Causes of increased Lumbar Lordosis
Developmental….
Postural Muscular Imbalance – Hypertonic/shortened LES and weak/stretched abdominals. Tight/shortened hip flexors and weak/stretched hamstrings: postural patterns, imbalances caused by ineffective training/exercise regimes, sports
Repeated extension of lumbar spine, e.g. dance of gymnastics.
Increased thoracic kyphosis – Poor posture, chronic respiratory problems, osteochrondritis/scheurmans (http://www.nursingcenter.com/pdf.asp?AID=1093874)
Spondylolithesis - Anterior slippage of one vertebrae on another. Depending on degree of slippage it increases sacral kyphosis and lumbar lordosis. Spondylolytic is with a fracture of the pars interarticularis leading to the slippage, most commonly at L5/S1. Non-spondylolytic is with no fracture and is most common at L3/4. Can be characterised as 5 different types using the Wiltse Classification System:
Neuromuscular – e.g. Cerebral palsy = Hypertrophy and hypertonicity in LES with contracture of hip flexor muscles. Abnormal course of Psoas Major between spine and proximal femur becomes more of an L-Sp extensor than hip flexor (usually secondary to severe scoliosis and associated kyphosis).
Connective Tissue – Hypermobility Syndrome e.g. Ehlers-Danlos Syndrome (EDS) = Inherited connective tissue disorder, defect in collagen (types I or III) synthesis which helps tissue resist deformation. Six major types (Hypermobility, Classical, Vascular, Kyphoscoliosis, Arthrochalasis & Dermatoparaxis) ranging from mild to life-threatening. Affects skin, joints, vessels, ligaments, muscles and viscera.
Marfan Syndrome = Genetic connective tissue disorder. Tend to be tall people with long limbs (disproportionally long arms) and long, thin fingers. Defective gene so Fibrillin 1 is not encoded properly. Consequently Fibrillin 1 binds (inappropriately) to another connective protein Transforming Growth Factor Beta (TGFβ) which has a deleterious effect on vascular smooth muscle development and extracellular matrix. Mutated Fibrillin and excessive TGFβ in lungs heart valves and aorta weakens the structures and causes the features of Marfan’s. It can affect – the skeletal system (scoliosis, pectus excavatum/carinatum not uncommon), eyes (near sightedness and astigmatism, subluxation of the lens), CVS (palpitations, tachycardia, angina, aortic aneurysm), Lungs (spontaneous pneumothorax) & CNS (weakening of dural sac → lower back/abdominal/leg pain, headaches).
Can also be a symptom of serious medical conditions, such as Stickler Syndrome, rheumatism osteogenesis imperfecta, lupus, polio, Down syndrome, morquio syndrome, cleidocranial dysostosis or myotonia congenita.
Degenerative – Hip OA leading to fixed flexion deformity and compensatory increased lumbar lordosis. Degenerative joint disease affecting articular cartilage. Chrondoblast activity outstrips chrondoclast activity as proteoglycan content reduces making cartilage less resilient. Cartilage is softened and roughened, eventually wearing away. Breakdown of the cartilage leads to irritation and inflammation of the synovial capsule. Initially this leads to hypermobility as the joint surfaces don’t want to be irritated by one another. Eventually the sub-chondral bone is exposed and osteoclast activity is increased to try and replace the cartilage with bone. This leads to osteophytic growths at the joint margins in an attempt to stabilise the joint or improve congruency. At this stage the joint becomes hypomobile (esp. in extension in the hip). Decreased Rom leads to a fixed flexion deformity at the hip and often a compensatory increase in lumbar lordosis. Hard, swollen joints that are stiff and painful, symptoms are worse with activity and morning stiffness characteristically is less that 1hour. NON-INMFLAMMATORY condition.
Should we do anything about it???
http://physther.net/content/83/10/907.full.pdf+html
Postural Muscular Imbalance – Hypertonic/shortened LES and weak/stretched abdominals. Tight/shortened hip flexors and weak/stretched hamstrings: postural patterns, imbalances caused by ineffective training/exercise regimes, sports
Repeated extension of lumbar spine, e.g. dance of gymnastics.
Increased thoracic kyphosis – Poor posture, chronic respiratory problems, osteochrondritis/scheurmans (http://www.nursingcenter.com/pdf.asp?AID=1093874)
Spondylolithesis - Anterior slippage of one vertebrae on another. Depending on degree of slippage it increases sacral kyphosis and lumbar lordosis. Spondylolytic is with a fracture of the pars interarticularis leading to the slippage, most commonly at L5/S1. Non-spondylolytic is with no fracture and is most common at L3/4. Can be characterised as 5 different types using the Wiltse Classification System:
Neuromuscular – e.g. Cerebral palsy = Hypertrophy and hypertonicity in LES with contracture of hip flexor muscles. Abnormal course of Psoas Major between spine and proximal femur becomes more of an L-Sp extensor than hip flexor (usually secondary to severe scoliosis and associated kyphosis).
