ORIGINAL RESEARCH

Knuckle Cracking and Hand Osteoarthritis

Kevin deWeber, MD, FAAFP, Mariusz Olszewski, MD, and Rebecca Ortolano, MD
Background: Previous studies have not shown a correlation between knuckle cracking (KC) and hand
osteoarthritis (OA). However, one study showed an inverse correlation between KC and metacarpopha-
langeal joint OA.
Methods: We 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 OA, and controls did not. Participants indicated frequency, duration, and details of their KC be-
havior and known risk factors for hand OA.
Results: The prevalence of KC 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, KC was not a risk for
OA in that joint. Total past duration (in years) and volume (daily frequency years) of KC of each joint
type also was not signicantly correlated with OA at the respective joint.
Conclusions: A history of habitual KCincluding the total duration and total cumulative exposure
does not seem to be a risk factor for hand OA. (J Am Board Fam Med 2011;24:169174.)
Keywords: Knuckle Cracking, Osteoarthritis
Knuckle cracking (KC) is a behavior that involves
manipulation of the nger joints that results in an
audible crack, and it is often done habitually. Prev-
alence estimates vary between 25% and 54%, de-
pending on the population studied.
1,2
The behavior
can become habitual because of immediate joint
tension release and increased joint range of mo-
tion.
3
During an attempt to crack a knuckle, the joint
is manipulated by axial distraction, hyperexion,
hyperextension, or lateral deviation. This lengthens
part or all of the joint space and greatly decreases
intra-articular pressure, causing gases that have dis-
solved in the synovial uid to form microscopic
bubbles, which coalesce. When the joint space
reaches its maximum distraction (up to 3 times its
resting joint space distance), joint uid rushes into
the areas of negative pressure. The larger bubbles
suddenly collapse into numerous microscopic bub-
bles, leading to the characteristic cracking sound.
The maneuver leaves the joint space wider than it
had been and synovial uid more widely distrib-
uted. 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.
4
Common urban legend suggests that KC will
lead to arthritis of the hand joints. Adverse effects
of KC have been cited but are not well supported in
the medical literature. Case reports of acute joint
damage from unusually vigorous and deviant KC
attempts are rare. One reported a thumb ulnar
collateral ligament sprain and a fth nger extensor
tendon sagittal band tear at the metacarpophalan-
This article was externally peer reviewed.
Submitted 6 July 2010; revised 15 October 2010; accepted
22 October 2010.
From the Department of Family Medicine, Uniformed
Services University of the Health Sciences, Bethesda, MD
(KD); the Department of Radiology, National Naval Med-
ical Center, Bethesda, MD (MO); and the Madigan Army
Medical Center, Tacoma, WA (RO).
Funding: Uniformed Services University of the Health
Sciences Grant HU81CV.
Conict of interest: none declared.
Disclaimer: The opinions contained herein are those of
the authors. They do not reect ofcial policy of the De-
partment of Defense, the Department of the Navy, or the
Uniformed Services University.
Corresponding author: Kevin deWeber, MD, FAAFP,
USUHS, Dept. FAP, 4301 Jones Bridge Road, Bethesda,
MD 20814 (E-mail: kdeweber@usuhs.mil).
doi: 10.3122/jabfm.2011.02.100156 Knuckle Cracking and Hand Osteoarthritis 169
geal (MCP) joint.
5
Another described a man with
chondrocalcinosis in the rst and fourth MCP
joints and ligamentous ossication in the third
MCP joint, presumably caused by chronic KC.
6
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 dam-
age.
7
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 sur-
faces.
1
Based on these facts, it is logical to theorize
that habitual KC may lead to gradual thinning of
articular cartilage and eventual clinical osteoarthri-
tis (OA). However, this claim remains unsubstan-
tiated in the medical literature.
A MEDLINE search using keywords joint
cracking and knuckle cracking revealed 2 studies
that addressed the incidence of OA in knuckle
crackers. The rst 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 preva-
lence of hand OA was 16% among those who
cracked knuckles and those who did not.
2
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, KC of the MCP joint was found to be neg-
atively 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 sug-
gests that KC may be associated with a lower prev-
alence of OA at the MCP joint.
