Phases of Osteoarthritis in the Finger Tips
Osteoarthritis (OA) can affect any joint in the body. Most people associate OA with hip, knee, and spine (back) pain. But it can also affect the fingers of the hand, right down to the very tip of the fingers. The joint that allows finger tip motion is called the distal interphalangeal (DIP) joint.

In this article, experts who understand and treat hand osteoarthritis (OA) discuss the two main types of OA that affect the hand. They summarize what is known about normal distal interphalangeal (DIP) joint anatomy. A description of the four phases of osteoarthritis progression in the DIP is provided along with drawings, photos, and X-rays to help us understand this process.

It is helpful to realize that the development of osteoarthritis is complex and multifactorial (i.e., there are many risk factors involved). It is safe to say that for as much as we do know about this disease, there is much more we do not understand about it. Scientists are actively exploring who gets osteoarthritis, why and how it develops, and what can be done to prevent (or treat) it.

Some of the more common risk factors being studied are age, genetics, sex (male versus female), race/ethnicity, hand dominance, and occupation. When it comes to osteoarthritis of the distal interphalangeal (DIP) joint, studies have shown a possible link to each one of these factors.

But the people who are affected don't all have the same risk factors and are not in the same age range. So it's a bit of a puzzle how demographics, environment, genetics, and joint mechanics interact to result in this final outcome we call osteoarthritis.

Aside from patient factors, scientists are examining the pathogenesis of osteoarthritis. Pathogenesis refers to the steps that take place as a normal joint is altered and becomes an arthritic joint.

All aspects of the joint and surrounding soft tissue are affected. These structures support and stabilize the joint and include the cartilage, first layer of bone (called the subchondral bone), ligaments, and tendons. Any injury, damage, shift, or change in these structures can also change the biomechanics, force, and load on a joint. And any of these events can become the first step in the cascade that eventually leads to arthritis.

What exactly are those changes and the chain of events? It might be helpful to look at this first by describing what is seen on X-rays and in the clinic. Early arthritic changes show up on X-rays as a slight narrowing of the joint space. This phase is referred to as the stationary non-erosive stage. The joint remains intact and stable.

The next phase is the destructive erosive phase. Here there is swelling and break down of the cartilage and subchondral layer. The tendons that attach to the bone start to thicken and degenerate. Inflammation of the joint fluid (synovitis) develops and creates an inflammatory phase (not unlike what happens with rheumatoid arthritis).

After the destruction, the joint tries to recover and remodel the damaged area. But all that happens is the formation of osteophytes (bone spurs), cysts, scar tissue, a thickened cartilage, and other bumps on the finger bones called Heberden's nodes.

Although we can describe what happens, it's still unclear what starts the process, what keeps it going, and why it happens. Where do the first signals come from -- the cartilage? The joint surface? The ligaments around the joint? There are theories but no firm knowledge about this.

While scientists continue to try and unravel all the details of the pathogenesis of osteoarthritis, the authors suggest finding better ways to detect those changes. Various ways to assign a level of severity have also been developed. Three of the most common scoring systems rely on X-rays to grade osteoarthritis. These are the Kellgren and Lawrence method, the Kallmann method, and the Verbruggen method.

The Kellgren and Lawrence grading system has four levels (one through four). Grade 1 is the normal joint. Up to one osteophyte (bone spur) can be seen around that joint and still be considered "normal". Grade two is assigned to the joint that has two osteophytes in separate places on the same joint. There are some slight changes in the bone under the joint but no deformities and no changes in the joint space.

Grade three shows a definite narrowing of the joint space, moderate osteophytes, and the start of joint deformity at the ends of the bones. In a joint labeled grade four, there are large osteophytes, loss of joint space, bone sclerosis (hardening), deformity, and the formation of cysts.

The Kallmann system differs from the Kellgren and Lawrence scoring in that the changes observed (spurs, joint space, cysts, deformity, sclerosis) are given a score of zero (none or absent)or one (present). Some of the defining characteristics (e.g., joint space narrowing, osteophytes) can also be given a score of two for moderate changes and three (large or severe).

Each of these systems has a slightly different way of assessing hand osteoarthritis. The third system (the Verbruggen assessment) was developed to help record smaller changes that take place quickly.

Using all three systems together provides a way to assess specifics about changes in the individual lesions as well as the progression in phases of osteoarthritis. None of the systems are enough as stand-alone methods. The authors note that the Verbruggen scoring method is less time consuming and might be the most reliable but further studies are needed to confirm this.

In summary, osteoarthritis of the distal interphalangeal (DIP) joints of the hand has both a nonerosive and an erosive stage with inflammation, destruction, and remodeling observed. This understanding has led to the development of scoring methods to help describe the process. Until knowledge of the disease process is complete, physicians must rely on grading joint damage using one (or more) of the scoring systems currently available.
Robert A. Kaufmann, MD, et al. Osteoarthritis of the Distal Interphalangeal Joint. In The Journal of Hand Surgery. December 2010. Vol. 35A. No. 12. Pp. 2117-2125.