Background: Intrauterine protein restriction in rodent models is associated with low bone mass which persists into adulthood. This study examined how early nutritional compromise affects the mechanical and structural properties of spinal tissues in sheep throughout the lifecourse.

Methods: Lumbar spines were removed from 19 sheep; 5 control animals and 14 that received a restricted diet in-utero. Eight animals (2 control/6 diet) were sacrificed at a mean age of 2.7 years and eleven at a mean age of 4.4 yrs. Two motion segments from each spine were tested on a hydraulically-controlled materials testing machine to determine their mechanical properties. Vertebral bodies were assessed for a number of structural parameters including cortical thickness and area, and regional trabecular density.

Results: Younger animals in the diet group showed a 25% reduction in forward bending stiffness (p< 0.05) and a 32% reduction in extension strength (p< 0.05) compared to controls of the same age. Furthermore, these young animals showed a 25% reduction in the thickness of the anterior cortex (p< 0.001) and an 18% reduction in the thickness of the superior cortex (p< 0.02). In older animals, no differences were observed in any of the mechanical parameters examined between diet and control groups, although animals in the diet group showed an average increase in cortical thickness of 14%, across all regions (p< 0.01).

Conclusions: These results suggest that early nutritional challenge can have detrimental effects on the mechanical and structural properties of spinal tissues in young animals but that adaptation occurs over the lifecourse to compensate for these differences in older animals.

Conflicts of Interest: None

Source of Funding: None

Introduction: Intrauterine protein restriction in rats is associated with low bone mass which persists with development through to adulthood. However, such adverse effects are not only restricted to bone. Intervertebral discs are the largest avascular structures in the body, and are particularly sensitive to their nutritional environment. We have examined the hypothesis that changes in the intervertebral disc (or ligaments), as a result of early nutritional compromise, affect the spine’s mechanical properties.

Material and methods: Lumbar spines were removed from 8 sheep (6 male, 2 female: mean age 2.7 yrs) that had received different diets early in their development: two animals received a control diet, three received low protein in utero (IU), and three received low protein both in utero and postnatally (PN). Fifteen motion segments (consisting of two vertebrae and the intervening disc and ligaments) were dissected from the spines and tested on a hydraulically-controlled materials testing machine. Compressive stiffness and bending stiffness were measured before and after creep loading, in both flexion and extension. Reflective markers attached to the specimens were tracked during loading, enabling intervertebral angles to be calculated. Bending moment-angular rotation curves were used to calculate bending stiffness. Repeated measures ANOVA was used to test for differences in stiffness with posture and creep, and between the dietary groups.

Results: Compressive stiffness increased after creep loading (p=0.002) but was unaffected by posture or dietary group. In contrast, bending stiffness was unaffected by creep but differed significantly between groups and with posture. When compared to controls, bending stiffness in the IU group was reduced by 35% in flexion and 26% in extension (p< 0.02). In the PN group, reductions of 28% in flexion and 15% in extension were observed (p=0.056).

Discussion: These results indicate that early protein restriction can affect the mechanical properties of the spine. These effects were evident in bending but not in compression, and tended to be greater in flexion than extension. These preliminary findings suggest that early protein restriction may affect the composition and mechanical function of the annulus fibrosus and the intervertebral ligaments which are the structures most involved in resisting flexion movements.

Introduction: Epidemiology suggests that an intrauterine nutrient restriction increases the likelihood of osteoporosis in later life, possibly due to differences in bone structure and strength. We hypothesise that, in an ovine model, early nutritional compromise reduces vertebral cancellous bone density and cortical thickness, and thereby reduces vertebral compressive strength.

Materials and methods: Lumbar spines were dissected from 8 sheep (6 male, 2 female: mean age 2.7 yrs). Spines were divided into different groups, based on the early diet of the sheep: group CC received a control diet, group IU received low protein in utero, and group PN received low protein both in utero and postnatally. Fifteen motion segments (consisting of two vertebrae and the intervening disc and ligaments) were prepared from the spines, and compressed to failure using a hydraulically-controlled materials testing machine to obtain yield strength. 1mm-thick bone slices were taken from the mid-sagittal and para-sagittal regions of each vertebral body and micro-radiographed. Digital images of the micro-radiographs were analysed to obtain the cancellous bone density in anterior and posterior regions, and the cortical thickness in the anterior, posterior, superior and inferior regions. Repeated measures ANOVA was used to test for differences in parameters at the different locations, and between the groups.

Results: The anterior cortex was 28% thinner for the IU group, and 23% thinner for the PN group compared to controls (both p< 0.001). In the PN group, the superior cortex was also 18% thinner than controls (p< 0.02). There was no significant difference between cancellous bone density in either region. Yield strength was 16% lower in the IU group compared to controls, but this did not reach significance.

Discussion: In the nutritionally compromised groups, cortical thickness was lower in regions of the vertebral body where fractures often occur in elderly people. However, the reduction in cortical thickness is not accompanied by a significant reduction in compressive strength in the sheep model. These findings suggest that the well-maintained cancellous bone protects the vertebra from fracture.

Introduction: The clinical condition was described as Ankylosing Hyperostosis of the Spine by Forestier (1950¹), was expanded by Resnick (1975) with the Extraspinal Manifestations². What is the nature of this unique formation, asymptomatic in 90% of cases? Several researchers questioned whether the hyperostosis was physiological or pathological. Initially, in 1985 B.M. Rotschild called it a phenomenon ³. Schlapbach in 1989 found no associated pathological condition ⁴. Hutton in his Editorial “Hyperostosis…a State not a Disease“ was doubtful ⁵.

