Arthritis with Nutritional Rehabilitation: A Case Report

Objectives: To discuss the rehabilitation of a patient suffering from arthritis, to describe the presentation of osteoarthritis and rheumatoid arthritis, and to discuss nutritional intervention.
Clinical Features: A 32-yr-old man suffered from migrating joint pain in his fingers, hand, wrist, feet, and knees.
Intervention and Outcome: The patient was originally treated with Indocin, to which he did not respond. Chiropractic care with nutraceutical intervention helped decrease those symptoms.
Conclusion: Nutraceuticals and associated nutrients may be helpful in treating patients suffering from osteoarthritis and rheumatoid arthritis.

Key words: Osteoarthritis; Rheumatoid Arthritis; Chondroitin Sulfate; Glucosamine hydrochloride -

Introduction

The diagnostic word arthritis has long created fear in the minds of patients. Degenerative arthritis, for example, can conjure up images of a painful and crippling future, with all its complications, and the prospect that it is unalterable (1). This term brings to mind a person with hot, painful, deformed joints. The painful future for these victims was further substantiated by the misconception that an ordinary nutritious diet was sufficient and that food and diet quackery was common and should be ignored (2).

Arthritis, in all its forms, affects more than 40 million Americans annually, with medical costs and lost wages exceeding $54.5 billion (Arthritis Foundation of Eastern Pennsylvania. Personal communication, 1997). Although arthritis exists in more than 100 forms, the two major types are osteoarthritis and rheumatoid arthritis. Osteoarthritis affects 16 million people in the United States, and rheumatoid arthritis affects 2.1 million people (Arthritis Foundation of Eastern Pennsylvania. Personal communication, 1997). The former affects women and men in a 3 to 1 ratio and the latter, 2 to 1.

Case Report

A 32-yr-old man sought alternative treatment for chief complaints of swelling and severe pain in his finger joints, hands, and wrists. He also suffered occasional pain in his knees and feet.

In August 1988, the patient first noticed swelling in his right index finger, which he believed he had broken. He was diagnosed with tendinitis and had the finger splinted; Tylenol was prescribed for pain. A few months later, the swelling moved to another finger on his right hand, and the patient questioned whether it might be job related.

After a few more months, swelling occurred in his left wrist. The patient saw another doctor, and numerous X-rays and blood tests were taken-among them, tests for AIDS and Lyme disease. A chest X-ray was performed to rule out allergy to pine pollen, a condition prevalent in men of his age in the area of Virginia in which he lived. His condition was diagnosed as job related.

In 1992, the swelling and pain were present in both hands and wrists. The patient went to a rheumatologist who diagnosed rheumatoid arthritis. Magnetic resonance imaging was performed several times, one of his right wrist being "dark." He was told there was a lot of "activity" in that wrist. During exploratory surgery on the right wrist, debris was removed from a cyst that had ruptured. He was then put on the anti-inflammatory drug Indocin.

By 1994, the anti-inflammatory drug was no longer working. It was making him nauseous and his pain returned. He went to another rheumatologist who also prescribed Indocin. After 4 months, he had no relief and very limited results. His stomach problems persisted, and the pain was by then affecting his emotional state. His hands were in such a debilitated state that he was afraid to hold or lift his newborn.

The patient began a nutritional regimen, including a pharmaceutical-grade nutraceutical containing glucosamine hydrochloride (HCl), manganese ascorbate, and chondroitin sulfate, along with a multi-vitamin/mineral mixture and vitamin C. After 2 wk on the nutritional regimen, the patient spoke enthusiastically of improvements in his health and mental outlook. He felt better, his pain decreased, his stomach no longer bothered him, and his personality was improving.

My reasons for combining these supplements were that ascorbate is a necessary cofactor for proteoglycan synthesis. Manganese must be present for the biosynthesis of proteoglycans to occur. Glucosamine HCl and manganese combine to stimulate the synthesis of hyaluronic acid (an important component of synovial fluid) and synthesis of core protein. Zinc, manganese, and vitamin C are helpful in the synthesis of amino acids to procollagen; copper, iron, silicon, and vitamin C stimulate the synthesis of procollagen to collagen. Chondroitin sulfate is the major glycosaminoglycan (the framework for collagen) and provides protection by inhibiting degradative enzymes (3). Besides the vitamin and minerals already mentioned in the synthesis process, the antioxidants vitamin E and P-carotene and the mineral selenium are necessary to protect cells from oxidation and free radicals. Free radicals are the end product of oxidation. They are responsible for initiating chain reactions of damaging molecular events (4). Magnesium and niacinamide have been helpful for bone remodeling and improved joint function, respectively (4).

