OSTEOARTHRITIS
Symptoms: mild early morning stiffness,
stiffness following periods of rest, pain that worsens on joint use, and loss of joint function.
Signs: local tenderness, soft
tissue swelling, joint crepitus, bony swelling, restricted mobility, Heberden’s (proximal interphalangeal joints) and/or less common
Bouchard’s (distal interphalangeal joints) nodes, and other signs of degenerative loss of articular cartilage.
X-ray findings: narrowed
joint space, osteophytes, increased density of subchondral bone, subchondral sclerosis, bony cysts, soft tissue swelling, and particular
swelling.
• Disease thought to be OA of specific joints: hands (Heberden’s and Bouchard’s nodes); hip (Malum coxae sinilis); temporomandibular (Costen’s syndrome); knee (Chondromalacia patellae); spine (ankylosing hyperostosis – interstitial skeletal hyperostosis).
• Weight-bearing
joints and peripheral and axial articulations are principally affected; hyaline cartilage destruction followed by hardening and formation
of large bone spurs (calcified osteophytes) in joint margins – pain, deformity, and limited joint motion; inflammation usually minimal.
• Two
categories: primary OA – ‘wear and tear’ after fifth and sixth decades, with no predisposing abnormalities; cumulative effects of
decades of use stress collagen matrix; damage releases enzymes that destroy collagen components; with aging, ability to synthesize
restorative collagen decreases;
secondary OA – predisposing factor for degeneration; factors include; congenital abnormalities in
joint structure or function (e.g. hypermobility and abnormality shaped joint surfaces), trauma (obesity, fractures, along joint surfaces,
surgery, etc.), crystal deposition, presence of abnormal cartilage, previous inflammatory disease of joint (RA, gout, septic arthritis,
etc. )
Diagnosis
Onset subtle – morning stiffness first symptom; then pain on joint motion worsened by prolonged activity and
relieved by rest; no signs of inflammation; clinical picture varies with joint involved; disease of hands – pain and limitation of
use; knee involvement – pain, swelling, and instability; hip – local pain and limp; spinal OA (very common) – compression of nerves
and blood vessels – pain and vascular insufficiency; RA associated with much more inflammation of surrounding soft tissues; best diagnostic
tool is X-ray or Medical Thermography of suspected joint – joint space narrowing, loss of cartilage, and presence of bone spurs (osteophytes).
• Pain:
lack of correlation between severity of OA (X-ray) and degree of pain; 40% of patients with worst X-ray classification for OA are
pain-free; cause of pain in OA is still not well-defined; depression and anxiety increase experience of OA pain.
Therapeutic considerations
Cellular and tissue response is purposeful and aimed at repair of anatomic defects; process is arrestable and sometimes
reversible; therapeutic goal is to enhance collagen matrix and regeneration by chondrocytes; studies to determine ‘natural course’
of OA show marked clinical improvement and radiologic recovery of joint space is almost 50% of cases with no therapy – medical intervention
may promote disease progression.
• Aspirin and Non-steroidal anti-inflammatory drugs (NSAIDs) : ASA is effective in relieving
pain and inflammation, and is inexpensive; therapeutic dose high and toxicity frequent – tinnitus, gastric irritation; side-effects
of other NSAD’s are gastrointestinal upset, HA’s, and dizziness – only recommended for short periods of time; unexpected side-effects
may increase rate of cartilage degeneration – inhibit collagen matrix synthesis and accelerate cartilage destruction; NSAID’s use
is associated with acceleration of OA; NSAID’s suppress symptoms but accelerate OA progression.
Hormonal considerations
Endocrine
forces may initiate or accelerate OA by altering chondrocyte’s microenvironment; all hormones act on connective tissue cells; fibroblasts,
osteoblasts and chondrocytes.
• Oestrogen: high prevalence of OA in women suggests oestrogen involvement; estradiol worsens OA; anti-oestrogen drug tamoxifen improves experimental OA by decreasing erosive lesions – therapeutic role of oestrogen blockade; botanicals (e.g. Glycyrrhiza glabra and Medicago sativa) is used for OA contain ‘phytoestrogens’ that bind to oestrogen receptors, acting as oestrogen antagonists; food sources of phytoestrogens are soy, fennel, celery, parsley, nuts, whole grains, and apples.