Connective Tissue – Hypermobility Syndrome e.g. Ehlers-Danlos Syndrome (EDS) = Inherited connective tissue disorder, defect in collagen (types I or III) synthesis which helps tissue resist deformation. Six major types (Hypermobility, Classical, Vascular, Kyphoscoliosis, Arthrochalasis & Dermatoparaxis) ranging from mild to life-threatening. Affects skin, joints, vessels, ligaments, muscles and viscera.
Marfan Syndrome = Genetic connective tissue disorder. Tend to be tall people with long limbs (disproportionally long arms) and long, thin fingers. Defective gene so Fibrillin 1 is not encoded properly. Consequently Fibrillin 1 binds (inappropriately) to another connective protein Transforming Growth Factor Beta (TGFβ) which has a deleterious effect on vascular smooth muscle development and extracellular matrix. Mutated Fibrillin and excessive TGFβ in lungs heart valves and aorta weakens the structures and causes the features of Marfan’s. It can affect – the skeletal system (scoliosis, pectus excavatum/carinatum not uncommon), eyes (near sightedness and astigmatism, subluxation of the lens), CVS (palpitations, tachycardia, angina, aortic aneurysm), Lungs (spontaneous pneumothorax) & CNS (weakening of dural sac → lower back/abdominal/leg pain, headaches).
Can also be a symptom of serious medical conditions, such as Stickler Syndrome, rheumatism osteogenesis imperfecta, lupus, polio, Down syndrome, morquio syndrome, cleidocranial dysostosis or myotonia congenita.
Degenerative – Hip OA leading to fixed flexion deformity and compensatory increased lumbar lordosis. Degenerative joint disease affecting articular cartilage. Chrondoblast activity outstrips chrondoclast activity as proteoglycan content reduces making cartilage less resilient. Cartilage is softened and roughened, eventually wearing away. Breakdown of the cartilage leads to irritation and inflammation of the synovial capsule. Initially this leads to hypermobility as the joint surfaces don’t want to be irritated by one another. Eventually the sub-chondral bone is exposed and osteoclast activity is increased to try and replace the cartilage with bone. This leads to osteophytic growths at the joint margins in an attempt to stabilise the joint or improve congruency. At this stage the joint becomes hypomobile (esp. in extension in the hip). Decreased Rom leads to a fixed flexion deformity at the hip and often a compensatory increase in lumbar lordosis. Hard, swollen joints that are stiff and painful, symptoms are worse with activity and morning stiffness characteristically is less that 1hour. NON-INMFLAMMATORY condition.
Should we do anything about it???
http://physther.net/content/83/10/907.full.pdf+html
Postural Muscular Imbalance – Hypertonic/shortened LES and weak/stretched abdominals. Tight/shortened hip flexors and weak/stretched hamstrings: postural patterns, imbalances caused by ineffective training/exercise regimes, sports
Repeated extension of lumbar spine, e.g. dance of gymnastics.
Increased thoracic kyphosis – Poor posture, chronic respiratory problems, osteochrondritis/scheurmans (http://www.nursingcenter.com/pdf.asp?AID=1093874)
Spondylolithesis - Anterior slippage of one vertebrae on another. Depending on degree of slippage it increases sacral kyphosis and lumbar lordosis. Spondylolytic is with a fracture of the pars interarticularis leading to the slippage, most commonly at L5/S1. Non-spondylolytic is with no fracture and is most common at L3/4. Can be characterised as 5 different types using the Wiltse Classification System:
- Dysplastic – Congenital malformation of the LS, with small, incompetent facets. Very rare but develops quickly and is associated with severe neurological symptoms.
- Isthmic – AKA Spondylolytic spondylolithesis. Most common. Spondylotic defect usually occurs between 6-16yrs and slippage occurs soon after. Progression is rare but it can predispose to disc degeneration. 90% are low grade (<50% slippage) and 10% high grade. Linked to high impact activities as thought to be a result of repetitive stress fractures leading to chronic non-union (linked to cartilaginous defect). 100% slippage = Spondyloptosis.
