This document provides information on ossification of the posterior longitudinal ligament (OPLL). It describes the anatomy and function of the PLL, defines OPLL as ectopic ossification of the PLL, and discusses the epidemiology, pathogenesis, clinical presentation, diagnostic evaluation, treatment options, and prognosis of OPLL. Key points include that OPLL most commonly affects the cervical spine, causes myelopathy, and surgical treatment may involve anterior corpectomy or posterior laminoplasty depending on the location and severity of ossification.

1. Ossification of Posterior
Longitudinal Ligament(OPLL)
Arjun Das
Resident of
Department of Orthopedics and Traumatology

2. Anatomy :PLL
 Runs along the posterior aspect of the vertebral body inside
the vertebral canal from the body of the axis to the sacrum.
At the level of C2 , spreads out and becomes the tectorial membrane
that inserts into the base of skull.
Composed of longitudinal fibers.
Arises from sup. Margin of 1 vertebra and attach to inferior margin of
vertebra
Forms the anterior wall of vertebral canal

4. Fibers wider at IVD and more adherent than vertebral body
PLL much thinner than ALL ,significant for pathophysiology of disc
herniations occurring posterolateral .
In cervical and thoracic regions has uniform width over bodies and
discs
In lumbar region widest at disc
Firmly anchored to Annulus fibrosus ,cartilage of vertebral endplates
and margins of vertebra
Cranial counterpart is Tectorial membrane

5. Comprise superficial and deep connective tissue layers
Tightens with cervical flexion
Superficial layer
More posterior
Continuation of Tectorial membrane at body of Axis
Consists of central band of fibers 8 to 10 mm wide
Described as “fan –like “giving denticulate appearance
More on thoracic and lumbar regions
Span upto 4 vertebral levels
Fibers more vertical orientation

6. Deep layer
Adherent to sup. Layer in midline
Continuation of Cruciform ligament of Atlas
Uniform diameter
2-3 mm wide at narrowest part
Also has denticulate appearance
Intersegmental
Fiber orientation can’t be established

7. Function
Proctective role than supportive role .
Sup . Layer : limit forward flexion
Deep layer :limit lateral flexion and rotation
Increased rotational and lateral flexion forces : creates more
denticulate appearance in lower thoracic and lumbar region
Elastin in PLL :role in dynamic motion of spine

8. Embryology
 At 6 WOG :vertebral column appears as hypocellular light zone
forming vertebral body
Hpercellular dark zone forming IVD
At 7 WOG : light zone ad dark zone distinct but ligament unclear
At 8 WOG : longitudinal arrangement of cells and collagen fibers
appears at the adult ALL but not at PLL
At 10 WOG : Dark zone decreases in width and origin of PLL appears
( unclear at vertebral body but clear at disc )

9. Nerve supply
Primary source : meningeal branch from spinal nerve
Gives ascending and descending branches which fuses and forms
Transverse branches
Transverse branches from opposite side forms network of nerve
fibers superficially
Innervates the PLL in vertebral segments

10. Physiological variants
PLL Is narrower and weaker .
Fibers of annulus fibrosus and edge of vertebral body m/c site of
attachment
Sometimes to posterior aspect of vertebra
PLL most developed at L3 and L4 (1.4mm thickness )
Ligament in mid portion of each vertebral body covers vascular
foramina
From L2 upwards ligament thins markedly

11. Ossification of Posterior Longitudinal
Ligament (OPLL)
Chronically ,progressive disease .
Ectopic enchondral and membranous ossification
Unkown etiology
Multifactorial condition : genetic and environmental factors
Original reported from japan

12. Epidemiology
Incidence
In Japanese > 30 yrs upto 3%
In the United States and Europe , upto 1.7%
Gender
Cervical : M>F (2:1)
Dorsal :F>M
Race
More in Japanese
Age
Started in 40s and become symptomatic in 50s

13. Risk factors
Gentic locus close to HLA ,on chr. 6
DM
Obesity
Acromegaly
Hypoparathyroidism
Bone forming conditions : DISH and Fluorosis

14. PATHOGENESIS
Ligament cells from pts with OPLL have osteoblast –like
characteristics
Factors that initiate these cells to form calcification and ossification
are :
Genetic factors :COL6A1, COL11A2 and NPPS
Hormonal factors :non –insulin dependent D.M, hypoparathyroidism
Environmental factors : mechanical stress in ligaments of spine
Life style
a/w DISH and Fluorosis

15. Pathogenesis of Neural injury in OPLL
A) Mechanical
 Static compression
Occupying ratio greater than 60 % indicates high risk of development of myelopathy
SAC < 6 mm
Dynamic compression
Degenerative spondylolisthesis
SAC 6-13 mm
Threshold of SAC
Normal : 13 mm
B) Vascular

16. Pathology
Site
Cervical (C2-C4) : 70 %
Dorsal (T1-T4) :15%
Lumbar (L1-L3 ) : 15 %
High frequency with cervical OPLL a/w thracolumbar OPLL

17. Character
Early : PLL hypertrophy
Then : Punctate calcification within PLL
Then : Actual ossification

18. Types of OPLL

19. Types of OPLL

20. Microscopic features
Early OPLL
Hypertrophy PLL d/to fibroblastic hyperplasia and increased collagen
deposition with punctate calcification
Immature form
Woven bone with fibrocartilaginous cell proliferation
Mature form
Lamellar bone with well developed haversian systems
Mostly endochondral ossification and sometime membranous

21. Pathological changes in cord
Demyelination and loss of axon
Always in posterior and posterolateral part of cord

22. Natural History Of OPLL
OPLL ↑in thickness 0.4mm/yr
Longitudinal expansion 0.67mm/yr
More with continuous or mixed type
Rapid progression in 4th decade and then decreases
Also occurs post –operatively
In 60-70 % after posterior decompression
In 36-64 % after anterior decompression and fusion
Matsunga et al . Demonstrated that 38 % pts presenting with myelopathy had
progressive worsening of symptoms if not operated .