1
Though somewhat useful, neither of these
studies specied which joints participants
cracked. Neither quantied the duration or fre-
quency of KC, both of which could have corre-
lations with the presence or absence of OA. Du-
ration 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.
8
The prevalence of symptomatic
hand OA has been reported to be 22% in persons
age 71 to 100 years among the general population.
9
Other risk factors include prior joint trauma, family
history of hand OA, and history of heavy labor
involving the hands.
10
Those with hand OA have
reduced maximal grip strength, more difculty
writing and handling small objects, and more dif-
culty carrying objects.
8
Given this burden of suf-
fering from hand OA and the lack of curative or
disease-modifying treatments, factors that poten-
tially protect against OA warrant further investiga-
tion. One such factor is knuckle cracking.
Materials and Methods
After approval by the Uniformed Services Uni-
versity of the Health Sciences and the National
Naval Medical Center institutional review boards
in Bethesda, MD, we conducted a retrospective,
nested, case-control study to examine KC behav-
ior in a population aged 50 to 89 years. Partici-
pants were selected from patients who had re-
ceived radiographs of the right hand within the
5-year period from October 2003 to October
2008. Patients consisted of persons with hand
OA; the controls did not have OA, based on
radiographic diagnosis. Gathering data about
only one hand is easier and still allows accurate
assessment of KC prevalence. Using power anal-
ysis we determined that we would need approxi-
mately 200 participants to reach statistical signif-
icance.
We identied eligible patients with hand OA
by querying the military electronic medical re-
cord database for persons with International
Classication of Diseases 9 codes of 715.04 (OA
of hand generalized), 715.14 (OA of hand local-
ized primary), 715.34 (OA of hand localized), and
715.94 (OA of hand). We reviewed reports of
their hand radiographs to ensure that hand OA
was present and to determine which joints were
affectedthe distal interphalangeal (DIP), prox-
imal interphalangeal (PIP), MCP, and/or the rst
carpometacarpal (1CMC) joints. We then
searched the same population in the database for
persons who did not have International Classi-
cation of Diseases 9 diagnoses of hand OA.
Those whose reports of their hand radiographs
conrmed the absence of OA or the presence of
170 JABFM MarchApril 2011 Vol. 24 No. 2 http://www.jabfm.org
any exclusion criteria were selected as controls.
We excluded persons who did not have a written
report of a right-hand radiograph within the
specied 5-year period and those with diagnoses
of inammatory arthritidies. We identied 141
controls without hand OA and 188 patients with
OA, for a total of 329 participants. The partici-
pant selection process is summarized in Figure 1.
Each participant was assigned a unique study
number and was mailed a packet containing the
study questionnaire. Participants were asked to re-
call and specify which joints on their right hand
they crack, using a drawing of a hand and indicating
locations of joints to assist them. We categorized
these into DIP, PIP, MCP, and 1CMC joint types.
In addition to KC duration, we asked participants
to quantify their frequency of KC daily, divided
into 5 ordinal categories (none, 15 times/day,
610 times/day, 1020 times/day, and 20 times/
day). Participants were also asked about specic
risk factors for OA, including family history of
hand OA, any fractures or dislocations of particular
joints, and a history of heavy labor using the hands for
5 years. Persons with OA were asked about the
presence and duration of their hand OA symptoms.
We used basic descriptive statistics to charac-
terize respondent demographics. To investigate
any association between KC and OA, we per-
formed Pearson
2
tests between the prevalence
of KC in controls and participants with OA. To
explore the relationship of OA with the duration
(in years) of KC for each joint type, we used
independent sample t tests to compare the mean
duration of KC in controls and those with OA.
Results
We received 215 surveys from the 329 partici-
pants (135 from patients with OA and 80 from
controls), for a response rate of 65%. The mean
age of respondents was 62 years (SD, 8 years). Of
the 215 respondents, 43 indicated they crack
their knuckles (20% prevalence). Women were
less likely to habitually crack knuckles than men:
17% (n 26) versus 29% (n 17), respectively
(P .05). The presence of other risk factors for
hand OA among patients and controls is summa-
rized in Table 1.