- Degenerative – Develops as a result of spondyloarthrosis. Facets remodel and become more saggital so a small degree of slippage may occur. Very common. Mostly asymptomatic but can worsen to causes stenosis and neurogenic claudication (most common indication for spinal surgery in older adults).
- Traumatic – Acute fracture of inferior facets of pars interarticularis. Very rare.
- Pathological – Damage to posterior elements from metastases or metabolic bone disease. Very rare. Linked with; Osseous TB - Form of osteomyelitis, infection of bone or bone marrow. Leukocytes attempting to engulf the infecting organism release enzymes cause osteolysis, Giant Cell Tumours - multinucleated giant cells, which are osteoclast like. Usually benign. Account for 20% of benign bone tumours and Metastases - arise from epithelial cells and form solid masses with bones. Any type of cancer can metastasise to bone but breast, lung and prostate most common. Unregulated osteoblast and osteoclast activity leads to altered bone architecture that is unable to withstand normal, day-to-day stresses.
Neuromuscular – e.g. Cerebral palsy = Hypertrophy and hypertonicity in LES with contracture of hip flexor muscles. Abnormal course of Psoas Major between spine and proximal femur becomes more of an L-Sp extensor than hip flexor (usually secondary to severe scoliosis and associated kyphosis).
Connective Tissue – Hypermobility Syndrome e.g. Ehlers-Danlos Syndrome (EDS) = Inherited connective tissue disorder, defect in collagen (types I or III) synthesis which helps tissue resist deformation. Six major types (Hypermobility, Classical, Vascular, Kyphoscoliosis, Arthrochalasis & Dermatoparaxis) ranging from mild to life-threatening. Affects skin, joints, vessels, ligaments, muscles and viscera.
Marfan Syndrome = Genetic connective tissue disorder. Tend to be tall people with long limbs (disproportionally long arms) and long, thin fingers. Defective gene so Fibrillin 1 is not encoded properly. Consequently Fibrillin 1 binds (inappropriately) to another connective protein Transforming Growth Factor Beta (TGFβ) which has a deleterious effect on vascular smooth muscle development and extracellular matrix. Mutated Fibrillin and excessive TGFβ in lungs heart valves and aorta weakens the structures and causes the features of Marfan’s. It can affect – the skeletal system (scoliosis, pectus excavatum/carinatum not uncommon), eyes (near sightedness and astigmatism, subluxation of the lens), CVS (palpitations, tachycardia, angina, aortic aneurysm), Lungs (spontaneous pneumothorax) & CNS (weakening of dural sac → lower back/abdominal/leg pain, headaches).
Can also be a symptom of serious medical conditions, such as Stickler Syndrome, rheumatism osteogenesis imperfecta, lupus, polio, Down syndrome, morquio syndrome, cleidocranial dysostosis or myotonia congenita.
Degenerative – Hip OA leading to fixed flexion deformity and compensatory increased lumbar lordosis. Degenerative joint disease affecting articular cartilage. Chrondoblast activity outstrips chrondoclast activity as proteoglycan content reduces making cartilage less resilient. Cartilage is softened and roughened, eventually wearing away. Breakdown of the cartilage leads to irritation and inflammation of the synovial capsule. Initially this leads to hypermobility as the joint surfaces don’t want to be irritated by one another. Eventually the sub-chondral bone is exposed and osteoclast activity is increased to try and replace the cartilage with bone. This leads to osteophytic growths at the joint margins in an attempt to stabilise the joint or improve congruency. At this stage the joint becomes hypomobile (esp. in extension in the hip). Decreased Rom leads to a fixed flexion deformity at the hip and often a compensatory increase in lumbar lordosis. Hard, swollen joints that are stiff and painful, symptoms are worse with activity and morning stiffness characteristically is less that 1hour. NON-INMFLAMMATORY condition.
Should we do anything about it???
http://physther.net/content/83/10/907.full.pdf+html
Postural Muscular Imbalance – Hypertonic/shortened LES and weak/stretched abdominals. Tight/shortened hip flexors and weak/stretched hamstrings: postural patterns, imbalances caused by ineffective training/exercise regimes, sports
Repeated extension of lumbar spine, e.g. dance of gymnastics.
Increased thoracic kyphosis – Poor posture, chronic respiratory problems, osteochrondritis/scheurmans (http://www.nursingcenter.com/pdf.asp?AID=1093874)
Spondylolithesis - Anterior slippage of one vertebrae on another. Depending on degree of slippage it increases sacral kyphosis and lumbar lordosis. Spondylolytic is with a fracture of the pars interarticularis leading to the slippage, most commonly at L5/S1. Non-spondylolytic is with no fracture and is most common at L3/4. Can be characterised as 5 different types using the Wiltse Classification System:
- Dysplastic – Congenital malformation of the LS, with small, incompetent facets. Very rare but develops quickly and is associated with severe neurological symptoms.
