The Locomotor System pathology is one of the best candidates for mesotherapeutic treatment. In the first place, we have the localisation of injuries, which are generally confined to specific joints. In the second place, we have the allopathic medicines which, normally taken either orally or in an intramuscular fashion, inevitably lead to an iatrogeny, which may on occasion prove to be very serious. In the third place, we have the wide range of medicines which are available to us. Fourthly, and most importantly, we have the fact that we are dealing with the most frequent pathology with which we are confronted in our surgeries and private clinics, where the technique and art of mesotherapy is practised.

The bibliographic material consulted, along with conversations held with fellow mesotherapists, lead us to the conclusion that there is a lack of unanimity as regards the mixtures of medicines used to date. These are generally mixtures made up of one or more products from the following groups: AINES, Decontracting agents, Vasodilators, Anaesthetics and Calcitonins. It must also be stated that practically all of those consulted have mentioned some occasional unpleasant reaction to a some mixture or other, or some difficulty encountered in trying to obtain the medicine that they deem to be an ideal product to treat a particular case.

      Osteoarthritis and Homoeopathic Managements

Conducted by: Dr. Rajeev Singh; B.Sc., B.H.M.S.; Gold Medallist; Jail Road; Rae Bareli           

Osteoarthritis:

                           Osteoarthritis, also erroneously called degenerative joint disease, represents failure of the diarthrodial (movable, synovial-lined). In idiopathic (primary) OA, the most common form of the disease, no predisposing factor is apparent. Second OA is pathologically indistinguishable from idiopathic OA but is attributable to an underlying cause:-

I.       Idiopathic

A.      Localized OA-

1.         Hands: Heber den’s and Bouchard’s nodes (nodal), erosive interphalengeal arthritis (nonnodal), 1st carpometacarpel joint.

2.         Feet: Hallux valgus, hallux rigidus, contracted toes (hammer/cock-up toes), talonavicular.

3.         Knee:

a.       Medial compartment

b.      Lateral compartment

c.       Patellofemoral compartment

4.         Hip:

a.       Eccentric (superior)

b.      Concentric (axial, medial)

c.       Diffuse (coxae senilis)

5. Spine:

1. Apophyseal joints.
2. Intervertebral joints (disks)
3. Spondylosis (osteophytes)

                 d. Ligamentous (Hyperostosis, Forestier’s disease, Diffuse- Idiopathic skeletal hyperostosis.

5.         Other single sites, e.g., Glenohumoral, Acromioclavicular,

Tibiotalar, Sacroiliac, Temporomandibular.

B.      Generalized OA:

 Generalized OA includes 3 or more of the areas listed above (Kellgren- Moore).

II.      Secondary

A.      Trauma

1.         Acute

2.         Chronic (occupational, sports)

B.      Congenital or developmental

1.         Localized diseases: Legg- Calve- Perthes, congenital hip dislocation, slipped epiphysis.

2.         Mechanical factors: unequal lower extremity length, valgus/ varus deformity, hypermobility syndromes.

3.         Bone dysplasias: epiphyseal dysplasia, spondyloepiphyseal dysplasia, osteonychondystrophy.

C.      Metabolic

1.         Ochronosis (alkaptonuria)

2.         Hemochromatosis

3.         Wilson’s disease

4.         Gaucher’s disease

D.      Endocrine

1.         Acromegaly

2.         Hyperparathyroidism

3.         Diabetes mellitus

4.         Obesity

5.         Hypothyroidism

E.      Calcium deposition diseases

1.         Calcium pyrophosphosphate dehydrate deposition

2.         Apatite arthropathy.

F.      Other bone and joint diseases

1.         Localized: fracture, avascular necrosis, infection, gout.

2.         Diffuse: rheumatoid (inflammatory) arthritis, Paget’s disease, osteopetrosis, osteochondritis.

G.      Neuropathic (Charcot joints)

H.      Endemic

1.         Kashin –Bech

2.         Mseleni

I.       Miscellaneous.

1.         Frostbite

2.         Caisson’ disease

3.         Hemoglobinopathies

                                  Under the age of 55 yrs the joint distribution of OA in men and women is similar; in older individuals, hip OA is more common in men, while OA of interphalengeal joints; knee joint and the thumb base is more common in women. Point mutation in the cDNA coding for articular cartilage collagen have been identified in families with chondrodysplasia and polyarticular secondary OA.

