Osteoarthritis in the hand and wrist

Introduction/epidemiology

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  Osteoarthritis (OA) is a heterogeneous disease that includes conditions with different etiology, distribution, heredity, clinical presentation, and progression.

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  It is characterized by mechanical and biological events that alter the homeostatic relationship of degradation and repair of the surrounding articular tissues.

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  Although all joint tissues are involved, including the subchondral bone, damage to the articular cartilage is the hallmark of the disease.

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  Osteoarthritis is the most common rheumatologic disorder in the world. It affects all races, sexes, and age groups.

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  It is a major cause of adult morbidity. It is the cause of disability in 10% of the population over the age of 60.

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  The age-standardized prevalence of hand osteoarthritis was 44.2% in women and 37.7% in men in the Framingham OA Study. Distal interphalangeal (DIP), proximal interphalangeal (PIP) and thumb base arthritis were more prevalent in women while metacarpophalangeal (MCP) and wrist OA were more frequent in men.

• ■

  It is estimated that 21% of the US population, or 46.4 million Americans, in 2005 were affected by osteoarthritis.

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  Symptoms of OA may include joint pain, swelling, tenderness, stiffness, and crepitus. OA is typically considered a noninflammatory condition to differentiate it from the inflammatory arthropathies such as rheumatoid and psoriatic arthritis.

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  There is no cure for osteoarthritis and no effective method of altering the progression of the disease process.

This chapter will review the presentation, evaluation, and treatments of osteoarthritis as it presents in the various joints of the hand and wrist. Both nonoperative and operative approaches will be discussed, with particular attention to the indications and contraindications of specific treatments.

Basic science/disease process

OA is characterized by a loss of articular cartilage. It can be either primary or secondary in nature. Primary OA (idiopathic OA) occurs in the absence of antecedent trauma. The pathogenesis is likely heterogeneous; genetics, joint shape, and underlying endocrine abnormalities can contribute. Secondary OA is the result of direct trauma to the joint and can occur as a result of fracture, dislocation or infection.

In order to understand the pathophysiology of osteoarthritis, one must first consider the normal anatomy and biochemistry of the synovial joint. Normal articular cartilage consists of an extensive extracellular matrix (ECM) composed primarily of proteoglycans, collagens (predominantly type II), and water. While chondrocytes compose only 1% of the volume of the cartilage ECM, they are responsible for maintaining its architecture and composition. The matrix is composed primarily of collagen, proteoglycans, proteins and glycoproteins. Cartilage proteoglycans belong to two major classes: large aggregating molecules (aggrecans), and smaller nonaggregating molecules. The aggrecan molecule consists of a central protein core with about 100 glycosaminoglycan (GAG) side branches composed of repeating, negatively charged disaccharides. Aggrecan molecules form proteoglycan aggregates by linking with a long central hyaluronan molecule. The result is a very large molecule with 10 ⁵ negatively charged groups. These groups fill voids in the cartilage framework and create a high osmotic pressure in the framework, providing a stiff construct resistant to compression. Nonaggregating proteoglycans and other matrix proteins serve a variety of functions in the matrix including framework stabilization, regulation of fibrillogenesis, and matrix metabolism through chondrocyte interactions. Such molecules include biglycan, decorin, fibromodulin, chondroadherin, cartilage oligomatrix protein, and fibronectin. The interstitial fluid provides an important function in terms of altering the cartilage friction coefficient with changes in pressure (load).