- Isthmic – AKA Spondylolytic spondylolithesis. Most common. Spondylotic defect usually occurs between 6-16yrs and slippage occurs soon after. Progression is rare but it can predispose to disc degeneration. 90% are low grade (<50% slippage) and 10% high grade. Linked to high impact activities as thought to be a result of repetitive stress fractures leading to chronic non-union (linked to cartilaginous defect). 100% slippage = Spondyloptosis.
- Degenerative – Develops as a result of spondyloarthrosis. Facets remodel and become more saggital so a small degree of slippage may occur. Very common. Mostly asymptomatic but can worsen to causes stenosis and neurogenic claudication (most common indication for spinal surgery in older adults).
- Traumatic – Acute fracture of inferior facets of pars interarticularis. Very rare.
- Pathological – Damage to posterior elements from metastases or metabolic bone disease. Very rare. Linked with; Osseous TB - Form of osteomyelitis, infection of bone or bone marrow. Leukocytes attempting to engulf the infecting organism release enzymes cause osteolysis, Giant Cell Tumours - multinucleated giant cells, which are osteoclast like. Usually benign. Account for 20% of benign bone tumours and Metastases - arise from epithelial cells and form solid masses with bones. Any type of cancer can metastasise to bone but breast, lung and prostate most common. Unregulated osteoblast and osteoclast activity leads to altered bone architecture that is unable to withstand normal, day-to-day stresses.
Neuromuscular – e.g. Cerebral palsy = Hypertrophy and hypertonicity in LES with contracture of hip flexor muscles. Abnormal course of Psoas Major between spine and proximal femur becomes more of an L-Sp extensor than hip flexor (usually secondary to severe scoliosis and associated kyphosis).
Connective Tissue – Hypermobility Syndrome e.g. Ehlers-Danlos Syndrome (EDS) = Inherited connective tissue disorder, defect in collagen (types I or III) synthesis which helps tissue resist deformation. Six major types (Hypermobility, Classical, Vascular, Kyphoscoliosis, Arthrochalasis & Dermatoparaxis) ranging from mild to life-threatening. Affects skin, joints, vessels, ligaments, muscles and viscera.
Marfan Syndrome = Genetic connective tissue disorder. Tend to be tall people with long limbs (disproportionally long arms) and long, thin fingers. Defective gene so Fibrillin 1 is not encoded properly. Consequently Fibrillin 1 binds (inappropriately) to another connective protein Transforming Growth Factor Beta (TGFβ) which has a deleterious effect on vascular smooth muscle development and extracellular matrix. Mutated Fibrillin and excessive TGFβ in lungs heart valves and aorta weakens the structures and causes the features of Marfan’s. It can affect – the skeletal system (scoliosis, pectus excavatum/carinatum not uncommon), eyes (near sightedness and astigmatism, subluxation of the lens), CVS (palpitations, tachycardia, angina, aortic aneurysm), Lungs (spontaneous pneumothorax) & CNS (weakening of dural sac → lower back/abdominal/leg pain, headaches).
Can also be a symptom of serious medical conditions, such as Stickler Syndrome, rheumatism osteogenesis imperfecta, lupus, polio, Down syndrome, morquio syndrome, cleidocranial dysostosis or myotonia congenita.
Degenerative – Hip OA leading to fixed flexion deformity and compensatory increased lumbar lordosis. Degenerative joint disease affecting articular cartilage. Chrondoblast activity outstrips chrondoclast activity as proteoglycan content reduces making cartilage less resilient. Cartilage is softened and roughened, eventually wearing away. Breakdown of the cartilage leads to irritation and inflammation of the synovial capsule. Initially this leads to hypermobility as the joint surfaces don’t want to be irritated by one another. Eventually the sub-chondral bone is exposed and osteoclast activity is increased to try and replace the cartilage with bone. This leads to osteophytic growths at the joint margins in an attempt to stabilise the joint or improve congruency. At this stage the joint becomes hypomobile (esp. in extension in the hip). Decreased Rom leads to a fixed flexion deformity at the hip and often a compensatory increase in lumbar lordosis. Hard, swollen joints that are stiff and painful, symptoms are worse with activity and morning stiffness characteristically is less that 1hour. NON-INMFLAMMATORY condition.
Should we do anything about it???
http://physther.net/content/83/10/907.full.pdf+html