Risk factors for OA:

Age

Female

Race

Genetic factors

Major joint trauma

Repetitive stress, e.g., vocational

Obesity

Congenital/ developmental defects

Prior inflammatory joint disease

Metabolic/ endocrine disorders

Pathology: Although the cardinal pathologic feature of OA is a progressive loss of articular cartilage, OA is not a disease of any single tissue but a disease of an organ, the synovial joint, in which all of the tissues are affected: the subcondral bone, synobium, meniscus, ligaments, and supporting neuromuscular apparatus as well as cartilage.

In the early stages the cartilage is thicker than normal, but with progression of OA the joint surface thins, the cartilage softens, the integrity of the surface is breached, and vertical clefts develop (fibrillation). Areas of fibrocartilaginous repair may develop, but the repair tissue is inferior to pristine hyaline articular cartilage in its ability to withstand mechanical stress.

Remodeling and hypertrophy of bone is also major feature of OA. Appositional bone growth occurs in the subchondral region, leading to the bony “sclerosis” seen radio graphically. The abraded bone under a cartilage ulcer may take on the appearance of ivory (eburnation). Growth of cartilage and bone at the joint margins leads to osteophytes (spurs), which alter the contour of the joint and may restrict movement. A patchy chronic synovitis and thickening of the joint capsule may further restrict movement.

Pathogenesis:

The main load on articular, the major target tissue in OA, is produced by contraction of the muscles that stabilize or move the joint. Although cartilage is an excellent shock absorber in terms of its bulk properties, at most sites it is only 1 to 2 mm thick, too thin to serve as the sole shock-absorbing structure in the joint.

OA develops in either of 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 are inferior.

Some cases of “idiopathic” OA of the hip may be due to subtle congenital or developmental defects, such as congenital subluxation/ dislocation, acetabular dysplasia, Legg- Calve-Perthes disease, or slipped capital femoral epiphysis, which increase joint congruity and concentrate the dynamic load.

Clinical conditions that reduce the ability of the cartilage or subchondral bone to deform are associated with development of OA. In ochronosis, accumulation of homogentisic acid polymers leads to stiffening of the cartilage; in osteopetrosis, stiffness of the subchondral trabeculae occurs. In both conditions, severe generalized OA is usually apparent by the age of 40. If the subchondral bone is stiffened, repetitive impact loading soon leads to breakdown of the overlying cartilage. Conversely, osteoporosis, in which the bone is abnormally soft, may protect against OA.

N. B.: Articular cartilage is composed of two major macromolecular species: proteoglycans, which are responsible for the compressive stiffness of the tissue and its ability to withstand load, and collagen, their low pH optimum makes it likely that the proteoglycanase activity of these enzymes will be confined to intracellular sites or immediate pericellular area. However, cartilage also contains a family of matrix metalloproteinase (MMPs), including stromelysin, collagenase and gelatinase, which can degrade all the components of the extracellular matrix at neutral pH. The level of MMP activity in the cartilage at any given time represents the balance between activation of the proenzyme and inhibition of the active enzyme by tissue inhibitors.

The turnover of normal cartilage is affected through a degenerative cascade for which many investigators consider the driving force to be IL1, a cytokine produced by mononuclear cells (including synovial lining cells) and synthesized by chondrocytes. IL-1 stimulates the synthesis and secretion of the latent MMPs and of tissue plasminogen activator. Both plasminogen and stromelysin may play a major role in activation of the latent MMPs. In addition to its catabolic effect on cartilage, IL-1, at concentrations even lower than those needed to stimulate cartilage degradation, suppresses PG synthesis by chondrocytes matrix repair.

The balance of the system lies with at least two inhibitor; tissue inhibitor of metalloproteinase (TIMP), and plasminogen activator inhibitor-1 (PAI-1), which are synthesized by the chondrocytes and limit the degradative activity of MMPs and plasminogen activator, respectively. If TIMP or PAI-1 is destroyed or is present in concentrations that are insufficient relative to those of active enzymes, stromelysin and plasmin are free to act on matrix substrates. Stromelysin can degrade the protein core of the PG and activate latent collagenase. Conversion of latent stromelysin to an active, highly destructive protease by plasmin provides a second mechanism for matrix degeneration.