Microscopically, articular cartilage can be divided into four zones based on the cartilage matrix composition and architecture. Zone 1 is the most superficial zone and is called the superficial or tangential zone. Here, the chondrocytes are flat and oriented parallel to the articular surface. The collagen is condensed, and proteoglycans are sparse. The thin collagen fibers are arranged parallel to the articular surface. This construct resists shear force and has been compared to a “tough skin” that protects the underlying intermediate and deep zones. In zone 2, the intermediate zone, the chondrocytes are isolated or in isogenous groups and are surrounded by oblique collagen fibers. This zone is the thickest and is rich in proteoglycans. Proteoglycans are complex macromolecules composed of a protein core with attached glycosaminoglycan chains (chondroitin sulfate and keratan sulfate). The negative charge of the glycosaminoglycans accounts for the hydration and large swelling pressure of cartilage. Zone 3 is the radiate layer and includes large, round chondrocytes oriented vertically with intervening radial collagen fibers. Zone 4 is the deepest layer or calcified layer. It lies adjacent to the subchondral bone and resists shear stress between cartilage and bone. Between zone 3 and zone 4 is the tidemark ( Fig. 18.1 ). With age, articular cartilage becomes thin and there is relative advancement of the tidemark zone that occurs together with replacement of calcified cartilage with bone. The result of this anatomic design is a shiny and slippery surface with a friction coefficient lower than any prosthetic replacement. This remarkable construct is able to withstand millions of loading cycles each year with forces that may reach up to 18 MPa.

In the healthy, homeostatic state, the chondrocyte responds to the mechanical and biochemical environment by altering the synthesis and degradation of its macromolecules. Two groups of enzymes function to degrade the extracellular matrix: matrix metalloproteinases (MMPs) and a d isintegrin a nd m etalloproteinase with t hrombo s pondin-like motifs (ADAMTS). MMPs break down collagen and ADAMTS functions to break down aggrecan. The main MMP in cartilage is MMP-13 that breaks down type II collagen and the main ADAMTS in cartilage are ADAMTS-4 and ADAMTS-5. The regulation of matrix degradation and synthesis is poorly understood, but cytokines play an important role in both anabolic and catabolic pathways. The interplay between these cytokines is complex. Anabolic activity seems to be a response of the structural needs of the matrix, as may occur in response to mechanical loading. Cytokines involved in the anabolic pathway include transforming growth factor-beta (TGF-β) and insulin-dependent growth factor I. Catabolism within the matrix involves a complex cascade that includes interleukin-1, stromelysin, aggrecanase, and plasmin, in response to stimulation or inhibition by TGF-β, tumor necrosis factor, tissue inhibitors of metalloproteinases, tissue plasminogen activator, plasminogen activator inhibitor, and other molecules.

Historical perspective

Osteoarthritis is evident across species, with evidence in other mammals, amphibians, certain species of birds, and even ancient dinosaurs. The disease is likely as old as man, with evidence of its existence in prehistoric man from 2 million years ago. The disease is considered synonymous with aging.

Pathophysiology

Osteoarthritis involves all of the tissues around the synovial joint, including the articular cartilage, joint capsule, ligaments, subchondral bone, metaphyseal bone, and the muscles acting across the joint. However, the principle pathological change is that of loss of articular cartilage. Other changes include subchondral sclerosis, subchondral cyst formation and marginal osteophytes.

The earliest microscopic findings of OA are that of fibrillation and fraying of the superficial zone cartilage along with decreased staining for proteoglycans in the superficial and transitional zones and in-growth of blood vessels into the tidemark from subchondral bone ( Fig. 18.1B ). Progression of the disease leads to clefts in the articular surface, fracture of the superficial cartilage and decrease in cartilage thickness. Enzyme activation leads to further destruction of the cartilage leading to complete loss of articular cartilage exposing dense, and eburnated bone.

Associated with these changes of the cartilage are alterations in the subchondral bone, specifically an increased density. This increased density can be seen as a sclerotic line on radiographic examination. These changes may be more pronounced at the joint periphery where the new bone formation may be so exuberant as to produce osteophytes. The exact pathophysiology of osteophyte formation is not known, however it may be related to the release of anabolic cytokines from the matrix that stimulate the abnormal bone and cartilage growth.

The changes in the joint also affect the periarticular tissues. The synovial membrane becomes inflamed as fragments of cartilage become embedded within them. As the joint loses motion due to mechanical factors and pain, the capsule and surrounding ligaments become stiff due to myotendinous contraction and ongoing edema. The lack of motion and use can lead to muscle atrophy.

Diagnosis

The most common symptoms of OA are pain, swelling, and stiffness of the affected joint. Pain is the primary feature of the condition and is the focus of treatment. Examination confirms swelling, tenderness, and limited range of motion. In the case of post-traumatic arthritis, there may be joint instability associated with previous ligamentous injury.

