The authors conducted a retrospective case-control study among persons aged 50 to 89 years who received a radiograph of the right hand during the last 5 years. Patients had radiographically proven hand osteoarthritis (wear and tear arthritis) OA, and controls did not. Participants indicated frequency, duration, and details of their knuckle cracking behavior and known risk factors for hand OA.
Results: The prevalence of knuckle cracking among 215 respondents (135 patients, 80 controls) was 20%. When examined in aggregate, the prevalence of OA in any joint was similar among those who crack knuckles (18.1%) and those who do not (21.5%; P = .548). When examined by joint type, knuckle cracking was not a risk for osteoarthritis in that joint. Total past duration (in years) and volume (daily frequency × years) of knuckle cracking of each joint type also was not significantly correlated with OA at the respective joint.
Conclusions: A history of habitual KC—including the total duration and total cumulative exposure—does not seem to be a risk factor for hand OA.
IntroductionKnuckle cracking (KC) is a behavior that involves manipulation of the finger joints that results in an audible crack, and it is often done habitually. Prevalence estimates vary between 25% and 54%, depending on the population studied.
The behavior can become habitual because of immediate joint tension release and increased joint range of motion.
During an attempt to crack a knuckle, the joint is manipulated by axial distraction, hyperflexion, hyperextension, or lateral deviation. This lengthens part or all of the joint space and greatly decreases intra-articular pressure, causing gases that have dissolved in the synovial fluid to form microscopic bubbles, which coalesce. When the joint space reaches its maximum distraction (up to 3 times its resting joint space distance), joint fluid rushes into the areas of negative pressure. The larger bubbles suddenly collapse into numerous microscopic bubbles, leading to the characteristic cracking sound. The maneuver leaves the joint space wider than it had been and synovial fluid more widely distributed. The stretching of joint ligaments required to produce the widened joint space also leaves the joint with greater range of motion. It typically takes at least 15 minutes for the joint to be able to be cracked again because of the time required for the microscopic bubbles to fully dissolve into solution and for the joint space to retract back to its resting position.
Common urban legend suggests that knuckle cracking will lead to arthritis of the hand joints. Adverse effects of knuckle cracking have been cited but are not well supported in the medical literature. Case reports of acute joint damage from unusually vigorous and deviant knuckle cracking attempts are rare.
The amount of force required to crack a knuckle has been shown in vitro studies to exceed the energy threshold that can lead to articular cartilage damage.
Based on these facts, it is logical to theorize that habitual knuckle cracking may lead to gradual thinning of articular cartilage and eventual clinical osteoarthritis (OA). However, this claim remains unsubstantiated in the medical literature. The cavitation effect of intra-articular bubble formation and collapse is also mechanically similar to cavitation of ship propellers, a process that has been shown to produce wear on the propeller surfaces.
A MEDLINE search using keywords "joint cracking" and "knuckle cracking" revealed 2 studies that addressed the incidence of OA in knuckle crackers. The first looked at 300 randomly selected persons older than age 45 (mean age, 63 years). Participants were assessed by a questionnaire and a physical examination of the hands. Those who cracked knuckles were more likely to have hand swelling and reduced grip strength, but the prevalence of hand OA was 16% among those who cracked knuckles and those who did not. The investigators did not specify which joints were cracked nor which joints were affected with OA.
Another study involved examination of the hand radiographs of 28 nursing home residents (average age, 78 years). Participants were asked to recall if they currently or previously cracked knuckles, but investigators did not specify which joints. In this study, knuckle cracking of the MCP (first knuckle of the fingers) joint was found to be negatively correlated with OA. The prevalence of KC in the 6 persons with OA of the MCP joint was 17%, whereas the prevalence of KC in the group without OA of the MCP joint was 64%. This suggests that KC may be associated with a lower prevalence of OA at the MCP joint.
Though somewhat useful, neither of these studies specified which joints participants cracked. Neither quantified the duration or frequency of KC, both of which could have correlations with the presence or absence of OA. Duration and frequency may be relevant because, based on the mechanical logic above, the more times that the maneuver is performed, the more the risk of mechanical wear on affected surfaces would, theoretically, increase.
OA of the hand increases in prevalence and severity with age.The prevalence of symptomatic hand OA has been reported to be 22% in persons age 71 to 100 years among the general population. Other risk factors include prior joint trauma, family history of hand OA, and history of heavy labor involving the hands. Those with hand OA have reduced maximal grip strength, more difficulty writing and handling small objects, and more difficulty carrying objects. Given this burden of suffering from hand OA and the lack of curative or disease-modifying treatments, factors that potentially protect against OA warrant further investigation. One such factor is knuckle cracking.
This study represents the most comprehensive evaluation to date of habitual KC and any association with hand OA. Our findings support the conclusions of 2 previous studies. It confirms that the presence of knuckle cracking is not associated with hand osteoarthritis. This is the first study to correlate the duration and the total volume of previous knuckle cracking with OA, in addition to the presence or absence of knuckle cracking. Participants described how frequently each day they crack each type of knuckle and for how many years they have been doing it. First, our results indicated that the duration of KC has no correlation to the presence of OA in the DIP, PIP, and MCP joints.
They also calculated "crack-years," which roughly quantified the total amount of exposure to this behavior. This allowed investigation of a possible "dose–response" relationship between the mechanical effects of knuckle cracking and OA. Again, when looking at knuckle cracking of each joint type, the authors found no significant correlation of "crack-years" with OA in the respective joint.
What we do not know yet are all the reasons why people crack their knuckles and the effect this has on their joints in the long term. Though some people may start knuckle cracking because of joint symptoms, patients with OA in our study started knuckle cracking long before the onset of OA symptoms. Some people may crack knuckles because of the sense of relief it can bring, some because of habit, and some from both. People may stop knuckle cracking when hand symptoms appear either because of fear of what knuckle cracking might do to their joints or because knuckle cracking becomes too uncomfortable.
What we can conclude, however, is that, in these cohorts of persons aged 50 to 89 years, a history of habitual KC—including the total duration and total cumulative exposure to KC—does not seem to be a risk factor for hand OA.
Reference: Translated from Orthopedics to English for better patient understanding by JTM