Revisiting scoliosis in the KNM-WT 15000 Homo erectus skeleton.

Owing to its completeness, the 1.5 million year old Nariokotome boy skeleton KNM-WT 15000 is central for understanding the skeletal biology of Homo erectus. Nevertheless, since the reported asymmetries and distortions of Nariokotome boy's axial skeleton suggest adolescent idiopathic scoliosis, possibly associated with congenital skeletal dysplasia, it is questionable whether it still can be used as a reference for H. erectus. Recently, however, the presence of skeletal dysplasia has been refuted. Here, we present a morphological and morphometric reanalysis of the assertion of idiopathic scoliosis. We demonstrate that unarticulated vertebral columns of non-scoliotic and scoliotic individuals can be distinguished based on the lateral deviation of the spinous process, lateral and sagittal wedging, vertebral body torsion, pedicle thickness asymmetry, and asymmetry of superior and inferior articular facet areas. A principal component analysis of the overall asymmetry of all seven vertebral shape variables groups KNM-WT 15000 within non-scoliotic modern humans. There is, however, an anomaly of vertebrae T1-T2 that is compatible with a short left convex curve at the uppermost thoracic region, possibly due to injury or local growth dysbalance. Asymmetries of the facet joints L3-L5 suggest a local right convex curve in the lower lumbar region that probably resulted from juvenile traumatic disc herniation. This pattern is incompatible with adolescent idiopathic scoliosis or other types of scoliosis, including congenital, neuromuscular or syndromic scoliosis. It is, however, consistent with a recent reanalysis of the rib cage that did not reveal any asymmetry. Except for these possibly trauma-related anomalies, the Nariokotome boy fossil therefore seems to belong to a normal H. erectus youth without evidence for adolescent idiopathic scoliosis or other severe pathologies of the axial skeleton.

No skeletal dysplasia in the Nariokotome boy KNM-WT 15000 (Homo erectus)--a reassessment of congenital pathologies of the vertebral column.

The Nariokotome boy skeleton KNM-WT 15000 is the most complete Homo erectus fossil and therefore is key for understanding human evolution. Nevertheless, since Latimer and Ohman (2001) reported on severe congenital pathology in KNM-WT 15000, it is questionable whether this skeleton can still be used as reference for Homo erectus skeletal biology. The asserted pathologies include platyspondylic and diminutive vertebrae implying a disproportionately short stature; spina bifida; condylus tertius; spinal stenosis; and scoliosis. Based on this symptom complex, the differential diagnosis of spondyloepiphyseal dysplasia tarda, an extremely rare form of skeletal dysplasia, has been proposed. Yet, our reanalysis of these pathologies shows that the shape of the KNM-WT 15000 vertebrae matches that of normal modern human adolescents. The vertebrae are not abnormally flat, show no endplate irregularities, and thus are not platyspondylic. As this is the hallmark of spondyloepiphyseal dysplasia tarda and related forms of skeletal dysplasia, the absence of platyspondyly refutes axial dysplasia and disproportionate dwarfism. Furthermore, we neither found evidence for spina bifida occulta nor manifesta, whereas the condylus tertius, a developmental anomaly of the cranial base, is not related to skeletal dysplasias. Other fossils indicate that the relatively small size of the vertebrae and the narrow spinal canal are characteristics of early hominins rather than congenital pathologies. Except for the recently described signs of traumatic lumbar disc herniation, the Nariokotome boy fossil therefore seems to belong to a normal Homo erectus youth without pathologies of the axial skeleton.

Evidence for juvenile disc herniation in a homo erectus boy skeleton.

STUDY DESIGN: An analysis and differential diagnosis of bony alterations in the lower lumbar vertebrae of a Homo erectus boy skeleton. OBJECTIVE: To analyze low back problems during early human evolution. SUMMARY OF BACKGROUND DATA: Back problems in modern humans are often attributed to our upright, bipedal locomotion that is thought to place huge mechanical stresses on the vertebral column. However, little is known of this situation during the course of human evolution. METHODS: We analyzed the lower lumbar spine of the most complete early hominid skeleton, the 1.5-million-year-old Homo erectus boy KNM-WT 15000 from Nariokotome, Kenya, who died at an age of approximately 8 years. We use bony alterations as indirect evidence for disc disease in the absence of soft tissue. RESULTS: We describe an extensive osteophytic anterior curved remodeling of the left superior articular process of L5 and formation of a new joint at the underside of the left pedicle of L4. This indicates collisional facet joint subluxation, most likely as the result of juvenile traumatic disc herniation. CONCLUSIONS: This indirect evidence of possible juvenile disc herniation in a Homo erectus boy skeleton represents the earliest known case of this typical human ailment that is intricately linked to upright bipedalism. The extensive bony remodeling of the articular processes of L4 and L5 suggests that the disc herniation occurred several months before his death. Disabling backache and recurrent sciatica might have, at least, temporarily restricted his daily activities, which indicates advanced social care and nursing in early Homo. We hypothesize that the early Homo intervertebral discs were more vulnerable to injury compared with modern humans because of a relatively small vertebral cross-sectional area.