Polypeptide mediators, e.g., insulin growth factor-1(IGF-1) and transforming growth factor beta (TGF beta), stimulate biosynthesis of PGs. They regulate matrix metabolism in normal cartilage and may play a role in matrix repair in OA.

Pathophysiology of Cartilage Changes in OA:

Although “wear” may be a factor in the loss of cartilage, strong evidence supports the concept that lysosomal enzymes and MMPs accounts for much of the loss of cartilage matrix in OA. Whether their synthesis and secretion are stimulated by IL-1 or by other factors (e.g. mechanical stimuli), MMPs, plasmin, and cathepsins all appear to be involved in the breakdown of articular cartilage in OA.TIMP and PAI-1 may work to stabilize the system, at least temporarily, while growth factors, such as IGF-1, TGF- beta, and basic fibroblast growth factors, are implicated in repair processes that may heal the lesion or, at least, stabilize the process.

The possible role of NO is to stimulate synthesis of MMPs by chondrocytes. Chondrocytes are a major source of NO, the synthesis of which is stimulated by IL-1 and tumor necrosis factor and by shear stresses on the tissue.

Clinical feature:-

A deep ache and is localized to the involved joint. Typically the pain is <by joint use and >by rest; but as the disease progresses, it may become persist. Nocturnal pain, interfering with sleep, is particularly in advanced OA of the hip. Stiffness of the involved joint upon arising in the morning or after a period of inactivity but usually lasts less than 20 min.

Because articular cartilage is aneural, the joint pain must arise from other structures.

Cause of joint pain in OA

Source Mechanism

Synovium - Inflammation

Subchondral bone- Medullary hypertension, microfractures

Osteophytes- Stretching of periosteal nerve endings.

Ligaments- Stretch

Capsule- Inflammation, distention

Muscle- SpasmIn some patient with OA, joint pain may be due to synovitis. Synovitis in OA may be due to phagocytosis of shards of cartilage and bone from the abraded joint surface, to release from the cartilage of soluble matrix macromolecules, or to crystals of calcium pyrophosphate or hydroxyapatite. In other cases, immune complexes, containing antigens derived from cartilage matrix, may be sequestered in collagenous tissue of the joint, leading to low grade synovitis. In contrast, in the earlier stages of OA, even in the patient with chronic joint pain, synovial inflammation may be absent.

Physical examination of the OA joint may reveal localized tenderness and bony or soft tissue swelling. Bony crepitus (the sensation of bone rubbing against bone, evoked by joint movement) is characteristic. Synovial effusions, if present, are usually not large. Palpation may reveal some warmth over the joint. Periarticular muscle atrophy may be due to disuse or to reflex inhibition of muscle contraction. In advanced stages of OA, there may be gross deformity, bony hypertrophy, subluxation and marked loss of joint motion. The notion that OA is inexorably progressive, however, is in correct. In many patients the disease stabilizes; in some, regression of joint pain and even of radiographic changes occurs.

Although the diagnosis of OA is often straightforward because of the high prevalence of radiographic changes of OA in asymptomatic individuals, it is important to ensure that joint pain in a patient with radiographic evidence of OA is not due to some other cause, such as soft tissue rheumatism (e.g., anserine bursitis at the knee, trochanteric bursitis at the hip), radiculopathy, referral of pain from another (e.g., crystal- induced synovitis, septic arthritis). These are all common pitfalls in the diagnosis of OA. It is usually not difficult to differentiate OA from a systemic rheumatic disease, such as rheumatoid arthritis, because, in latter diseases, joint involvement is usually symmetric and polyarticular, with arthritis in wrists and metacarpophalangeal joints (which are generally not involved in OA ), and there are also constitutional features such as prolonged morning stiffness, fatigue, weight loss, or fever.

Laboratory and Radiographic findings:

In the early stages, the radiograph may be normal, but joint space narrowing becomes evident as articular cartilage is lost. Other characteristic radiographic findings include subchondral bone sclerosis or cysts, and osteophytosis. A change in the contour of the joint, due to bony remodeling, and subluxation may be seen. More than 90% of persons over the age of 40 have some radiographic changes of OA in weight bearing joints; only 30% of these are symptomatic.

