More recent dynamic CT [21] and MRI studies [22] proved occult instability to be one of the most popular causes of LBP in apparently normal conventional neuroradiological studies (Fig. 3.2).

Directly connected to disc degeneration is the chronic facet joint syndrome (CFJS): the asymmetrical spinal load at the level of facet joints is the main cause of pathological degeneration of the joint cartilage, as well as bone remodeling [23].

Facet joint disease, generally related to chronic arthritis and/or segmental degeneration, remains one of the most common causes of chronic lumbar pain both in young and elderly patients. The mechanism of facet joint syndrome pain is both related to mechanical and inflammatory damage of the facets, both concurring in generating local painful arthritis [24].

Medial branches of the dorsal rami are responsible for facet joint innervation [25]. Anatomical studies demonstrated the presence of “free and encapsulated nerve endings in lumbar facet joints.” Moreover, P-substance and calcitonin-related peptide have been discovered in facets, as additional cause of local pain [26, 27].

A frequent (5–25 % of all LBP causes) [28–31] and frequently misunderstood cause of LBP in adult males, and particularly females, is chronic sacroiliac joint arthritis secondary to acquired focal instability. The sacroiliac joint (SIJ) is the strongest and richest joint in human body as for ligaments (anterior sacroiliac, interosseous, sacrospinous, and sacrotuberous) and muscles (gluteus maximus, piriformis, and biceps femoris) concur to stabilize the joint [32]. Despite the great stability of this joint, there are several conditions that can reduce the stability of SIJ, generating chronic pain in a patient. SIJ ligaments are weaker in female patients as they are estrogen dependent, preparing the sacrum to the delivery nutation: as a consequence, postpartum chronic pain at the level of the sacrum can occur even after months after the delivery [33]. Another frequent cause of SI chronic pain is biomechanical changes in lumbar spinal unit mobility, as a consequence of surgical procedures like posterior interbody fixation (PIF) – generally performed in case of lumbar instability but conversely generating sacral instability: it has been calculated that 75 % of patients underwent PIF treatment suffer from painful SIJ instability in 5 years [34, 35]. Clinical symptoms related to SIJ disease are numerous, and no specific clinical sign supports the diagnosis. This uncommon uselessness of clinical symptoms analysis is related to the complexity of SIJ innervation, as the posterior surface of the joint receives collaterals from L3 to S4 dorsal rami [36] while anterior articulation is supplied by L2 to S2 nerves [37, 38]. Consequently, SIJ syndrome is responsible for pain referred in several different areas of the body, as the lower limbs, pelvis, coxofemoral area, buttock, and abdomen, overlaying other common causes of radicular pain. Even if several physical maneuvers are suggested to evocate the pain and propose a SIJ disease, diagnosis and neuroradiological examinations (MRI, bone scanning) – inserire immagini – can show focal SIJ abnormalities proposing a SIJ syndrome, only diagnostic block of the SIJ injecting intra-articular anesthetics (lidocaine) is considered the gold standard method to confirm the disease [39].

Finally, after-surgery LBP, usually known as failed back surgery syndrome (FBSS), is one of the most frequent causes of back pain in patient underwent surgical treatment, the etiology being controversial and complex. Epidural fibrosis is generally considered one of the most common causes of LBP after surgery, with patients having extensive epidural scars having 3.2 more frequent LBP and radicular pain that those with mild epidural fibrosis [40]. Moreover, epidural scars are responsible for neurological impairment demonstrated by electrophysiology and nerve root tethering as well as nerve inflammation induced by high local cytokines, and other inflammatory agent level has been described [41, 42]. In FBSS, the pain moves from a mechanic/inflammatory origin through a neuropathic pain: patients affected by it suffer from an increased sensitivity and responsiveness of receptors that generate an amplified reaction to mild algogenous stimuli (“hyperalgesia”) and/or misinterpretation of stimuli coming from non-nociceptive receptors (“allodynia”), generally related to abnormal activation of nonneuronal cells as microglia, together with changes in local pain neurotransmitter molecules, increasing pain feeling [43].