Spinal stenosis is a narrowing of the spaces in the spine that results in pressure being placed on the spinal cord and/or nerve roots. Although stenosis can develop without symptoms, it may produce numbness, tingling, pain and difficulty in walking, as well as a heavy/tired feeling in the legs. It is estimated that 250,000 to 500,000 Americans currently have symptoms of spinal stenosis.

Skeletal fluorosis is one cause of stenosis. In the advanced stages of fluorosis, the spine may develop extensive ligament calcifications and bony spurs (resembling spondylosis) which can press up against the spinal cord. Among patients with skeletal fluorosis, the cervical region of the spine is the most common site for cord compression. Fluoride-induced stenosis has been reported in the thoracic region as well. In thoracic cases, the spine can be compressed as a result of OLF (“ossification of ligamentum flavum”). Recent research from China has found that patients with OLF had significantly elevated levels of fluoride in their bone, indicating fluoride may play a causative role in the disease, even where signs of skeletal fluorosis may not otherwise be apparent. (Wang 2008).

In western countries such as the United States, case reports show that patients with fluorosis-induced stenosis have been misdiagnosed as suffering from other forms of disease. (Fisher 1989; Webb-Peploe 1966; Sauerbrunn 1965). The extent to which this misdiagnosis occurs remains unknown.

Fluoride & Spinal Stenosis:

“Spinal cord compression in flourosis is a common complication. These complications are mainly due to compression of the spinal cord by thickening and ossification of posterior longitudinal ligament and ligamentum flavum. Surgical decompression is the treatment of choice for fluorotic spinal cord compression. . . . The recurrence of spinal cord compression in the fluorotic spine 20 years after laminectomy is a very unusual event and hence the patient should be kept under observation for a long duration.”
SOURCE: Kumar P, et al. (2011). Fluorotic cervical compressive myelopathy, 20 years after laminectomy: A rare event. Surg Neurol Int. 2:11.

“Fluorosis and epidural lipomatosis are each rare caues of compressive myelopathy, and have never been described previously as a combined cause of spinal stenosis leading to myelopathy. We describe an unusual case of thoracic myelopathy due to coexistence of both conditions.”
SOURCE: Kalia LV, et al. (2010). Thoracic myelopathy from coincident fluorosis and epidural lipomatosis. Can. J. Neurol. Sci. 37:276-78.

“We present a rare case of high cervical myelopathy caused by ossification of the posterior longitudinal ligament and ligamentum flavum in a patient from an area endemic for skeletal fluorosis. The clinical presentation of skeletal fluorosis and treatment options are discussed.”
SOURCE: Kumar H, et al. (2009). Skeletal fluorosis causing high cervical myelopathy.J Clin Neurosci. 16(6):828-30.

“Objective: To determine the association between levels of basic metabolic elements and degeneration and ossification of the ligamentum flavum (LF). . . . The fluoride content in LF [ligamentum flavum] from nonfluorosis patients with OLF was also significantly higher than that in the control group, even though there was no difference between their serum F levels. A reasonable explanation was that patients without fluorosis may have endured a period of excessive F intake, which promoted the development of OLF. After that period, although the intake of F decreased to within normal limits, OLF still developed. So when compared, the F content of the LF of nonfluorosis patients was much higher than that in the controls; however, the serum F remained normal. The exact sources of F in nonfluorosis patients are still not known. It is reported that F can activate intracellular c- AMP, causing a significant increase of intracellular Ca and could stimulate the activation and proliferation of osteoblast-like cells with enhanced expression of messenger ribonucleic acid and the proteins c-fos and c-jun. Although it has not been confirmed that the retention of Ca in chondrocytes caused by F leads to the degeneration and necrosis of chondrocytes followed by chondral matrix calcification and endochondral ossification, these findings suggest that F and Ca might play important roles during the development of OLF.”
SOURCE: Wang Z, et al. (2008). Changes in basic metabolic elements associated with the degeneration and ossification of ligamenta flava. Journal of Spinal Cord Medicine 31:279-84.