Symptoms can dissipate with time and are not always correlated with the radiographic severity of disease. Osteoarthritis may also be present in the absence of pain. In a classic study looking at arthritis among miners in their 40 s, Kellgren and Lawrence found that only 24% of miners with radiographic OA had pain and 8% of radiographically normal knees had pain.

Radiographs are the most helpful test in making the diagnosis. In primary and secondary OA, joint spaces are narrowed radiographically due to a loss of radiolucent articular cartilage. Subchondral bone remodeling can manifest as increased density within the subchondral bone or sclerosis. Osteophytes and loose bodies may also be present ( Fig. 18.2 ).

In 1957, Kellgren and Lawrence described a grading system for the radiographic appearance of OA. Findings considered included: (1) the presence of peripheral osteophytes; (2) periarticular ossicles (commonly found in association with DIP and PIP joints); (3) narrowing of joint cartilage and subchondral sclerosis; (4) small pseudocystic areas with sclerotic walls, typically in the subchondral bone; and (5) altered shape of the bone ends. The authors then classified the arthritis into five grades:

• 1.

  Normal joint

• 2.

  Doubtful

• 3.

  Minimal (but definitely present)

• 4.

  Moderate

• 5.

  Severe

This system has been broadly applied for grading osteoarthritis in various joints; unfortunately, the grading system can be ambiguous as there are no specific cut-off criteria between the grades. In an analysis by Schiphof and colleagues, the authors note inconsistency in the application of the grading system within multiple cohort studies and have recommended the development of a single validated classification system.

Management of OA of the fingers

Hand and finger arthritis is one of the most common presentations of primary OA. Its onset is insidious with progressive aesthetic deformity followed by pain and functional limitation. Epidemiological studies of the joint-specific prevalence of hand arthritis consistently show the distal interphalangeal joint to be the site most frequently affected by OA, followed by the thumb carpometacarpal (CMC) joint, and the PIP joint. These studies typically defined OA based on the radiographic features described by Kellgren and Lawrence, which include the presence of osteophytes, joint space narrowing, subchondral sclerosis and subchondral cysts.

Distal interphalangeal joint (DIP) arthritis

Diagnosis

OA of the distal phalangeal (DIP) joint is common and affects females more frequently than males. Clinically, patients present with enlarged joints and hard, knobby protuberances overlying the DIP joints of multiple fingers. These so-called Heberden’s nodes are pathognomonic for the condition and are attributed to osteophyte formation with overlying soft-tissue thickening. These should be differentiated from a mucous cyst . A mucous cyst is a dorsal synovial cyst, often limited to a single digit. They are often associated with lateral deviation of the distal phalanx, and a limited range of motion ( Fig. 18.3 ).

Radiographically, joint space narrowing and osteophyte formation are common findings. However, the radiographic appearance of the DIP is not consistently associated with the patient’s symptoms. Frequently, the only significant concern for the patient is the aesthetic appearance. Even patients with severe DIP deformity may have little pain or functional impairment and the presence of Heberden’s nodes alone is not generally considered an indication for surgery.

DIP arthrodesis

Indications

The single most common indication for arthrodesis is intractable pain at the DIP joint that has failed all conservative treatments. Other less common indications include chronic mallet deformity, missed flexor tendon avulsions or distal phalanx non-unions.

Techniques

A multitude of fixation techniques have been described, including interosseous wiring, percutaneous pinning, tension band wiring, bio-resorbable pinning, plating, oblique lag screw fixation, and axial compression screw fixation. Regardless of the technique chosen, the joint is prepared in a similar manner and the requirements for a successful outcome are: (1) full apposition of the cancellous bone surfaces; (2) preservation of distal phalanx bone stock to allow for hardware purchase; (3) fusion in approximately 5–10° of flexion if possible; and (4) stable fixation.