The most commonly cracked joint was the PIP
(15.9%; n 34), followed by the MCP (13.5%;
n 29), DIP (6.1%; n 13), and 1CMC (2.3%;
n 5) joints. Based on analysis of the radiograph
reports of all participants, we also determined
which joint types were affected with OA. When
participants indicated a history of trauma to a
specic joint, we excluded OA data only for that
joint. The joint most commonly affected by OA
was the DIP joint (68.4%; n 91), followed by
the 1CMC (57.1%; n 76), PIP (54.1%; n
72), and MCP (28.6%; n 38) joints.
Table 2 lists the prevalence and duration of
KC at each specic joint type among the OA
versus control groups. The prevalence of any KC
among the controls (23.2%; n 19) was not
signicantly different from prevalence in persons
with OA (18.0%; n 24; P .361). When
Figure 1. Selection of participants. OA, osteoarthritis.
Table 1. Presence of Other-Hand Osteoarthritis (OA)
Risk Factors among Patients and Controls
Risk Factor
Patients with
Hand OA
(n)
Controls
(n) P
Age (years) 64.4 (135) 57.0 (80) .001
Female sex (%) 74.8 (101) 68.8 (55) .335
Family history
of hand OA
48.9 (66) 32.5 (26) .039
5 years heavy
labor
19.3 (26) 16.2 (13) .857
Values presented as % (n).
doi: 10.3122/jabfm.2011.02.100156 Knuckle Cracking and Hand Osteoarthritis 171
examined by specic joint type, prevalence of KC
in the DIP, PIP, MCP, and 1CMC joints was
similar in patients and controls. For the DIP,
PIP, and MCP joints, there were no signicant
associations between duration of KC and the
presence of OA. There was insufcient data for
the 1CMC joint.
We next explored the relationship of OA with
the total volume of KC behavior to which each
joint type was exposed. For each frequency cat-
egory we interpolated to facilitate calculations.
The category 1 to 5 times/day was scored as 3;
6 to 10 times/day was scored as 8; and 10 to 20
times/day was scored as 15. No participants
cracked knuckles more frequently than this. The
product of frequency duration (years) resulted
in an estimation of total KC exposurewhat we
call crack-years, similar to the quantication of
tobacco use in pack-years. We calculated this for
each joint type.
The mean total KC exposure for the DIP joint
was 108 crack-years (SD, 17 crack-years). An
independent sample t test failed to reveal a sig-
nicant association between DIP crack-years and
the presence or absence of OA (P .418). The
mean KC exposure in the PIP joint was 70 crack-
years (SD, 44 crack-years) and, again, there was
no signicant association between crack-years of
the PIP joint among the OA group compared
with the control group (P .214). The mean
MCP joint exposure was 75 crack-years (SD, 52
crack-years), with no signicant relationship to
OA (P .503). There were insufcient data for
the 1CMC joint.
We attempted to determine which came rst:
the OA or the KC by asking patients with OA to
indicate how many years have they noticed OA
symptoms. Many patients with OA were asymp-
tomatic or did not answer. However, for those
who did answer and who also cracked knuckles,
we used the paired-samples t test to compare the
duration of KC to the duration of OA symptoms
and found that, for all joint types, the duration of
KC was signicantly greater than the duration of
OA symptoms (see Table 3).
Lastly, we performed binary logistic regression
analyses to evaluate the relative contributions of
KC, age, sex, family history of hand OA, and his-
tory of prolonged heavy labor to the risk of hand
OA. Analyses conrmed a strong association be-
tween family history of OA and the presence of
hand OA (odds ratio, 2.98; P .009) and between
age and hand OA (odds ratio, 1.20 per additional
year of age; P .001). Knuckle cracking, sex, and
heavy labor were not associated with OA (P .626,
P .222, and P .632, respectively) after control-
ling for other risk factors.
Discussion
This study represents the most comprehensive
evaluation to date of habitual KC and any asso-
ciation with hand OA. Our ndings support the
conclusions of 2 previous studies
1,2
that the pres-
ence of KC is not associated with hand OA. Ours
is the rst study to correlate the duration and the
total volume of previous KC with OA, in addition
to the presence or absence of KC. Participants
Table 2. Prevalence and Duration of Habitual Knuckle
Cracking in Patients and Controls by Joint Type
Joint Cracked Controls Patients with OA P
DIP (% n) 9.2 (11) 2.2 (2) .097
Duration*
(years)
26.3 36.0 .257
PIP (% n) 16.1 (23) 15.5 (11) .911
Duration*
(years)
28.3 21.6 .556
MCP (% n) 14.3 (25) 10.0 (4) .474
Duration*
(years)
26.4 25.0 .764
1CMC (% n) 2.9 (4) 1.3 (1) .746
Duration*
(years)
Data unavailable Data unavailable
Any joint 23.2 (19) 18.0 (24) .361
*Independent sample t test was used.
