Ankle Arthritis Etiology and Prevention

CHAPTER PREVIEW

CHAPTER SYNOPSIS:

Ankle arthritis is less prevalent than that of the other major lower extremity joints. Neuropathic arthritis is increasing in prevalence, as is ankle pain due to obesity. Newer techniques to reverse cartilage damage and to evenly distribute load are showing promise in experimental animals, but no therapy has yet been proved effective in humans. For those with inflammatory arthritis, the anticytokine therapies are showing preservation of joint space and bone quality.

IMPORTANT POINTS:

Most ankle arthritis is related to prior trauma; with the increasing prevalence of obesity, there may be more primary osteoarthritis of the ankle. Instability and loose body are amenable to early surgical intervention. Early treatment of sepsis and effective management of crystalline arthritis will protect the joint.

CLINICAL/SURGICAL PEARLS:

1

Realignment of the lower leg may limit the progression of medial or lateral ankle degeneration.
2

Preserving range of motion through exercise has a protective element.
3

In sports, fracture and ligament damage prevention are worthwhile strategies.

CLINICAL/SURGICAL PITFALLS:

Surgery to repair ligaments around the ankle should include arthrotomy to remove loose bodies or to repair osteochondral lesions on the medial and lateral corners of the talus, when present.

VIDEO AVAILABLE:

In rheumatism, as in other form of diseases, prevention is ultimately likely to be more effective than cure. —Jonas Kellgren

HISTORY/INTRODUCTION/SCOPE OF THE PROBLEM

The physician bears the role of expert on the explanation and treatment of disease. Fundamental understanding of the pathogenesis of ankle arthrosis is critical to appropriate management; since numerous factors can contribute to the ankle joint’s dysfunction, it is important to be aware of the natural history of each. This debilitating and progressive disorder merits renewed attention due to recent advances in treatment.

This chapter focuses on various causes of ankle arthritis with specific interest in the role played by prior traumatic injury in tibiotalar pathology. In addition, there is a discussion on the natural history of ankle degenerative joint disease and whether there are any effective modes of preventing disease progression.

CHARACTERIZATION OF ANKLE OSTEOARTHRITIS

The Outerbridge classification of chondral injury has been adopted by most orthopedists as an effective mode of communicating pathologic findings of articular cartilage. Typically used for describing osteochondral lesions, articular cartilage is graded from 1 to 4 based on the depth and diameter of the defect ( Table 2-1 ). The correlation between radiographic and clinical diagnosis based on symptoms is inexact. Radiographically, the most common method for describing arthritis in a joint is based on Kellgren-Lawrence criteria ( Table 2-2 ). However, this grading scale has limitations ; this system is broadly applicable to all joints without particular focus on characteristics unique to the ankle. Additionally, the Kellgren-Lawrence system places great emphasis on the presence of osteophytes, but the degree of joint space narrowing has been considered a more important diagnostic feature.

TABLE 2-1

Outerbridge Grading System with Modification

Grade	Outerbridge	Modification
1	Softening and hypertrophy of cartilage	Softening and hypertrophy of cartilage
2	Fissures and fragmentation comprising less than ½-inch diameter	Fibrillation and fissuring of less than 50% of the cartilage depth
3	Fissuring and fragmentation comprising an area greater than ½-inch diameter	Fibrillation and fissuring of greater than 50% of the cartilage depth, but without exposed bone
4	Erosion of cartilage down to but not penetrating subchondral bone	Erosion of cartilage down to but not penetrating subchondral bone

From Outerbridge RE: The etiology of chondromalacia patella. J Bone Joint Surg Br 43:752–757, 1961; Williams RJ 3rd, Ranawat AS, Potter HG, et al: Fresh stored allografts for the treatment of osteochondral defects of the knee. J Bone Joint Surg Am 89:718–726, 2007; and Steadman JR, Briggs KK, Rodrigo JJ, et al: Outcomes of microfracture for traumatic chondral defects of the knee: Average 11-year follow-up. Arthroscopy 19:477–484, 2003.

TABLE 2-2

Kellgren-Lawrence Criteria

Grade	Presence of Arthritis
0	None	No radiographic evidence of osteoarthritis
1	Doubtful	Presence of small osteophytes of doubtful significance
2	Minimal	Presence of osteophytes with mild joint space narrowing
3	Moderate	Presence of osteophytes with moderate joint space narrowing
4	Severe	Presence of osteophytes, significant joint space narrowing, and subchondral sclerosis

Kellgren-Lawrence Classification Features	Description
1	Formation of osteophytes on the joint margins
2	Periarticular ossicles
3	Narrowing of joint cartilage associated with subchondral bone sclerosis
4	Presence of pseudocysts with sclerotic walls in the subchondral bone
5	Altered bone-end morphology

Data from Huch K, Kuettner KE, Dieppe P: Osteoarthritis in ankle and knee joints. Semin Arthritis Rheum 26, 1997.