New vertebral and rib material point to modern bauplan of the Nariokotome Homo erectus skeleton.

The double S shape of the vertebral column is one of the most important evolutionary adaptations to human bipedal locomotion, providing an optimal compromise between stability and mobility. It is commonly believed that a six element long lumbar spine facilitated the critical adoption of lumbar lordosis in early hominins, which contrasts with five lumbars in modern humans and four in chimpanzees and gorillas. This is mainly based on the juvenile Homo erectus skeleton KNM-WT 15000 from Nariokotome, Kenya. Yet, the biomechanical advantage of a long lumbar spine is speculative. Here we present new vertebral and rib fragments of KNM-WT 15000. They demonstrate that the sixth to the last presacral vertebra possesses rib facets and therefore indicate the presence of only five lumbar and twelve thoracic segments, as is characteristic of modern humans. Moreover, they show that no additional element was located between the sixth to the last presacral vertebra and Th11 as suggested in the original description. The transition from thoracic to lumbar type orientation of the facet joints that takes place at Th11 is thus at the same segment as in over 40% of modern humans, suggesting an identical lumbar mobility and capacity for lordosis. Taken together, KNM-WT 15000 had one vertebra less than previously thought irrespective of whether rib-free lumbar vertebrae or vertebrae that bear lumbar-like articular processes are counted. Furthermore, the new rib fragments imply a rearrangement of the ribs that results in a symmetrical rib cage. This challenges previous claims for idiopathic or congenital scoliosis. We conclude that the bauplan of the hominin axial skeleton is more conservative than previously thought.

Confirmation of microevolutionary increase in spina bifida occulta among Swiss birth cohorts.

Previous studies on the prevalence of spina bifida occulta have indicated a microevolutionary increase in its frequency and possible population differences in the prevalence of the condition. We studied the frequencies of closed and open sacral canals at each sacral level among two birth cohorts in Switzerland. Transverse CT scans and multiplanar reconstruction images of sacra of 95 males and 96 females born in 1940-1950 and 99 males and 94 females born in 1970-1980 in Switzerland were reviewed. We found that individuals born later have significantly more open sacral arches at all sacral levels compared to those born 30-40 years earlier. When results were related to previously published data on Australian cohorts, the trend was the same, but Swiss in both cohorts were less likely to have an open section than Australians at all locations apart from S2. This study confirmed a microevolutionary trend in the opening of sacral canal among two different generations in Switzerland and demonstrated a population difference in the prevalence of spina bifida occulta.

Tobacco smoke: a risk factor for pulmonary arterial hypertension? A case-control study.

BACKGROUND: Smoking is a well-known risk factor for cardiovascular, lung, and many other diseases. Smoking can induce pulmonary arterial hypertension (PAH) in animal models; PAH is common in smokers with COPD and thereby not correlated with the degree of airway obstruction. The impact of tobacco smoke exposure on the development of PAH in humans is not known. METHODS: In a case-control study we assessed smoking and secondhand smoke exposure in all patients with PAH and chronic thromboembolic pulmonary hypertension (CTEPH) seen at our pulmonary hypertension clinic from 2002 until July 2008. Data from patients with PAH were compared with CTEPH and healthy control subjects from the Swiss Health Survey 2007. RESULTS: Ninety-one patients with PAH were compared with 64 patients with CTEPH and 18,747 control subjects (women 58, 36, 10,331, respectively). Tobacco smoking was significantly more common in PAH compared with CTEPH and control subjects. This difference could be attributed to men. Patients with PAH also smoked longer and more heavily compared with patients with CTEPH. In addition, secondhand smoke exposure was significantly longer in nonsmokers with PAH compared with control subjects. CONCLUSION: Our data indicate that tobacco smoke exposure may be a risk factor for men with PAH. Considering smoking as a risk factor for PAH will have implications in counseling patients and especially their hitherto unaffected relatives. Further research on the pathogenetic role of smoking in PAH is warranted.