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.

Introduction: Flat Back Syndrome resulting from decreased lumbar lordosis or increased thoracolumbar kyphosis was initially described by Doherty¹ in post scoliotic surgery patients. This decompensation was later coined as fixed sagittal imbalance and was also detected in patients operated for ankylosing spondylitis or with fractured vertebrae. Various clinical symptoms were included in the syndrome such as stooped posture, knee/ hip flexion compensation, fatigue of para-spinal muscles, neck pain and upper spinal deformities, imbalanced gait. Surgical corrections were described by Kostuik², Lagrone³, Farcy⁴ and others. The “normal” assessments were varying, but accepted according to Propst-Proctor⁵ and Bernhardt & Bidwell Segmental measurements⁶. The clinical diagnosis was supported by radiological evaluation using the Cobb technique and a plumbline alignment from odontoid to promontorium. This evaluation required multiple sets of x-ray films.

Methods: Our preliminary study is aiming at describing in detail the clinical syndrome in patients with lower dorsal and upper lumbar vertebral compressions. Scanogram CT- imaging of the spine is suggested for diagnosis, a rapid technique reported to be with at least 40% reduced radiation^7,8. The scanogram is suggested to be functional as it is repeated in prone and in supine positions. The two films were superimposed and rigidity assessed, angles were measured (Cobb) at the T/L junction (two above and two levels below the fracture) and of the lumbar lordosis (from Inferior L1 to superior L5).

Results: This technique was applied to eight patients: the clinical syndrome is detailed with one additional, as yet unreported feature, namely the sleeping position. These were patients with two, three or four vertebral compressions, resulting in imbalance of the dorsolumbar junction and deformity of the lumbar lordosis. All patients had increased T/L kyphosis of varying degrees, all but one had parallel loss of lordotic curvature.

Discussion: A different imaging technique, functional and less irradiating is suggested for the diagnosis of fixed sagittal imbalance of the dorsolumbar spine and is applied to deformities resulting from fractured vertebrae. The clinical syndrome is enlarged with one feature, namely sleeping in prone position. These early impressions need a larger prospective study for confirmation.

Introduction: Described by Jacques Forrestier at the beginning of the 20th century, the disease was named ankylosing hyperostosis of the spine1. Since that time various other names have been accorded to it, the most comprehensive being dish: diffuse, idiopathic, skeletal, hyperostosis2. The disease is often misdiagnosed by radiologists, unrecognised by surgeons and considered a silent condition. To diffuse this myth of ‘innocence ‘ I am presenting syndromes collected from over 80 patients, during some 20 years.

Methods: the clinical syndromes were recorded, with emphasis on general health and family history. The physical examination recorded the rigidity of spinal movements and neurological changes. All patients were exposed to plain films and CT scan of the spine, to barium meal and /or laryngoscopy.

Results: Only clinical assessment and radiological illustrations were the aim of this review: Cervical syndromes: – painful ankylosis; stenosis with myelopathy (3);

-Tracheal compression with laryngeal nerve palsy;

-Esophageal compression with endoscopic implications. (4).

Dorsal syndromes: painful ankylosis, spinal stenosis & myelopathy (5,6,);

Lumbar syndromes: painful hyperlordotic ankylosis, spinal stenosis (7);

Sacroiliac fusion (8); calcifications of iliosacral and iliolumbar ligaments.

Extra spinal calcifications: peri articular at elbow, hips and in operative scars: Achilles’ repair; Post-laparatomy abdominal wall ossification (9).

Particular features: early onset (age 40); incidence in families with two brothers and another with three brothers.

Discussion: Presentation of multilevel spinal syndromes and extra-spinal symptomatic calcification/ossification is intended to dispel the “innocence” of this disease. Except the ankylosis, often asymptomatic, the approximate symptomatic disease was found to be of 10%.