Another grading system has been devised by Scranton and McDermott with the express purpose of characterizing ankle arthritis; again, emphasis has been placed on the presence and size of anterior osteophytes rather than on joint space narrowing ( Table 2-3 ). Nevertheless, a discrepancy exists in the correlation between radiographic findings and the existence of intra-articular pathology. A cadavaric study has shown that cartilage degeneration often exists in the ankle even in the absence of radiographic degenerative changes. In that study, radiographic changes associated with arthritis were detected only when full-thickness cartilage loss had occurred. This finding implies that the osseous structures of the ankle may resist degeneration better than other joints throughout the body.

TABLE 2-3

Scranton and McDermott Grading System

Type	Characteristics
I	Synovial impingement; radiographs show inflammatory reaction, up to 3-mm spur formation
II	Osteochondral reaction exostosis; radiographs manifest osseous spur formation greater than 3 mm in size. No talar spur is present.
III	Significant exostosis with or without fragmentation, with secondary spur formation on the dorsum of the talus seen. Often with fragmentation osteophytes
IV	Pantalocrural arthritic destruction; radiographs suggest medial, lateral, or posterior degenerative, arthritic changes.

Data from Scranton PE Jr, McDermott JE: Anterior tibiotalar spurs: A comparison of open versus arthroscopic debridement. Foot Ankle 13:125–129, 1992.

The relative distribution of arthritis among the hip, knee, and ankle has been reported at 19%, 41%, and 4.4%, respectively. This relative infrequency has led to a variety of theories attempting to explain the ankles’ resilience to the development of ankle arthritis. Some of these theories include the following:

•

The ankle is constrained and therefore perhaps more stable than other joints of the body. The ankle joint is a rolling joint and exhibits congruency at a higher load.
•

The temperature of the ankle is approximately 1° less than the core body temperature. It is believed that the lower temperature may foster slower metabolic activity in this joint.
•

The ankle joint has the thinnest cartilage compared with the hip and knee. An inverse relationship has been found between cartilage thickness and its compressive modulus. It has been proposed that the most congruent joints have the thinnest cartilage to better equalize stresses. The loaded ankle joint has a smaller surface contact area (273 to 417 mm ²) than the hip (1100 to 1700 mm ²) or the femorotibial joint (1120 mm ²). During gait, the contact area and pressure distribution pattern within the ankle joint change. This change in pressure distribution may have a beneficial effect on cartilage lubrication and nutrition.
•

The tensile strength of the talar cartilage decreases only slightly with age, unlike the femoral head.
•

Compared with the knee, normal ankle cartilage is stiffer and more resistant to indentation. The cartilage matrix is more uniform than that of the hip or knee. It has been postulated that cartilage exposed to high stress adapts through increased stiffness and uniformity.
•

There may be a view among physicians that ankle arthritis is a common complication of ankle injury, and until recently good options for treatment were lacking. Subsequently, patients are encouraged to live with their disability for as long as possible to avoid undergoing arthrodesis or arthroplasty.
•

Nevertheless, in those affected, the impact of ankle arthrosis can be profoundly disabling.

EPIDEMIOLOGY

Estimates of the incidence and prevalence of tibiotalar arthritis suggest a rather small group relative to those with hip and knee arthritis. The NHANES I study group of physician-diagnosed musculoskeletal abnormalities observed a 0.8% rate of ankle arthritis compared with a 12% rate in the knee; notably, this population consisted of individuals equally distributed in age from 25 to 74 years and therefore underestimated the actual rates of ankle disease among the more likely affected older subset of the population. Post mortem studies of prevalence have revealed grade 3 and 4 chondral changes in the ankles of 18% of an elderly population. Surprisingly, radiographic imaging on the joints in this study did not show arthritic changes until grade 4 chondral lesions were present. This suggests that ankle degeneration must be quite advanced before it becomes radiographically detectable.

It is important to note that certain subsets of the population are at a higher risk for the development of ankle arthritis. Roughly 70% of all individuals with ankle arthritis have a history of prior trauma, whereas rheumatoid arthritis (RA) accounts for 6% to 12% of cases of ankle arthritis; idiopathic, 7% to 15%; and neuropathic, 5%.

CAUSES OF ANKLE ARTHRITIS

As with arthritis of other joints, certain factors determine pathogenesis and progression. Age, joint morphology, genetics, and environmental factors all are important determinants in ankle arthritis ( Fig. 2-1 ). The ankle differentiates itself because its particular susceptibility is to the development of posttraumatic arthritis. The dynamics of load-bearing are exceedingly important for the ankle, and the concept of pathologic loading becomes quite important. Pathologic loading is ill defined, but for the purposes of this text, it shall mean one of two things.