Most techniques utilize a transverse skin incision dorsally overlying the joint. Oblique or axial extensions are made proximally and distally and skin flaps are raised to complete an H-shaped exposure centered over the joint. Alternatively, a mid-lateral or a Y-shaped dorsal incision can be used. Specific care should be taken to avoid injury to the germinal nail matrix located just distal to the extensor insertion. The extensor tendon and joint capsule are sharply divided in a transverse orientation, the collateral ligaments are divided, and the joint is maximally flexed to allow access to the articular surfaces.

With the base of the distal phalanx and the condyles of the middle phalanx exposed, a rongeur is used to remove dorsal and lateral osteophytes. The articular surfaces are decorticated until cancellous bone is visualized. Alternatively, osteotomies can be created with a small oscillating saw to achieve precise apposition of the cancellous bone. If power saws or burrs are to be utilized, copious irrigation should be maintained throughout the cutting process to avoid the risk of thermally induced osteonecrosis which can elevate the risk of non-union postoperatively.

Interosseous wiring

Interosseous wiring involves securing the distal and middle phalanx together by means of one or two dental wires passed through bone tunnels. Interosseous wiring can be used to achieve some compression of the joint and is usually used in conjunction with Kirschner (K) wires for greater stability. Zavitsanos et al . described a technique which allows the K-wires to be completely buried, minimizing the risk of infection. The wires may be palpable and bothersome under the thin dorsal skin so wire removal can be completed after union.

K-wire fixation

After the joint is prepared, two crossed 0.045-inch K-wires are passed across the joint. Alternatively, an axial K-wire and a single oblique wire can be used. A minimum of two wires needs to be used to prevent rotation. The wires are typically cut beneath the skin at the fingertip. This enables the patient to continue to use the finger in activities of daily living. The DIP joint is immobilized in a splint to protect the fusion. Once union is documented radiographically, the wires can be removed. Wire removal can be done in the office under digital block anesthesia.

Tension band wiring

With the joint surfaces prepared, two 0.045-inch K-wires are placed parallel across the joint. Distally, the pins are buried in the distal volar cortex of the distal phalanx while proximally the pins exit on the dorsal cortex of the middle phalanx. A transverse canal is made dorsal to the wires in the proximal distal phalanx. A 28-gauge dental wire is passed through this canal and secured proximally around the K-wires exiting on the dorsal proximal phalanx in a figure-of-eight fashion. The dental wire is twisted and secured and the K-wires are bent to assure the construct is as low-profile as possible. The tension band construct is remarkably stable and early motion may be permitted in selected patients. If the hardware is bothersome it can be removed after bony union.

Clinical tips

Tension band wiring

• Take down the collateral ligaments for clear visualization of the entire joint.

• A ronguer or small saw can be used to prepare the joint for fusion.

• K-wires can be placed retrograde from the joint into the middle phalanx to assure an appropriate trajectory that will capture a sufficient portion of the distal phalanx.

• After confirming the correct length of the parallel K-wires, back them out of the bone slightly, bend, and cut to length prior to gently tapping back into place. This will allow for better coaptation to the bone and make hardware irritation less likely.

Axial compression screw

A single axial compression screw ( Fig. 18.4 ) can be used to reliably achieve DIP joint fusion. A traditional lag screw technique can be used but will result in prominent hardware at the fingertip and is discouraged. Buried headless compression screws are preferred. The technique for the use of a threaded headless compression screw initially involves preparation of the joint surfaces followed by the placement of an antegrade axial K-wire through the distal phalanx exiting at the hyponychium. The bone surfaces are then coapted in the position of fusion and the same wire is drilled retrograde back into the middle phalanx. The position of the wire and arthrodesis are checked fluoroscopically, the screw length is determined, and the wire is advanced across the PIP joint. A cannulated drill is used to prepare the channel for screw placement taking care to drill the appropriate length for the screw, and a cannulated, fully threaded; self-tapping screw is inserted in a retrograde fashion to complete the fusion (see Fig. 18.4 ).

The screw should be long enough to engage the cortical isthmus of the middle phalanx. Occasionally, the intramedullary canal of the middle phalanx is too wide for the thread to engage the endosteal cortex even at the isthmus (e.g., thumb), and the chances of a stable construct are reduced. Additionally, specific attention should be paid to the anteroposterior (narrowest) diameter of the distal phalanx to ensure that the screw thread diameter is not greater than this measurement, otherwise dorsal fracturing and nail bed deformity can occur.