• Insulin,
growth hormone (GH) and somatomedin (SMM): diabetics have greater incidence and more severe OA than non-diabetics; insulin insensitivity
or deficiency, increased GH, and decreased SMMs (insulin-like growth factors secreted by liver in response to GH); insulin stimulates
chondrocytes to increase synthesis and assembly by proteoglycans; most prominent early change in articular cartilage is decreased
proteoglycans and state of aggregation – insulin insensitivity or deficiency predisposes to OA; excessive GH is detrimental
to bone and joint structures – increased incidence of OA in acromegaly; women with primary osteoporosis have high basal GH than controls;
GH detrimental to chondrocytes; SMMs mediate normal chondrocyte activity; impaired hepatic function, diabetes, and malnutrition suppresses
liver secretion – increased risk of OA.
• Thyroid: hypothyroidism increases risk of OA compared with age – and sex-matched population
samples.
Dietary considerations
Achieve normal body weight – minimize stress on weight-bearing joints affected with OA; healthy
diet, rich in complex carbohydrates and dietary fiber.
• Nightshade vegetables: Childers’ theory – genetically susceptible individuals might develop arthritis from long-term, low level consumption of the solanum alkaloids found in Solanacea (nightshade) plants; tomatoes, potatoes, aubergine, peppers, and tobacco; alkaloids may inhibit normal collagen repair; theory as yet unproven, but diet beneficial to some patients.
• Antioxidant nutrients:
Nutritional supplements
• Glucosamine sulphate (GS): stimulate
manufacture of glycosaminoglycans (GAGs) and promotes incorporation of sulphur into cartilage; with age, there is reduced ability
to synthesise sufficient glucosamine – cartilage loses gel-like nature and ability to absorb shock – may be the major factor leading
to OA; significantly more effective than placebo in improving pain and movement after 4 weeks in double-blind crossover; longer GS
use gives greater therapeutic benefit; rate and severity of GS side-effects not different from placebo; head-to-head studies; better
long-term results than NSAID’s relieving OA pain and inflammation despite little anti-inflammatory or analgesic effect of GS; NSAID’s
offer only symptomatic relief and may promote disease process; GS treats root cause (cartilage synthesis), improving symptoms and
helping body to repair damage; higher dosages may be required for obese patients; patients with peptic ulcers should take GS with
food; individuals taking diuretics may need increased dosage to compensate for reduced efficacy; improvement with GS lasts 6-12 weeks
after end of treatment – taken for long periods of time or in repeated short-term courses; high safety and excellent tolerability
– suitable for long-term use.
• Chondroitin sulphate (CS): contains mixture of intact or partially hydrolyzed GAGs of molecular
weights 14,000 to > 30,000; composed of repeating units of derivatives of GS; absorption rate of GS = 90-98%; absorption of intact
CS = 13% - CS 50-300 times larger than GS; key reason why GS is effective is small molecular size, allowing diffusion through joint
cartilage to chondrocyte; CS levels are typically elevated in synovial tissues of OA patients; less effective than GS.
• Niacinamide: Kaufman
and Hoffer – treatment of RA and OA with high-dose niacinamide improves joint function, range of motion, muscle strength and endurance,
and sedimentation rate; benefits within 1-3 months of use; peak benefits between 1 and 3 years of continuous use; 29% improvement
in global arthritis impact vs. 10% worsening with placebo; pain levels do not change, but niacinamide patients reduce NSAID use; reduces
• Methionine: S-adenosylmethionine (
• Superoxide dismutase (SOD): intra-articular injections of SOD have significant therapeutic effects;
whether oral SOD is absorbed is yet to be determined; preliminary indications unfavourable.
• Vitamin E: significantly beneficial
– anti-oxidant and membrane stabilising actions; in vitro, it inhibits activities of lysosomal enzymes and stimulates increased deposition
of proteoglycan.
• Vitamin C: deficient intake is common in elderly – altered collagen synthesis and compromised connective tissue
repair; in vitro vitamin C has anabolic effect on cartilage; excess of ascorbic acid needed in human chondrocyte protein synthesis;
in vivo study of experimental OA in guinea pigs – cartilage erosion is much less, and overall histologic and biochemical changes in
and around OA joint are much milder in animals on high doses of vitamin C; vitamin C and E have synergistic effects – enhance stability
of sulphated proteoglycans.