1

Chronic abnormal loading of cartilage that results progressive joint deterioration.
2

Acute loading of the joint that results in an overwhelming injury to chondrocytes from which they cannot recover. Another consequence of acute joint loading is the development of metaphyseal bone bruising as noted on magnetic resonance imaging. The significance of this finding in the context of arthritis development is unknown, but the involvement of subchondral bone can affect basilar chondrocyte metabolism.

These two entities probably exist on a spectrum. In the case of the former, ligamentous laxity may cause decades of abnormal loading before symptoms arise. However, in high-energy injuries such as pilon fractures, joint degeneration can occur relatively rapidly.

Idiopathic

The ankle joint consists of the articulation between the tibia, fibula, and talus. Tibiotalar motion is only made possible by the stabilizing bony, ligamentous, and musculotendonous support structures of the ankle. Small disruptions in articular contact can have profound influences on joint congruence, location of loading, shear stresses, and concentration of load transmitted. For example, with hindfoot valgus deformities, the talus shifts laterally and a more concentrated load may be transmitted through the lateral aspect of the talar dome to the lateral plafond. This type of loading may become pathologic over time and may eventually lead to ankle joint degeneration.

Idiopathic tibiotalar osteoarthritis (OA) is rare but may more accurately have its origin in a remote injury previously thought to be unrelated. It can take more than 20 to 30 years for degenerative symptoms to arise following ankle ligamentous injury. Nevertheless, idiopathic arthritis merits discussion as it introduces the mechanisms of cartilage degeneration.

The pathogenesis of OA requires some kind of initiating event such as mechanical stresses, genetic predisposition, or merely the changes associated with normal aging ( Table 2-4 ). Responses to these changes depend on the depth of injury to the articular surface. Tibial and talar cartilages are roughly comparable in their mean thickness (1.2 mm), but the talus has substantially more matrix depth on its shoulders.

TABLE 2-4

Biochemical Changes of Articular Cartilage

	Aging	Osteoarthritis (OA)
Water content (hydration: permeability)	↓	↑
Collagen	Content remains relatively unchanged	Becomes disorderly (breakdown of matrix framework)
		Content ↓ in severe OA
		Relative concentration ↑ (due to loss of proteoglycans)
Proteoglycan content (concentration)	↓ (also the length of the protein core and GAG chains decreases)	↓
Proteoglycan synthesis		↑
Proteoglycan degradation	↓	↑↑↑
Chondroitin sulfate concentration (includes both chondroitin 4 and 6–sulfate)	↓	↑
Chondroitin 4–sulfate concentration	↓	↑
Keratin sulfate concentration	↑	↓
Chondrocyte size	↑
Chondrocyte number	↓
Modulus of elasticity	↑	↓

Cartilage cells are normally shielded from their environment by the extracellular matrix they produce. Nutrition occurs via diffusion rather than via systemic blood supply. Normal loading conditions predispose chondrocytes to maintain the cartilage matrix, whereas injurious loading activates degradation pathways. These cells are relatively inactive in normal adult joints, but in the event of injury (micro or macro), resulting in exposure to their environment, chondrocytes become activated to initiate degradation pathways. During this process, chondrocytes produce cytokines that fuel inflammation, as well as degradative enzymes, including matrix metalloproteinases (MMPs) that break down the type II collagenous matrix within the joint.

Studies have indicated that the chondrocytes of the ankle may possess biochemical properties that create a joint more resistant to arthritic changes than other load-bearing joints such as the knee. Several studies have indicated that ankle chondrocytes are less disposed to respond to inflammation than are comparable knee chondrocytes. Ankle chondrocytes are less responsive to interleukin (IL)-1β inflammatory pathways than are comparable knee chondrocytes. An additional difference is the lack of ankle chondrocyte expression of MMP-8, a protease thought to be important in matrix degeneration. Also, ankle cartilage has been observed to be more cellular and contain a higher relative concentration of proteoglycans. Perhaps these chondrocytes’ comparatively increased hardiness reflects an adaptive characteristic made necessary by the tremendous demands placed on the ankle joint.

Cell Response to Pathologic Loading

The development of OA begins with some type of insult to articular cartilage that is sufficient to activate chondrocytes to become metabolically active and to initiate degradation pathways. However, not all load-related cartilaginous injuries progress to OA. Excessive loading that does not result in visible cartilaginous injury can increase the metabolic activity of chondrocytes. This can result in an anabolic response from chondrocytes and does not necessarily portend activation of degradation pathways. However, at a certain point, pathologic loading exceeds the chondrocytes’ ability to compensate, and the cellular metabolism shifts from anabolic (matrix maintenance) to catabolic (matrix degeneration) ( Fig. 2-2 ).