In recent personal observations, protection by ossification was recorded in a severe trauma case and in vertebrae weakened by malignant infiltration.

Methods: A phylogenetic review of the animal world, followed by an ontogenetic study of mammals/ humans, could assist in a decision regarding the nature (physio-or pathological) of the hyperostosis.

Results: The phylogenetic lineage on one side showed the oldest record of hyperostosis in dinosaur (144 million years ago=mya). Ossifications were found in the anterior, lateral, posterior longitudinal ligaments, in C1–C2 transverse ligament. In the other phylogenetic, Hyperostosis was in historic and contemporary mammals.

The next step in this study is in the ontogenetic line of the Humans. The oldest skeleton (Ethiopia, 4.5 mya) showed “bridged vertebrae“. The first definite hyperostosis was in the Shanidar skeleton (Iraq, 40–12,000 BCE) with“flowing osteophytes”. In the historic Humans since 9500 BCE, hyperostosis was found in Europeans, Egyptians, Indians (Chile) and Incas. In the Christian era, hyperostosis was present in Roman-British/ Celt populations, Franks, Saxons, British, Swiss and N. Americans. In the 20th C, it is pandemic.

Discussion: a. Impressions from the animal world: Paleopathology was established as a scientific branch in 1912 (Ruffer), and exemplified its value in understanding the nature of diseases. Moodie questioned the function of the long spinal “bony rods”, considered them with a protective function. Others ⁶ suggested spinal hyperostosis as induced by “mechanical stress”. Shore⁷ (1936) described the spondylitis ossificans ligamentorum as due to mechanical strain.

b. Impressions from the Hominid world: The ontogenetic line shows a constant presence of hyperostosis in prehistoric and historic periods. Parallel to human migration from Africa, hyperostosis expanded globally.

c. The theory of logical probability: It is postulated that hyperostosis is a condition, as no pathology (other than inflammatory) could have expanded and persisted in many species along millions of years, as it would have been removed by the rules of the Darwinian Selection. Possibly triggered by strain in younger age, functional in the past, it is today an atavistic older age “condition“, with increased osteoblastic activity in connective tissues of ligaments and tendons. At times it is incidentally discovered and is occasionally excessive. Once presented with clinical manifestations, it becomes defined an illness and should be called the Forestier-Resnick syndrome.

INTRODUCTION: The clinical condition was described as Ankylosing Hyperostosis of the Spine by Forestier (1950¹), was expanded by Resnick (1975) with the Extraspinal Manifestations². What is the nature of this unique formation, asymptomatic in 90% of cases? Several researchers questioned whether the hyperostosis was physiological or pathological. Initially, in 1985 B.M. Rotschild called it a phenomenon³. Schlapbach in 1989 found no associated pathological condition⁴. Hutton in his Editorial “Hyperostosis…a State not a Disease“ was doubtful⁵.

In recent personal observations, protection by ossification was recorded in a severe trauma case and in vertebrae weakened by malignant infiltration.

METHODS: A phylogenetic review of the animal world, followed by an ontogenetic study of mammals/ humans, could assist in a decision regarding the nature (physio-or pathological) of the hyperostosis.

RESULTS: The phylogenetic lineage on one side showed the oldest record of hyperostosis in dinosaur (144 million years ago=mya). Ossifications were found in the anterior, lateral, posterior longitudinal ligaments, in C1-C2 transverse ligament. In the other phylogenetic, Hyperostosis was in historic and contemporary mammals.

The next step in this study is in the ontogenetic line of the Humans. The oldest skeleton (Ethiopia, 4.5 mya) showed “bridged vertebrae“. The first definite hyperostosis was in the Shanidar skeleton (Iraq, 40–12,000 BCE) with “flowing osteophytes”. In the historic Humans since 9500 BCE, hyperostosis was found in Europeans, Egyptians, Indians (Chile) and Incas. In the Christian era, hyperostosis was present in Roman-British/Celt populations, Franks, Saxons, British, Swiss and N. Americans. In the 20th C, it is pandemic.

DISCUSSION: (a) Impressions from the animal world: Paleo-pathology was established as a scientific branch in 1912 (Ruffer), and exemplified its value in understanding the nature of diseases. Moodie questioned the function of the long spinal “bony rods”, considered them with a protective function. Others⁶ suggested spinal hyperostosis as induced by “mechanical stress”. Shore⁷ (1936) described the spondylitis ossificans ligamentorum as due to mechanical strain.

(b Impressions from the Hominid world: The ontogenetic line shows a constant presence of hyperostosis in prehistoric and historic periods. Parallel to human migration from Africa, hyperostosis expanded globally.

(c) The theory of logical probability: It is postulated that hyperostosis is a condition, as no pathology (other than inflammatory) could have expanded and persisted in many species along millions of years, as it would have been removed by the rules of the Darwinian Selection. Possibly triggered by strain in younger age, functional in the past, it is today an atavistic older age “condition“, with increased osteoblastic activity in connective tissues of ligaments and tendons. At times it is incidentally discovered and is occasionally excessive. Once presented with clinical manifestations, it becomes defined an illness and should be called the Forestier-Resnick syndrome.