No lab studies are diagnostic for OA, but specific lab investigation may help in identifying one of underlying causes of secondary OA. Because primary OA is not systemic, the ESR, serum chemistry determinations, blood counts and urinalysis are normal. Serum alkaline phosphatase increased. Synovial fluid analysis reveals mild leukocytosis (<2000 WBC/micro liter), with a predominance of mononuclear cells.

OA at Specific Joint Sites:

Interphalangeal Joints: Heberden’s nodes, bony enlargements of distal Interphalangeal joints. Most common form of idiopathic it is. A similar process at the proximal Interphalangeal joints leads to Bouchard’s nodes. Presents acutely with pain, redness and swelling, sometimes triggered by minor trauma. Gelatinous dorsal cysts filled with hyaluronic acid may develop at the insertion of the digital extensor tendon into the base of the distal phalanx.

Erosive OA: Erosive OA is more destructive than typical nodal OA; x-ray evidence of collapse of the subchondral plate is characteristic, and bony ankylosis may occur. The synovium is much more extensively infiltrated with mononuclear cells than in OA. Joint deformity and functional impairment may be severe.

Generalized OA: It is characterized by involvement of 3 or more joints. Heberden’s and Bouchard’s nodes are prominent. Symptoms may be episodic, with “flare ups” of inflammation marked by soft tissue swelling, redness and warmth. ESR may be elevated.

Thumb Base: The second most frequent area is the thumb base. Swelling, tenderness, and crepitus on movement of the joint are typical. Osteophytes may lead to a “squared appearance.

The Hip: Congenital or developmental (e.g. acetabular dysplasia, Legg- Calve- Perthes disease, slipped capital epiphysis) can lead to cases of hip OA. Pain from hip OA generally referred to the inguinal area but may be referred to the buttock or proximal thigh. Pain can be evoked by putting the involved hip through its range of motion. Flexion may be painful initially, but internal rotation will exacerbate pain. Loss of internal rotation occurs early, followed by loss of extension, adduction and flexion due to capsular fibrosis and buttressing osteophytes.

The Knee: OA of the knee may involve the medial or lateral femorotibial compartment and/or the patellofemoral compartment. Palpation may reveal bony hypertrophy (osteophytes) and tenderness. Effusions, if present, are generally small. Joint movements commonly elicit bony crepitus. A positive “shrug’ sign ( pain when the patella is compressed manually against the femur during quadriceps contraction) may be a sign of patellofemoral OA.

                                Chondromalacia patellae, which also is characterized by anterior knee pain and a positive shrug sign, a syndrome of patellofemoral pain, often bilateral, in teenagers and young adult. It is more common in female. It may be caused by a variety of factors (e.g., abnormal quadriceps angle, patella alta, trauma).Exploration of the knee may reveal softening and fibrillation of cartilage on the posterior aspect of the patella but this is usually not progressive.The Spine: Degenerative disease of the spine can involve the apophyseal joints, intervertebral disks and paraspinous ligaments. The diagnosis of the spinal OA should be reserved for patients with involvement of the apophyseal joints and not only disk degeneration. Symptoms of spinal OA include localized pain and stiffness. Nerve root compression by an osteophyte blocking a neural foramen, prolapsed of a degenerated disk, or subluxation of an apophyseal joint may cause radicular pain and motor weakness.

                                Marked calcification and ossification of paraspinous ligaments occur in diffuse idiopathic skeletal hyperostosis (DISH). Although DISH is often categorized as a variant of OA, dearthrodial joints are not involved. Ligamentous calcification and ossification in the anterior spinal ligaments give the rise of “flowing wax” on the anterior vertebral bodies. However radiolucency may be seen between the newly deposited bone and the vertebral body, differentiating DISH from marginal osteophytes in spondylosis. Intervertebral disc spaces are preserved, and sacroiliac and apophyseal joints appear normal, helping to differentiate DISH from spondylosis and from ankylosing spondylitis, respectively. DISH occurs in the middle-aged and elderly and is more common in men than in women. The radiographic changes are generally much more severe than might be predicted from the mild symptoms.