• Panthothenic acid: acute deficiency in the rat causes pronounced failure of cartilage growth and
lesions similar to OA; clinically improves OA symptoms.
• Vitamin A and E, pyridoxine, zinc, copper, and boron: required for synthesis
of collagen and maintenance of normal cartilage; deficiency of any one of these allows accelerated joint degeneration; supplements
at appropriate potencies may promote cartilage repair; boron used to treat OA in
Physical therapy
Exercise,
heat, cold, diathermy, and ultrasound often improve joint mobility and reduce pain in OA, especially when administered regularly;
benefit of physical therapy –achieving proper hydration within the joint capsule; short-wave diathermy may be of greatest benefit;
combining short-wave diathermy with periodic ice massage, rest, and appropriate exercises may be most effective approach; ultrasound
and laser therapy also helpful; best exercises are isometrics and swimming – increase circulation to joint and strengthen surrounding
muscles without excess strain on joints; increasing quadriceps strength improves clinical features and reduces pain on knee OA; walking
helps improve functional status and relieve pain in knee OA.
Botanical medicines
When inflammation is present, botanicals and
nutritional factors possessing anti-inflammatory activity is indicated e.g. bromelain, curcumin, and ginger.
• Yucca: double-blind trial – saponin extract of yucca has positive therapeutic effect; results gradual with no direct joint effects; improvement due to indirect effects on gastrointestinal flora; bacterial lipopolysaccharides (endotoxins) depress the biodynthesis of proteoglycans; yucca may decrease bacterial endotoxin absorption, reducing inhibition of proteoglycan synthesis; other saponin-containing herbs and other ways of reducing endotoxin load may be useful.
• Harpagophytum procumbens (Devil’s claw): experimental animal models of
inflammation – Devil’s claw has anti-inflammatory and analgesic effect comparable to phenylbutazone; other studies indicate little,
if any, anti-inflammatory effect; equivocal research from mechanism of action is inconsistent with current anti-inflammatory models
or failure to use quality-controlled (standardised) extracts; main components of Devil’s claw are saponins –therapeutic effect in
OA may be similar to that of yucca.
• Boswellia serrata: large branch tree native to India: exudative gum resin (‘salai guggul’)
used for centuries; newer preparations concentrated for active components (boswellic acids) give better results; boswellic acid extracts
have anti-arthritic effects in animal models; mechanisms of action – inhibit inflammatory mediators, prevent decrease in GAG synthesis,
and improve blood supply to joint tissues; herbal formulas with Boswellia yield good clinical results in OA and RA.
Therapeutic approach at ICIM
Clinical study of comprehensive, integrated program for OA yet to be conducted; therapeutic approach – reduce joint
stress, promote collagen repair, and eliminate foods and other factors that inhibit collagen repair; control all diseases or predisposing
factors; avoid NSAIDs as much as possible; if aspirin used, deglycyrrhizinated Glycyrrhiza glabra (licorice) may protect the gastrointestinal
tract from damaging effects and ASA should be discontinued ASAP.
• Diet: avoid simple, processed, and concentrated carbohydrates; emphasise complex-carbohydrate, high-fiber foods; minimise fats; eliminate Solanacea foods (tomatoes, potatoes, tobacco, aubergine, peppers); liberally consume flavonoid-rich berries or extracts.
• Supplements
- glucosamine sulphate
- niacinamide
- vitamin
E
- vitamin A
- vitamin C
- vitamin B6
- pantothenic acid
-
- Zinc
- Copper
- Boron
• Botanical
medicines
- Medicago sativa
- Yucca leaves
- Harpagophytum procumbens (Devil’s claw)
- Boswellia serrata (Frankincense)
• Physical
therapy and exercise: avoid physical activity that induces physiologic or traumatic strain (occupational or recreational overuse);
normalise posture; orthopedically correct structural abnormalities to limit joint strain; monitored daily non-traumatic exercise (isometrics
and swimming); short-wave diathermy, hydrotherapy, and other PT modalities which improve joint perfusion.
This article is to be used for information and guide line purpose. Any advice and/or suggestions from this article should be supervised by your health professional. ICIM can offer a medical professional at the centre to guide you through your health complaints. Contact ICIM for more information.
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ICIM Medics, St. Johns Grove, Johnstown, Naas, Co. Kildare, Ireland.
Tel: 00353 (0)45 844 819 - www.icim.ie - info@icim.ie
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