“On the basis of clinical examination, MRI, and X-ray findings, the patient was diagnosed as a case of endemic skeletal fluorosis who presented as compressive myelopathy causing quadriparesis.”
SOURCE: Gupta AK, et al. (2008). Quadriparesis–A rare presentation of skeletal fluorosis. J. Indian Academy of Clinical Medicine 9:201-04.

“Myeloradiculopathy caused by skeletal fluorosis was thought to be a result of compression of the spinal cord by osteophytes and vertebral osteosclerosis. However, myelopathy caused by OLF [ossification of ligamentum flavum] in patients with skeletal fluorosis has recently been recognized. Thus, fluorosis should be considered a potential contributing factor for OLF, especially in patients from high-fluoride areas. . . . Seventy-four thoracic OLF patients who underwent surgical management in the authors’ hospital between 1993 and 2003 were retrospectively studied. The diagnostic criteria for thoracic OLF were: numbness in the lower limbs and below the relative spinal cord segment, motor weakness in the lower extremities and difficulty walking, and increased patellar and Achilles reflexes and lower limb muscle tension upon physical examination. X-ray, Computed Tomography (CT), and magnetic resonance imaging (MRI) were used to confirm the diagnosis in each patient. Based on the following diagnostic criteria, 23 patients were determined to have OLF caused by fluorosis. . . . The diagnostic criteria for fluorosis were: (1) habitation in an endemic fluorosis region since birth, (2) dental fluorosis, (3) regular consumption of water with fluoride levels above 1.2 ppm, and (4) urine fluoride level above 1.5 mg/l. Other clues used for diagnosis were X-ray findings of diffuse densification of bone and calcification of bony insertions of many ligaments, discs, and interosseous membranes (i.e., interosseous membranes of the ribs, forearm, and leg). . . . In conclusion, fluorosis can cause ossification of the thoracic ligamentum flavum, as well as other ligaments. Comparing with other OLF series, a larger number of spinal segments were involved.”
SOURCE: Wang W, et al. (2007). Thoracic ossification of ligamentum flavum caused by skeletal fluorosis. Eur Spine J. 16(8):1119-28.

“Ossification of the ligamentum flavum (OLF) is increasingly being recognized as a cause of myeloradiculopathy. However, the cause of such OLF has been identified only occasionally. The purpose of this case report is to highlight one more cause of OLF causing myelopathy. Two middle-aged men residing in an area endemic for fluorosis presented with the insidious onset of myelopathy. Clinical examination revealed evidence of thoracic cord compression in both patients. Plain x-rays revealed markedly increased bone density characteristic of fluorosis. Magnetic resonance imaging revealed OLF in the lower thoracic region causing cord compression (at one level in the first patient and at three consecutive levels in the second patient). Plain x-rays of the forearm revealed ossification of the interosseous membrane, which is characteristic of fluorosis. Both patients underwent decompressive laminectomy with removal of the OLF. The laminae and ossified yellow ligaments formed one mass of bone, which was removed with rongeurs and drills. After surgery, the first patient demonstrated improvement in motor power, whereas the second patient did not demonstrate any change in neurological status. CONCLUSION: Fluorosis should be entertained in the differential diagnosis of OLF, especially in patients from endemic areas. The magnetic resonance imaging appearance of the spine in such cases is characteristic. In properly selected cases of fluorotic myelopathy, surgery is indicated. However, the prognosis is guarded, and long-term follow-up of these patients is necessary given the nature of the underlying disease.”
SOURCE: Muthukumar N. (2005). Ossification of the ligamentum flavum as a result of fluorosis causing myelopathy: report of two cases. Neurosurgery. 56(3):E622.

“Ossification of the transverse atlantal ligament (OTAL) is extremely rare and may cause upper cervical canal stenosis and spastic quadriparesis… Each of the two cases of OTAL (Ossification of the transverse atlantal ligament) presented here had been diagnosed with fluorosis. As previously discussed, the etiology of OTAL may be of multiple origins, such as injury, and acquired or congenital abnormalities. Although there have been no English articles reporting that OTAL can be caused by fluorosis, we would argue that, together with many other ligaments and membranes, the atlantal transverse ligament may be ossified (in fluorosis).”
SOURCE: Wang W, et al. (2004). Ossification of the transverse atlantal ligament associated with fluorosis: a report of two cases and review of the literature. Spine 29 :E75-8.