The patient slowly weaned himself off the Indocin when he began using the nutritional supplements. Since then, he has had only minor flare-ups lasting 24 hr or less. Before the nutritional regimen, the patient had flare-ups every 4 days. He has gone 4 months without an exacerbation. To evaluate objective outcomes in case reports of this nature, the following assessment tools can be used: for pain level, (a) Numerical Pain Scale and (b) Visual Analog Scale; for disability, (a) Oswestry and (b) Roland Morris; for psychometrics, (a) Health Status Questionnaire and (b) Modified Zung Depression Index.

Osteoarthritis has long been described as simple "wear and tear" on the joints associated with the aging process. This fraying of the articular cartilage and bone produces a dull aching sensation in those joints. It is estimated that 97% of all individuals over the age of 60 have osteoarthritis that is advanced enough to be evident on X-ray (5).

Recent studies have shown that as a joint is used, enzymes are released that digest cells in the articular cartilage, destroying them; at the same time, other cells are in the midst of rebuilding the cartilage (4). The cartilage in the joints work on a plus-and-minus system. As long as we stay equal or on the positive side, osteoarthritis will not occur. This is one of the reasons we should work out on an every-other-day basis, or a hard-day followed by an easy-day pattern. This concept is reinforced by research that shows that musculoskeletal problems increase when one trains more than three times per week (6). Joints are constantly undergoing normal remodeling, a process of wear and repair. The current thought is that breakdown races ahead of repair in osteoarthritis, becoming a destructive process because of the imbalance (7). Scientists are not sure why this imbalance occurs, but suspect it has to do with abnormal biomechanical stress. The biomechanical misalignment in the bone structure places increased stress on the articular cartilage in the joint, which leads to excessive chondrocyte damage and excessive proteolytic enzyme release (8). It is not understood whether excessive proteolytic enzyme is released, the repair process is slowed, or a combination of the two occurs, but the end result is osteoarthritis. Tables 1-3 detail diagnostic issues with regard to osteoarthritis.

The old approach to fighting this disease was to use powerful anticancer drugs and steroids to slow down the body's hyperimmune defense system. This approach was only moderately effective, with side effects as distressing as the disease itself.

Two new treatment approaches have been advanced. One is genetically engineered proteins, and the other is custom

1. Morning stiffness
2. Pain on motion, or tenderness in at least one joint (observed by a physician)
3. Swelling (soft-tissue thickening or fluid, not body overgrowth alone) in at least one joint (observed by a physician)
4.Swelling (observed by a physician) of at least one other joint (an interval free of joint symptoms between the two joint involvements may not be more than 3 months)
5. Symmetrical joint swelling (observed by a physician) with simultaneous involvement of the same joint on both sides of the body (bilateral involvement of proximal interphalangeal, metacarpophalangeal, or metatarsophalangeal joints is acceptable without absolute symmetry). Terminal phalangeal joint involvement will not satisfy this criteria
6. Subcutaneous nodules (observed by a physician) over body prominences, on extensor surfaces, or in juxta-articular regions                                                                                                                                                                                                                 7. Roentgenographic changes typical of rheumatoid arthritis (which must include at least bony decalcification localized to or most marked adjacent to the involved joints and not just degenerative changes). Degenerative changes do not exclude patients from any group classified as rheumatoid arthritis                                                                                                                         8. Positive agglutination test-demonstration of the "rheumatoid factor" by any method that, in two laboratories, has been positive in not more than 5% of normal controls-or positive streptococcal agglutination test (the latter is now obsolete)          9. Poor mucin precipitate from synovial fluid (with shreds and cloudy solution)                                                                                 10. Characteristic histologic changes in synovium with three or more of the following: marked villous hypertrophy, proliferation of superficial synovial cells often with palisading, marked infiltration of chronic inflammatory cells (lymphocytes or plasma cells predominating) with tendency to form "lymphoid nodules," deposition of compact fibrin either on surface or interstitially; foci of necrosis                                                                                                                                                                           11. Characteristic histologic changes in nodules showing granulomatous foci with central zones of cell necrosis surrounded by a palisade of proliferated macrophages, and peripheral fibrosis and chronic inflammatory cell infiltration, predominantly perivascular.