The major advantages of this technique over other methods of DIP fusion are buried hardware and stable fixation. Immobilization time with the use of compression screws has been shown to be significantly shorter when compared to other techniques for DIP fusion. Patients may often be splinted for only 1–3 weeks, allowing patients to return to work earlier. One disadvantage of this technique is the difficulty in achieving the optimal prehensile position at the DIP as the joint is typically fused straight due to the conical shape of the screw. Other reported complications have included a single case of skin necrosis of the finger tip requiring secondary amputation ; this was likely due to unrecognized prominent hardware.

Complications of DIP fusion

Infection

Traditional fixation techniques for small joint arthrodesis include interosseous wiring, crossed K-wires or a combination of these techniques. The rate of deep infection and osteomyelitis with these techniques remains up to 20% in some studies. Surgeons who prefer this technique should consider burying the K-wires during the consolidation phase, as infection and non-union rates are much lower when buried techniques are utilized.

Non-union

Reported non-union rates for DIP arthrodesis range from 0% to 20%. Several studies have reported low rates of non-union with screw techniques as well as traditional techniques, however a clear relationship between fixation technique and the rate of non-union has not been shown for DIP arthrodesis.

Kirschner wire and interosseous wire techniques produce significantly less compression across the fusion site than compression screw techniques and compression itself has been shown to achieve more rapid fusion. In a biomechanical cadaver study comparing fixation techniques, the use of a single buried axial compression screw (Herbert screw) was shown to be superior in terms of fixation strength when compared to a combined K-wire/tension band technique. Despite this biomechanical study, retrospective clinical studies have noted similar non-union rates when comparing compression screws, interosseous wiring, and crossed K-wires techniques; it is thought that non-union rates most closely correlate with the amount of cortical bone and condition of the bone stock at the time of operative procedure.

Proximal interphalangeal (PIP) joint arthritis

Within the hand, the PIP joint is the third most frequently affected by OA. The joint is more commonly affected in females. The PIP joint has been described as the “functional locus of the finger” as it produces 85% of intrinsic digital flexion and contributes 20% to the overall arc of finger motion. Despite this, a full range of motion is not absolutely necessary for good hand function, and a 45–90° flexion arc allows for most activities.

As in DIP arthritis, PIP joints affected by OA are often enlarged and painful. Patients will complain of their inability to wear or remove rings from the affected fingers. Bouchard’s nodes are pathognomonic for PIP OA and are bony protuberances at the joint, analogous to Heberden’s nodes at the DIP joint. Range of motion at the PIP joint tends to be preserved until late in the disease process. Radiographic findings include joint space narrowing, subchondral sclerosis, and osteophytes (see Fig. 18.2 ).

PIP arthrodesis

PIP arthrodesis can be accomplished using the same techniques as described for DIP arthrodesis. The optimal position of PIP fusion varies according to the digit, with some authors recommending 40° of flexion for index, 45° for the long, 50° for the ring, and 55° for the small finger ( Fig. 18.5 ) ; however, this can be tailored according to the patient’s occupation and recreational activities. Preoperative splints simulating fusion at various angles can be used to allow the patient to make a more informed decision.

Techniques

The PIP is approached dorsally through a longitudinal incision centered over the joint. The extensor tendon and joint capsule are split longitudinally and dissected radially and ulnarly. The central slip should be elevated subperiosteally off the base of the middle phalanx. The proximal origins of the collateral ligaments are divided and the joint is flexed to expose the joint surfaces. The bone ends are prepared using angled saw cuts on both phalanges. Alternatively, rongeurs or a burr can be used to create a concave–convex (cup and cone) configuration on the opposing bone surfaces. The digit is necessarily shortened by preparation of the bone surfaces. Prolapse of the volar plate in between the bone ends may result in non-union; the volar plate should be resected if this occurs. Fixation can be achieved by one of the following techniques.

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