“A 70 years old farmer from Yemen was referred as a case of osteoarthritis of both knees for preoperative rehabilitation procedures. Six years before he developed skeletal stiffness. By 70 years he became dependent for ambulation and many other self-care activities. He showed quadriparesis resulting from compression of spinal cord and nerve roots at multiple levels associated with multiple joint involvement.” (This patient was diagnosed by the authors as suffering from skeletal fluorosis.)
SOURCE: Khamees MF, et al. (1995). An uncommon presentation of fluorosis. Electroncephalography & Clinical Neurophysiology 97: S229.

“Two cases of ossification of the posterior longitudinal ligamentum with cervical myelopathy are reported. The radiologic studies determined the etiology, in the first case, it was fluorosis and the second DISH disease.”
SOURCE: Chaabane M, et al. (1995). [Rare causes of ossification of the posterior common vertebral ligament causing cervical compression. Apropos of 2 cases]. [Article in French] J Radiol. 76(1):43-6.

“The authors report four cases of spinal cord compression (three at cervical level and one at dorsal level) due to vertebral osteosclerosis secondary to chronic fluoride intoxication. Roentgenograms showed typical diffuse densification of vertebral bodies, calcifications of bony insertions of many ligaments, discs and interosseous membranes… Spinal computed tomography showed severe cord compression due to posterior osteophytes.”
SOURCE: Mrabet A, et al. (1995). [Spinal cord compression in bone fluorosis. Apropos of 4 cases] [Article in French]. Rev Med Interne.16(7):533-5.

“A case of skeletal fluorosis with spinal cord compression from Kekirawa following consumption of water with high fluoride content for about 20 years is described.”
SOURCE:Disanayake JK, et al. (1994). Skeletal fluorosis with neurological complications. Ceylon Med J. 39(1):48-50.

“Plain roentgenology of the skull was normal, but of the cervical spine revealed marked fluorotic changes and a fracture of C6. Ossification of the posterior longitudinal ligament (OPLL) was seen. He was suspected of having fluorotic cervical canal stenosis with compressive myelopathy, precipitated by trauma… At operation, the characteristic changes of a fluorotic spine were observed in the form of ossified spinal ligaments and hardened bone… The spine was like a continous column of bone, typical of fluorosis… Neurological sequelae in skeletal fluorosis manifest as radiculomyelopathy, principally due to mechanical compression of the spinal cord and nerve roots… Though the disease develops slowly with relentless progression, the neurological manifestations may sometimes be precipitated by minor trauma.”
SOURCE: Prasad VS, Reddy DR. (1994). Posttraumatic pseudomenigocoele of cervical spine in a patient with skeletal fluorosis: Case report. Paraplegia 32:627-30.

“A sizeable number of patients suffering from ossified posterior longitudinal ligament (OPLL) may have fluoride intoxication as the underlying cause.”
SOURCE: Reddy DR, et al. (1993). Neuro-radiology of skeletal fluorosis. Annals of the Academy of Medicine, Singapore 22(3 Suppl):493-500.

“A lumbar computer tomographic scan demonstrated severe calcification of the posterior longitudinal ligament and ligamentum flavum extending from T7 though L3 resulting in marked stenosis of the spinal canal and secondary spinal cord atrophy.”
SOURCE: Dhuna AK, et al. (1992). Skeletal fluorosis. An unusual cause of progressive radiculomyelopathy. Spine 17:842-4.