Tables 4 and 5 discuss other diagnostic criteria for rheumatoid arthritis. Table 6 provides a differential.

Table 4
Key Roentgen Observations Rheumatoid Arthritis (5)
1. Characterized by destructive and proliferative changes in synovial joints and periarticular soft tissue structures
2. Systemic multiplicity of joint involvement with a tendency to
bilateral symmetry
3. Periarticular soft tissue swelling and edema
4. Progressive deossification
5. Thinning of articular cortices
6. Progressive reduction on interosseous spacing
7. Late-stage subluxations, fibrous and osseous ankylosis

Table 6
The Hand in Rheumatoid Osteoarthritis (2)
Criteria                         Rheumatoid Arthritis                                                                  Osteoarthritis
Charater of swelling     Synovial, capsular, "soft tissue",     Bony with irregular spurs, occassional soft cysts 
                                 Bony only in late stages

Tenderness                    Usual                                   None or minimal except during occasional late onset

Distal interphalangeal involvement      Not usual except thumb      Characteristic

Proximal interphalangeal involvement      Characteristic      Frequent

Metacarpal phalangeal involvement      Characteristic      Never except thumb

Wrist involvement      Usual or common      Never except base of thumb

Conclusion

Because it was once believed that articular cartilage could not heal itself, arthritis was a dreaded disease. Research has now shown that this feared result is not inevitable (10, 11). Cartilage can repair itself, and this healing process can be enhanced with the use of nutraceuticals (4). Nutraceuticals are nutritional compounds that the body needs and can use normally. There is now considerable evidence to suggest that arthritis can be reversed (12). In addition, research has narrowed the causes of these two diseases, and the role of chondroprotective agents has become clear. In rheumatoid arthritis, it seems to be primarily the chondroitin sulfate that protect the joints by inhibiting the degradative enzymes (3). .In osteoarthritis, it seems to be glucosamine HCl and the chondroitin sulfate that protect joints (3). Chondroitin sulfate performs its enzymatic duties as a chondroprotector in this disease. Glucosamine HCl performs a twofold role by driving the chondrocytes from a destructive mode to a more repair mode and then being able to greatly elevate the rate of repair (4). Chondrocytes, which are the main cellular component of articular cartilage, play a unique role in the biological tissue. They exist as both a destroyer and a rebuilder that maintain a homeostatic environment.

2. Berkow R. The Merck manual of diagnosis and therapy. 13th ed. West Point (PA): Merck Sharp & Dohme; 1977. p. 1317-1336.

3. Cosamin DS. Informational pamphlet. Baltimore: Nutramax Laboratories; 1996.

4. Bucci L. Pain free. Fort Worth (TX): The Summit Group; 1995. p. 80-105.

5. Erhardt R. X-ray seminars. Dunwoody, GA: R. Erhardt; 1978.

6. Taylor P, Ward A, Rippe JM. Exercising to health: how much, how soon? Physician Sports Med 1991:19:95-105.

7. Cailliet R. Knee pain and disability. Philadelphia: F. A. Davis; 1973. p. 97.

8. Cailliet R. Ankle and foot pain. Philadelphia: F. A. Davis; 1968. p. 82.

9. Greenfield GB. Radiology of bone diseases. 3rd ed. Philadelphia: J. B. Lippincott; 1979. p. 686-687.

10. Radin EL, Burr DB. Hypothesis: joints can heal. Sem Arthritis Rheum 1984;13:293-302.

Il. Reiman I, Christensen SB, Diemer NS. Observations of reversibility of glycosaminoglycan depletion in articular cartilage. Clin Orthop Rel Res 1982;168:258-264.

12. Bland JH, Cooper SM. Osteoarthritis-a review of the cell biology involved and evidence for reversibility: management rationally related to known genesis and pathophysiology. Semin Arthritis Rheum 1984;14:106-133.