathic bone hypertrophy (Figure 1), and 111 controls. Case information collected included underlying disease (Charlson underlying disease score), trauma mechanism, fracture characteristics (Table 2), nerve damage, complications, and in-hospital mortality. The relationship between spinal rigidity disease and mortality, and other possible risk factors for mortality were analyzed by logistic regression. The results showed that patients with spinal rigidity disease were 5 years older than control cases and were predominantly male. There were no significant differences in Charlson’s underlying disease scores between groups, but obesity and type II diabetes were more common in patients with diffuse idiopathic bone hypertrophy. In many cases of ankylosing spondylitis and diffuse idiopathic bone hypertrophy, the fractures originated from hypoenergetic trauma and were mostly in hyperextension (Table 3). In terms of nerve damage, ankylosing spondylitis (57.1%) and diffuse idiopathic bone hypertrophy (30.0%) were higher than controls (12.6%), with no significant improvement in the majority of cases (Table 4). Complications and mortality were also significantly higher than in the control group (Table 5). Logistic regression analysis suggested age and diffuse idiopathic bone hypertrophy, as independent factors statistically associated with mortality. These results show that in patients with ankylosing spondylitis and diffuse idiopathic bone hypertrophy, spinal fractures are often of the unstable hyperextension type and often combined with nerve damage. Complications and mortality are higher than in patients with normal spinal fractures. Advanced age and diffuse idiopathic bone hypertrophy are predictors of spinal fracture mortality. The AO fracture classification and the thoracolumbar spine injury classification and severity scoring system usually recommend surgical treatment of patients with these fractures. Diffuse idiopathic bone hypertrophy combined with fracture should be suspected in any spinal fracture over the age of 50 years with one or more of hypertension, obesity, and type II diabetes. Awareness of the risk of this type of fracture allows effective measures to be taken to avoid worsening secondary nerve damage.