“In advanced stages of neurofluorosis, the clinical picture is rather uniform, with complete incapacitation and the bedridden state of severe spastic paraparesis, or quadriparesis with incontinence of urine and flexor spasms… [F]luorotic changes resulted in considerable encroachment on the diameter of the intervertebral foramina and spinal canal. These changes tend to be most marked in the cervical region. This explains the clinical similarity of neurofluorosis to cervical spondylosis.”
SOURCE: Haimanot RT. (1990). Neurological complications of endemic skeletal fluorosis, with special emphasis on radiculo-myelopathy. Paraplegia 28:244-51.

“A middle-aged male resident of Benghazi, northeastern Libya, with radiological features of skeletal fluorosis associated with cervical radiculomyelopathy is reported… His problem is of special interest because he lived in a non-tropical, non-endemic area [1-2 ppm] where cases of advanced fluorosis would not be expected.”
SOURCE:Maloo JC, et al. (1990). Fluorotic radiculomyelopathy in a Libyan male. Clinical Neurology and Neurosurgery 92(1):63-5.

“We report a case of spinal cord compression with paraplegia as a result of endemic skeletal fluorosis… Kyphosis of the spine was present without other apparent bone deformity… [M]yelography demonstrated partial spinal cord compression at the level of T2 and T3 vertebrae.. A radiographic skeletal survey revealed osteosclerosis of the axial skeleton with sparing of the skull and prominent calcification of the interosseous membranes and ligamentous insertions… Magnified computed tomographic scan images of the thoracic vertebrae demonstrated marked narrowing at the T2 and T3 levels due to bony exostoses protruding into the spinal canal… Neruologic symptoms are a late occurrence and signify far advanced disease… Involvement of the peripheral and central nervous system has led to the description of neurologic manifestations as a radiculomyelopathy. Radicular features include muscle weakness with asymmetric atrophy, fasciculation, nerve root pain, and acroparesthesias. Onset of these symptoms is usually insidious. Myelopathic features are characterized by a more abrupt onset and include spastic paraplegia or quadriplegia, hyperreflexia, Babinski reflex, clonus, or a variety of sensory deficits. The course is usually progressive, and there is predilection for cervical spine involvement. Neurogenic bladder or bowel incontinence has been reported as a conequence of spinal cord involvement.”
SOURCE: Fisher RL, et al. (1989). Endemic fluorosis with spinal cord compression. A case report and review. Archives of Internal Medicine 149: 697-700.

“All five cases of fluorosis in this study had the clinical picture suggestive of cervical myelopathy. The diagnosis of fluorosis was based on the residence in the endemic area and the radiological features of fluorosis, which included osteosclerosis, calcification of the interosseous membrane/ligaments, periosteal bone formation, and irregular osteophytes… The spinal cord involvement is commonest in the cervical region and has been reported to constitute 56% of 136 patients of fluorosis with neruological complication. Although the lumbar vertebrae are the first to show the changes caused by fluorosis, the compression of cauda equina rarely occurs because its roots are easily accomodated.”
SOURCE:Misra UK, et al. (1988). Endemic fluorosis presenting as cervical cord compression. Archives of Environmental Health 43:18-21.

“Intraosseous Schwannoma of the cervical spine is very rare. Its association with skeletal fluorosis is also extremely rare. A case of succesfully treated intraosseous neurofibroma of the cervical spine associated with skeletal fluorosis causing tetraparesis is reported. The clinical features, diagnostic aspects and the management is described and the literature is reviewed.”
SOURCE: Naidu MRC, et al. (1988). Intraosseous schwannoma of the cervical spine associated with skeletal fluorosis. Clinical Neurology & Neurosurgery 90:257-60.

“The mean canal body ratio was higher in fluorosis at every level of the vertebra as compared to that of normal controls. In other words, the spinal canal was narrow at every level in fluorosis as compared to normal controls.”
SOURCE: Kapila AK, et al. (1983). Measurement of spinal canal body ratio in fluorotic spine. Fluoride 16: 11-19.