OA, osteoarthritis; DIP, distal interphalangeal; PIP, proximal
interphalangeal; MCP, metacarpophalangeal; 1CMC, rst car-
pometacarpal.
Table 3. Comparison of Habitual Knuckle Cracking
Duration (Any Frequency) with Duration of Hand
Osteoarthritis (OA) Symptoms Using Paired Samples
t Test
Joint (n)
Duration of OA
Symptoms (Years)
Duration of KC
(Years) P
DIP (7) 7.6 27.1 .006
PIP (19) 9.7 25.1 .001
MCP (15) 7.9 23.1 .003
1CMC (3) 8.0 33.3 .091
OA, osteoarthritis; DIP, distal interphalangeal; PIP, proximal
interphalangeal; MCP, metacarpophalangeal; 1CMC, rst car-
pometacarpal; KC, knuckle cracking.
172 JABFM MarchApril 2011 Vol. 24 No. 2 http://www.jabfm.org
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.
We also calculated crack-years, which roughly
quantied the total amount of exposure to this
behavior. This allowed investigation of a possible
doseresponse relationship between the me-
chanical effects of KC and OA. Again, when
looking at KC of each joint type, we found no
signicant correlation of KC crack-years with
OA in the respective joint.
Our study methodology, though useful to nd
large enough numbers of participants with and
without OA to generate adequate statistical
power, does have limitations. Our sample was
limited to people who presented to a health care
facilitylikely with hand symptomsand who
received a radiograph of their hand. Radio-
graphic diagnosis of OA is preferred over physi-
cal examination because radiograph ndings of-
ten will appear before physical examination
ndings. The time frame of 5 years was some-
what arbitrary but reected a period of time in
which only minor radiographic changes to OA in
the hand joints might occur. We chose the age
range of 50 to 89 years to nd enough patients
with OA and enough people who had been crack-
ing knuckles for many years. Limiting analysis to
only the right hand was also somewhat arbitrary
but was scientically sound because knuckle
cracking is typically a bilateral behavior.
The use of participants who received radio-
graphs of their hand during the last 5 years intro-
duced a selection bias that affects the generalizabil-
ity of our results. This also likely explains the lower
prevalence of KC in our study population (20%)
compared with other studies of less selective pop-
ulations. Prevalence reported in other studies in-
cluded 25% in adults older than 45 years,
5
34% in
11-year-old children,
1
and 54% among nursing
home residents with a mean age of 78 years.
1
The
subset of persons in our study does not accurately
reect the general population, most of which do
not have hand symptoms. However, because both
cohorts in this study met the same inclusion and
exclusion criteria, biases were likely similar in both
and probably will not diminish the usefulness of
differences between the 2 cohorts. Future studies
that randomly select asymptomatic persons for ra-
diographs of the hand would more accurately re-
ect the general population, though this method-
ology would subject large numbers of people to the
risks of radiation.
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 KC because of joint symptoms,
patients with OA in our study started KC 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 KC when hand symptoms
appear either because of fear of what KC might do
to their joints or because KC becomes too uncom-
fortable. These are all factors that were not ac-
counted for in this study but contribute to the
complex nature of this behavior. We did not ascer-
tain if KC was painful, neutral, or even relieved OA
symptoms, so we do not know the reason for the
difference.
What we can conclude, however, is that, in these
cohorts of persons aged 50 to 89 years, a history of
habitual KCincluding the total duration and total
cumulative exposure to KCdoes not seem to be a
risk factor for hand OA.
The authors would like to thank Cara Olsen, Assistant Professor
of Preventive Medicine and Biometrics at Uniformed Services
University; and Roberta Williams, National Capital Area IT
Management Specialist, for their invaluable assistance with data
management.
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