23. Causes of late deterioration
Post operative progression of OPLL
Progressive deformity and instability
Thoracic myelopathy secondary to OPLL or OLF or both
Degenerative lumbar stenosis

24. Diagnostic criteria
Radiological
OPLL visible on lateral view X-ray
CT scan may be used for better assessment
Clinical
Cervical myelopathic symptoms
Radicular symptoms
Abnormality of cervical range of movement

25. Clinical picture
Accidental discovery
Onset
Usually graudual progressive but may be acute (after trauma )
Pain
Axial neck and upper limb pain
Motor abnormalities
Weakness
Incoordination
Clumsiness
Muscle wasting
Bladder –bowel dysfunction
Sensory symptoms

26. Neurological deficits
Myelopathy or myeloradiculopathy rather than radiculopathy alone
Associated co-existing conditions
DM
Hypoparathyrodism
Mytonic muscular dystrophy
Acromegaly
Obesity

27. Radiological features

28. X- ray
• Normal AP diameter of
cervical canal :17mm from C3-C7
• Absolute stenosis : 10 mm or less
• Relative stenosis : 10 – 13 mm

29. CT- SCAN

31. Dural calcification

32. CT signs of Dural Penetrance (Single –layer
and Double –layer Signs )

33. MRI
High incidence of associated
disc herniation in pts with
cervical OPLL.
Pathological changes in spinal
cord.

34. Treatment
Conservative management
Surgical management

35. Conservative management
Indications
Axial pain without or with subclinical myelopathy
Main insult is dynamic compression (less than 60 % stenosis or 6-13mm SAC)
Severe co morbidity
Measures
Collar
Traction
Careful life style
Analgesics and anti –inflammatory drugs
Anti depressants and anticonvulsants
Opiods

36. Surgery : Indications
Is there a rule for prophylactic surgery ?
Myelopathy or radiculo-myelopathy with predominant myelopathy
Role of prophylactic surgery in asymptomatic patient
Severe canal compromise :
•SAC <6mm or
•Occupational ratio >60 %
Presence of cord signal in MRI
SSEP is affected
Young age (< 65yrs )

37. Surgical procedures
Anterior surgery :single/ multilevel (upto 4)
Corpectomy with removal of calcified mass
Corpectomy without removal of calcified mass (ant .floating method )
Open Window Corpectomy/Skip cervical corpectomy ( removal of post ½ of body
leaving ant one )
Oblique Cervical Corpectomy
With fusion and Halo Vest or with fusion and fixation

38. Surgical procedures
Posterior surgery
Laminectomy
Laminectomy + fixation and fusion
Laminoplasty (open door or double door laminoplasty )
Combined anterior and posterior surgery

39. Choice of approach
Factors in favor of ant .approach
Presence of facilities and expertise
Occupying ratio more than 60 %
Hill- shaped calcification
Kyphotic deformity or degenerative instability
Limited corpectomy levels (upto 4 )
Fessler et al. found pts with anterior approach t/t have improvement of
1.24 Nurick grades than laminectomy pts by 0.07.

40. Factors allowing posterior approach
Comorbidity prevent more lengthy procedures
Occupying ratio less than 60 %
Plateau – shaped calcification
Preserved lordotic spine or maximum straightening

41. Radiological signs help in choosing approach
Gwinn et al. proposed simple straight line method to effective spinal canal
lordosis
Anterior surgery :better achieve decompression in lost effective lordosis

42. In 2008 ,Fusiyoshi et al . Proposed a new concept called K-line .

43. Fusiyoshi et al . Proposed in K line(-) ventral approach have a better
chance of neurological outcome .
K line (-) pts have kyphosis that prohibits a dorsal approach as spinal
cord has less potential to shift following decompression .

45. Anterior corpectomy and fusion
Advantages
Improved myelopathy scores
Direct removal of pathology
Disadvantages
Increased complications
Anterior approach related (dysphagia ,hoarseness ,prolonged intubation )
Graft expulsion
Pseudoarthrosis
C5 root palsy

46. Laminoplasty
Advantages
Decreased approach related complications
Better tolerated in pts >65 years
Improved stability
Disadvantages
Increased neck pain
Less improvement in myelopathy scores
Persistent ossified bar/ligament
C5 root palsy

48. Prognosis
Patient’s factors :
Old age
Preoperative neurological status and duration of symptoms
H/O trauma causing acute presentations
Disease’s factors
Occupying ratio of OPLL or SAC
Saggital shape of ossification (hill –shaped ) esp. with post. Decompression
Management’s factors
Progression more with posterior decompression

49. • Thank you