Spondylosis (spinal osteoarthritis) is a degenerative disorder that may cause loss of normal spinal structure and function. Although aging is the primary cause, the location and rate of degeneration is individual. The degenerative process of spondylosis may affect the cervical (neck), thoracic (mid-back), or lumbar (low back) regions of the spine.
Spondylosis often affects the following spinal elements:
Intervertebral Discs As people age, certain biochemical changes occur affecting tissue found throughout the body. In the spine, the structure of the intervertebral discs (annulus fibrosus, lamellae, nucleus pulposus) may be compromised. The annulus fibrosus (eg, tire-like) is composed of 60 or more concentric bands of collagen fiber termed lamellae. The nucleus pulposus is a gel-like substance inside the intervertebral disc encased by the annulus fibrosus. Collagen fibers form the nucleus along with water and proteoglycans. The degenerative effects of aging can weaken the annulus fibrosus’ structure, causing the ‘tire tread’ to wear or tear. The water content of the nucleus decreases with age affecting its ability to rebound following compression (e.g. shock absorbing quality). The structural alterations from degeneration may decrease disc height and increase the risk for disc herniation.
Facet Joints (or Zygapophyseal Joints)
The facet joints are also termed zygapophyseal joints. Each vertebral body has four facet joints that work like hinges. These are the articulating (moving) joints of the spine that enable extension, flexion, and rotation. Like other joints, the bony articulating surfaces are coated with cartilage. Cartilage is a special type of connective tissue that provides a self-lubricating and low-friction gliding surface. Facet joint degeneration causes loss of cartilage and formation of osteophytes (eg, bone spurs). These changes may cause hypertrophy or osteoarthritis, also known as degenerative joint disease.
Bones and Ligaments
Osteophytes (eg, bone spurs) may form adjacent to the end plates, which may compromise blood supply to the vertebra. Further, the end plates may stiffen due to sclerosis; a thickening or hardening of the bone under the end plates. Ligaments are bands of fibrous tissue connecting spinal structures (eg, vertebrae) and protect against the extremes of motion (eg, hyperextension). However, degenerative changes may cause ligaments to lose some of their strength. The ligamentum flavum (a primary spinal ligament) may thicken and buckle posteriorly (behind) toward the dura mater (a spinal cord membrane).
Spondylosis Symptoms and Different Spinal Levels
Cervical (Neck) The complexity of the cervical (neck) anatomy and its wide range of motion make this spinal segment susceptible to disorders associated with degenerative change. Neck pain from spondylosis is common. The pain may spread into the shoulder or down the arm. When a bone spur (osteophyte) causes nerve root compression, extremity (eg, arm) weakness may result. In rare cases, bone spurs that form at the front of the cervical spine, may cause difficult swallowing (dysphagia). We have an article that presents a cervical spondylosis case; you should definitely read it if you have spinal osteoarthritis in your neck.
Pain associated with degenerative disease is often triggered by forward flexion and hyperextension. In the thoracic spine disc pain may be caused by flexion–facet pain by perextension.
Lumbar (Low Back)
Spondylosis often affects the lumbar spine in people over the age of 40. Pain and morning stiffness are common complaints. Usually multiple levels are involved (eg, more than one vertebrae). The lumbar spine carries most of the body’s weight. Therefore, when degenerative forces compromise its structural integrity, symptoms including pain may accompany activity. Movement stimulates pain fibers in the annulus fibrosus and facet joints. Sitting for prolonged periods of time may cause pain and other symptoms due to pressure on the lumbar vertebrae. Repetitive movements such as lifting and bending (eg, manual labor) may increase pain.