Treatment: Treatment is aimed at reducing pain, maintaining mobility and minimizing disability.

Nonpharmacological Measures:

Reduction of Joint Loading: Correction of poor posture and a support for excessive lumber lordosis can be helpful. Excessive loading of the involved joint should be avoided. Patient with OA of the knee or hip should avoid prolonged standing, kneeling, and squatting. In patient with medial-compartment knee OA, a wedge insole may decrease joint pain. In patient with unilateral OA of the hip or knee, a cane, held in contra lateral hand, may reduce joint pain by reducing the joint contact force.

Physical therapy: Application of heat to the OA joint may reduce pain & stiffness. An exercise program should be designed to maintain range of motion, strengthen periarticular muscle, and improve physical fitness.

A Rational Approach to the Nonsurgical Management of OA: Nonpharmacological measures may comprise instruction of the patient in principles of joint protection; thermal modalities; exercises to strengthen periarticular muscles; weight reduction; if the patient is obese; avoidance of excessive loading of the arthritic loading of the arthritic hip or knee joint by use of shoes with well-cushioned soles and a cane of walker, when appropriate, and prescription of orthotics for the patient with varus or valgus knee deformity. Medial tapping of the patella may reduce knee pain in patient with patellofemoral OA. If the above measures are ineffective, tidal irrigation of the joint with a large quantity of saline or Ringer’s lactate warrants consideration.

Homoeopathic Treatments:

Intending to say everything we had to say on the pathological character of the diseases under OSTEOARTHRITIS, GOUT, NEURALGIA, etc., we here point out more particularly the parts to which the remedies have specific curative relations. This knowledge is the required in every case, but in many cases it is, since two or three remedies may correspond to the general state of the patient, and one of them only to the part affected. But in homoeopathic treatment, totality of symptoms and individualization of patient should be on top.

1. Aconite, Antim crud, Ars alb, Bell, Bry., Calc., Caust, China, Cocc., Colo, Ferr, Guicum, Heper, Iodium, Ledum, Magn. acet, Nux vom, Phos, Acid phos, Puls, Rhod, Sab, Sass., Sulph.

2. Abrot, Apoc. andr, Arn, Canth, Chel, Cic, Colch, Con, Dulc, Meny, Mez, Natr, Phyt, Sang, Stann, Staph, Thuja,

3. Ant. tart, Chin. sulph, Cina, Kali bich, Nux j, Ran. scler, Visc. alb .

Acute Arthritis: 1. Aconite, Apoc. andr.,Bell , Bry, China, Heper, Nux vom, Puls,

2. Ant., Arn, Ars., Cocc, Fer, Kreo, Phy., Sulph, ; with gastric discomfort, Antim crud; with severe pain in hands and knee Cocc.

Chronic Arthritis: 1. Abrot., Benzoic acid, Caust, Kalmia, Lach, Natr. sulph, Sil, 2.Calc, Col, Guicum, Iod, Mang, Phos acid, Rhod, Sass., Sulph,

Erratic Arthritis: 1. Arn, Mang, Nux mosch, Nux vom, Puls, 2. Asaf, Daph, Plumb, Rhodo.

Osteoarthritis with osteophytes and tophi: 1. Arn, China, Cocc, Hep, Rhus, Sulph; 2. Ant, Bry, China ars.

Arthritis with haemorrhoidal or menstrual difficulties: Berb vulg.

OA with Heberden’s and Bouchard’s nodes: 1. Calc, Lyc, Rhod, 2. Antim crud, Amm. Phos, Abrot, Graphites, Led, Nux v; 3. Agn cast, Bry., Carb. an, Carb veg, Nitr, Nux m, Ran, Sabin, Staph. 4. Aur, Dig, Phos, Sep, Sil, Zinc. Painless: Nitr.

Arthritic affections of drunkards: 1. Aconite, Calc, Nux v, Sulph, 2. Ars, China, Hep, Iod, Lach, Led, Puls.

Arthritis of persons having rich living: Antim crud, Calc, Iod, Nux v, Puls, Sulph.

Arthritis of persons working in water: Antim crud, Ars, Calc, Dulc, Nux v, Puls, Rhus, Sarasaparilla.