“X-ray examination revealed generalized increased bone density of the spine, ribs, and pelvis, suggestive of skeletal fluorosis. Extensive accompanying osteophytosis was present… The sagittal diameters of both the cervical and lumbar spine were below the 90 per cent tolerance levels… A diagnosis of fluorotic radiculomyopathy was made and confirmed by the consulting rheumatologist… The characteristic vertebral changes of skeletal fluorosis and severe osteophytosis were probably the basis for his neurological deficits. Although trauma may have precipitated his radiculomyopathy, the neurological symptoms are adequately explained by the marked narrowing of the sagital diameter of the spinal canal and vertebral osteophytosis secondary to fluorosis. Any trauma which might have caused edema of the spinal cord could have produced neurological damage because of the narrowed bony spinal canal. Thus, the role of trauma is equivocal since bony encroachment on the spinal cord was probable. Wolf has stated that cord compression is likely to occur when the cervical canal is 10 mm or less. The bony canal at C-4 in this patient was 9.5 mm.”
SOURCE: Goldman SM, et al. (1971). Radiculomyelopathy in a southwestern indian due to skeletal fluorosis. Arizona Medicine 28: 675-677.

“A series of 70 cases of skeletal fluorosis with neurological manifestations was studied… The F concentration of water consumed by the patients varied between 1.2 and 11.8 ppm… In 50 cases there was evidence of involvement of the cervical cord… The lowest F concentration in water causing skeletal fluorosis and quadriplegia was 1.35 ppm. Singh et al (1961) recorded spastic paraplegia in a 50 year old male who consumed water containing 1.2 ppm F.”
SOURCE:Siddiqui AH. (1970). Neurological complications of skeletal fluorosis with special reference to lesions in the cervical region. Fluoride 3:91-96.

“The case of a 57-year-old man with skeletal fluorosis leading to spinal cord compression is described. Myelography showed a partial block at T11, and following decompression of the lower thoracic cord there was considerable improvement in symptoms and signs. The diagnosis of fluorosis was confirmed by the radiological appearances, by the histology of the bone removed at operation, and by the raised level of the bone fluoride.”
SOURCE:Webb-Peploe MM, Bradley WG. (1966). Endemic fluorosis with neurological complications in a Hampshire man. Journal of Neurology, Neurosurgery and Psychiatry 29:577-583.

“A 64-year-old white male was admitted to the Veterans Administration Hospital, McKinney, Tex, on May 11, 1962, because of severe respiratory distress and semicoma. He had been a complete invalid in a nursing home for a year… This case of a patient with chronic fluoride intoxication, extensive osteosclerosis, and fluorotic radiculomyelopathy is believed to be the first reported from the United States.”
SOURCE:Sauerbrunn BJ, et al. (1965). Chronic fluoride intoxication with fluorotic radiculomyelopathy. Annals of Internal Medicine 63: 1074-1078.

“compression of the cord (in fluorosis) is almost inevitable.”
SOURCE:Singh A, et al. (1963). Endemic fluorosis. Epidemiological, clinical and biochemical study of chronic fluoride intoxication in Punjab. Medicine 42: 229-246.

“The earliest symptom of spinal cord involvement, present in all cases, was weakness of both lower limbs. This usually started in one leg, with later progression to the other. In 18 cases, after a variable interval, the upper limbs became involved, producing a spastic quadriplegia… The pattern resembled in many ways that of spondylitic myelopathy…The signs of fluorotic myelopathy result chiefly from narrowing of the spinal canal or intervertebral foramina and compression may occur at a single or at multiple sites.”
SOURCE:Singh A, et al. (1963). Endemic fluorosis. Epidemiological, clinical and biochemical study of chronic fluoride intoxication in Punjab. Medicine 42: 229-246.

“The neurological complications of endemic fluorosis have received scant attention, and we first became interested in this aspect while investigating obscure cases of paraplegia, associated with increased density of the spine and other bones, in Punjab – a northern state of India. Almost all the patients came from a small area of Punjab and had in fact skeletal fluorosis with compression paraplegia… The neurological complications are the result of deposition of fluoride in the spine, leading to narrowing of the spinal canal and compression of the cord… It did not differ significantly from other compression paraplegias.”
SOURCE:Singh A, et al. (1961). Skeletal fluorosis and its neurological complications. Lancet 1: 197-200.