Continuous Passive Motion, or CPM

The influence of environment on repair of tissues is known to exert a powerful influence in the quality of tissue repair. It is the place of the physician to provide the optimal environment for repair of tissues. For the same reason that surgery is performed under aseptic conditions, skin is apposed by sutures, and hemostasis is secured during surgery, the proper environment for maturation and differentiation of the repair tissues in articular cartilage is necessary.

Limited repair of damaged articular cartilage has been the accepted norm in orthopedic medicine. Further degenerative changes, including arthritis, are the expected sequelae of most articular injuries. Because of the acceptance of these qualities, joint replacement arthroplasty has gained much popularity in both the medical and lay society. The expected benefits of these procedures are often guarded because of the mechanical and physiologic constraints that have become prominent over time. As a result of these factors, many physicians are reexamining joint preservation arthroplasty.

The repair of well vascularized, nonarticular tissues has been well studied. Three traditional phases of repair are understood. Immediately post injury is the phase of necrosis. This phase is characterized by varying degrees of cell death, largely dependent upon the degree of injury and the interruption of oxygen tension. The second phase, that of inflammation is characterized by establishment of a fibrovascular mass that serves as a scaffold for the impending repair phase. The third phase is cellular proliferation and differentiation, as well as production of cell products, including collagen.

Although the reparative process varies considerably among tissues, these phases can be expected in all tissues except that of articular cartilage. Because of the unique qualities of articular cartilage, the traditional phases of repair are interrupted after the first phase‑cell death. The second phase of repair does not occur in articular cartilage because of the avascular nature of this tissue and because hyaluronic acid and other constituents of synovial fluid inhibit clot formation and secondary fibrous lattice‑work assembly. Although frequently silent, superficial cartilage injury is often a cause of chronic discomfort, swelling, and joint limitation. These types of lesions frequently progress to chronic joint disease with secondary degenerative arthritis.

The response of articular cartilage to penetrating full thickness injury produces a much different sequence of events. When the lesion penetrates beyond the tide mark region, a vascularized repair sequence can then begin. Bleeding and secondary clot formation can occur within the base of the defect.  Later, proliferation of the capillary buds within the base of the defect can allow a fibrovascular lattice‑work to be established with secondary invasion of pluripotential mesenchymal cells and later differentiation into hyaline-like tissue.

The early healing process of this matrix then forms a tissue that morphologically and histologically resembles articular cartilage, at least for the first several months. Initially, tissue specific type II collagen is produced. However, several weeks after the injury, type I collagen becomes present. By one year after the injury the articular repair tissue generally loses the morphologic features of hyaline cartilage and becomes more fibrous.  This is characterized by a decrease in the proteoglycan content and an increased amount of type I collagen. This type of repair tissue is called fibrocartilage.

Fibrocartilage repair of articular defects is generally accepted as the norm and is the expected potential of articular repair in full‑thickness defects. Clinically, the fibrocartilage repair of articular defects, although often initially symptomless, is frequently fraught with increasing amounts of pain, stiffness, and further progression toward degenerative arthritis.

With respect to collagen based tissues, environment is known to participate in directing the quantity and quality of the repair tissue.  Strain is thought to orient the deposition of collagen fibers.  Load and oxygen tension help determine the quality and type of tissue produced by primitive mesenchyme.  Protection from mechanical stimuli is thought to lead to unorganized and poorly differentiated repair tissue.

Immobilization or rest of injured, infected, or arthritic joints has long been an unchallenged tenet of orthopedics.  According to Salter, Hugh Owen Thomas, the great British orthopedic surgeon, embraced rest as his creed and believed that an overdose was impossible.  Although Thomas immobilized with splints, traditional orthopedic care of these maladies has been referred to by some as the “plaster entrapment syndrome". The rationale for immobilizing joints has not been well defined.  Robert Salter suggests that, perhaps, joints have been immobilized because it is possible.

The effects of immobilization on articular cartilage have been reported in the literature. Consistently the effects have been deleterious to the homeostasis and repair of normal articular cartilage. Evans et al. described cleft formation, matrix fibrillation, and alteration of articular cartilage in rats whose knees have been immobilized.  Flattening of articular cartilage, degeneration of peripheral areas and synovial adherence were described by Hall.  Troyer described decreased affinity from metachromatic stains and abnormal chondrocytes in immobilized animals.  Decreased proteoglycan synthesis, decreased aggregation of molecular complexes, fibrillation, fibrin plaque formation, and proliferation of fibrous connective tissue have been described by others.  The effects of prolonged immobilization on humans has also been reported, most of which are comparable to those in animal studies.

In the clinical setting, the effects of immobilization are well known. The effects often present therapeutic challenges to the clinician, therapist, and patient to rebuild the quality of musculoskeletal tissues to what it was before injury.  Muscle atrophy is, by far, the most obvious side‑effect of immobilization. This atrophy begins almost immediately after immobilization and is clinically recognized within days after cast application.

Bone atrophy also begins very quickly after immobilization and can be recognized radiographically within weeks. It appears logical to assume that other musculoskeletal structures, including tendons, ligaments and the collagen matrix will also atrophy when they are protected from the stimulus of physiologic loading. 

In response to these clinical observations, a school of thought has developed within the physician community to mobilize injured parts as quickly as possible by providing the proper environment for the repair of local tissues to take place.  Most recently this philosophy of care has been developed and promoted with respect to bone injury by the A.O./A.S.I.F. group of fracture surgeons.  By performing rigid internal fixation of bone, early mobilization and prevention of fracture disease has occurred while the optimum environment for the repair of bone has been provided.

The positive effects of intermittent motion on articular and periarticular tissues have been well documented.  In 1950, Saaf reported on a study in guinea pigs in which exercise of the shoulder joint produced a temporary increase in the size and number of chondrocytes in articular cartilage. Ekholm studied articular cartilage nutrition with gold isotopes. He demonstrated increased uptake of the gold isotope in the articular cartilage and synovial fluid in exercised joints. Intra‑articular tibial fractures in monkeys were studied by Hohl and Luck in 1956. The animals that were allowed uninhibited movement had a markedly increased range of motion and fewer intra‑articular adhesions than those that were immobilized after injury.  Mooney and Ferguson, in 1966, described the effects of early immobilization in rabbit metatarsophalangeal joints that had sustained an arthroplasty very similar to a Keller operation.  A greater amount of chondroid tissue was noted in joints immobilized one week postarthroplasty than in those immobilized for longer periods of time. The rabbits immobilized for a longer duration exhibited larger amounts of, and more mature, fibrous tissue.

The logical extension of the process of analysis of motion versus immobilization was carried out by Robert Salter et al. The question they raised was “If intermittent motion of joints is beneficial to the repair, what would it be with the consequence of constant motion?”  The obvious obstacle to this question was that continuous active motion is not possible because of muscle fatigue, the need for sleep, and lack of cooperation of an animal model.  The problem was solved by devising a passive motion machine that moves the joint through its normal range constantly at one cycle every 40 seconds.

The results of an animal model study performed on rabbits in 1980 revealed that in three (3) weeks an adult animal's healing of full‑thickness defects of hyaline articular cartilage was present in 3% of the animals that were immobilized, in 5% of the animals that were allowed intermittent active motion, and in 44% of the animals that were managed immediately after the operation with continuous passive motion.  Although the long‑term results of the repair of these full‑thickness defects are not completely known, the quality of repair of these articular defects, noted three (3) and four (4) months into therapy, has been maintained for periods as long as I year.

On the basis of the results of Salter's investigations (as well as others), the following conclusions can be made: