SANDHIGAT VATA (OSTEOARTHRITIS).
1) NIRUKTI:-
The disease in which the vitiated Vata afflicts the joints leading to a painful swelling and ultimately destruction of the joints is called as Sandhigata Vayu.
2) VYAKHYA:-
3) HETU:-The Risk factors in OA are: - a) Age,
b) Female gender,
c) Race,
d) Genetic factors,
e) Major joint trauma,
f) Repetitive stress, e.g. , vocational,
g) Obesity,
h) Congenital/developmental defects,
i) Prior inflammatory joint disease,
j) Metabolic/endocrine disorders.
3) PURVARUPA:-
4) RUPA: - The joint pain of OA is often described as a deep ache and is localized to the involved joint. Typically, the pain of OA is aggrevated by joint use and relieved by rest, but, as the disease progresses, it may become persistent. Nocturnal pain, interfering with sleep, is seen particularly in advanced OA of the hip and may be enervating. Stiffness of the involved joint upon arising in the morning may be prominent but usually lasts less than 20 min. Systematic manifestations are not a feature of primary OA.
Causes of joint paint in patients of OA with the corresponding mechanisms.
| SOURCE. | MECHANISM. |
| Synovium. | Inflammation. |
| Subchondral bone. | Medullary hypertension, microfractures. |
| Osteophyte. | Stretching of periosteal nerve endings. |
| Ligaments. | Stretch. |
| Capsule | Inflammation, distension. |
| Muscle. | Spasm. |
5) PRAKARANURUPA RUPA: - In Idiopathic OA, the most common form of the disease, no predisposing factor is apparent. Secondary OA is pathologically indistinguishable from idiopathic OA but is attributable to an underlying cause.
(A) Idiopathic/Primary: -
(a) Localized OA: -
(1) Hands: Heberden’s and Bouchard’s nodes (nodal), erosive inter-phalangeal arthritis (nonnodal), 1st carpometacarpel joint.
(2) Feet: hallux valgus, hallux rigidus, contracted toes, talonavicular.
(3) Knee: * Medial compartment,
* Lateral compartment
* Patellofemoral compartment.
(4) Hip: * Ecentic (superior)
* Concentric (axial, medial)
* Diffuse (coxae senilis)
(5) Spine: * Apophyseal joint
* Intervertebral joints or disks
* Spondylosis or osteophytes
* Ligamentous (hyperostosis, Forestier’s disease, diffuse idiopathic skeletal hyperostosis)
(6) Other single sites: - e.g. glenohumeral, acromioclavicular, tibiotalar, sacroiliac, temporomandibular.
(b) Generalized OA includes 3 or more of the area listed above (Kellgren-Moore).
(B) Secondary: -
(a) Trauma: * Acute
* Chronic (occupational, sports)
(b) Congenital or developmental: * Localized diseases Legg-Calve-Perthes, congenital hip dislocation, slipped epiphysis.
* Mechanical factors: - Unequal lower extremity length, valgus/varus deformity, hypermobility syndromes.
* Bone dysplasias: epiphyseal dysplasia, spondyloepiphyseal dysplasia, osteonychondystrophy
(c) Metabolic: * Ochronosis (alkaptonuria)
* Hemochromatosis
* Wilson’s disease
* Gaucher’s disease
(d) Endocrine: * Acromegaly
* Hyperparathyroidism
* Dibetes mellitus
* Obesity
* Hypothyroidism
(e) Calcium deposition diseases: * Calcium pyrophosphate dehydrate deposition
* Apatite arthropathy
(f) Other bone and joint diseases: * Localized: Fracture, avascular necrosis, infection, gout
* Diffuse: Rheumatoid (inflammatory) arthritis, Paget’s disease, osteopetrosis, osteocondritis
(g) Neuropathic: Charcot joints
(h) Endemic: * Kashin-Beck
* Mseleni
(i) Miscellaneous: * Frostbite
* Caisson’s disease
* Hemoglobinopathies
6) SAMPRAPTI: - OA develops either in two settings: (1) the biomaterial properties of the articular cartilage and subchondral bone are normal, but excessive loading of the joint causes the tissues to fail, or (2) the applied load is reasonable, but the material properties of the cartilage or bone marrow are inferior.
If the material properties of the cartilage or bone marrow are inferior, then their will be ruksha and dry gunas in excess leading to vitiation of vata followed by pain. If the material properties of the cartilage and subchondral bone are normal, the excessive load held may go out of the bearing capacities of the joints, leading to stress on ligaments followed by pain. The age and female gender are considered to be the risk factors since the joints and articulating mechanisms are poorly developed in younger age and in females. Since OA can transmit as heredity disease through the poorly developed joints; race and genetic factors are considered to be the risk factors. Major joint trauma and Prior inflammatory joint disease indicate week biomaterial properties of the joint leading to it limited capacities. Vocational movements will lead to more need of lubrication to the joint which will lead to Vata vitiation due to less moistness and chala guna. In obese people; OA in the lower extremities is common since, their lower extremities are not capable enough to bear their whole body weight.
7) UPADRAVA: -
8) UDARKA:-
10) ARISHTA LAKSHANA:-
11) VYADHI VYAVACHCHHATI: -The diagnosis of OA is usually based on clinical and radiographic features. The characteristic radiographic findings include narrowing joint space, subchondral bone sclerosis, subchondral cysts and osteophytosis.
No laboratory studies are diagnostic for OA, but specific laboratory testing may help in identifying one of the underlying causes of secondary OA. Analysis of synovial fluid reveals mild leukocytosis (more than 2000 white blood cells per microliter), with a predominance of mononuclear cells. Synovial fluid analysis is of particular value in excluding other conditions, such as calcium pyrophosphate diydrate deposition disease, gout or septic arthritis.
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