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Osteoarthritis

Volume 11, Issue 4

Diagnosing and Managing Hand

Osteoarthritis
Pain and decreased function are the cornerstone of osteoarthritis of the hand (HOA).
An individualized stepped-up approach may have broadest appeal in pain
management of HOA.
CITE THIS ARTICLE
Hegeman T, Goldstein L. Diagnosing and Managing Hand Osteoarthritis. Pract Pain Manag. 2011;11(4).

Oct 21, 2015 Timothy W. Hegeman

Leonard Goldstein, DDS, PhD, Assistant Vice President for Clinical Education
Development

Osteoarthritis (OA) is the most significant cause of musculoskeletal morbidity in the

elderly, and the hand is the most frequently affected area of the body.¹ A study in
the United States found that among people older than 26 years, the prevalence of
radiographic-confirmed osteoarthritis of the hand (HOA) and symptomatic HOA
were 27.2% and 6.8%, respectively.²

The disability of HOA is primarily due to the combined impact of pain and
decreased functionality, which significantly decreases quality of life for those who
suffer from it.³ The small size of the bones and joints in the hand also make it a
unique site for treatment. Current guidelines on the management of HOA are
centered primarily on pain management, as there is a dearth of disease-modifying
medical treatments, and surgical interventions are not as well developed as for OA
of the knee, hip, and shoulder.

This paper aims to review the suspected causes and risk factors of HOA, to outline
the appropriate diagnostic approach for a patient who presents with possible HOA,
and to describe the appropriate management of a patient with HOA.

Evolving Etiology and Risk Factors

Once regarded as simply a “wear and tear” phenomenon, the etiology of OA has
become remarkably complex. No longer thought of as solely a disease of cartilage,
the model for OA development involves the entire joint and includes such
pathological changes as loss of articular cartilage, osteophyte formation at the
joint margins, subchondral bone remodeling with cysts and sclerosis, ligamentous
dysfunction, muscle dysfunction, and synovial inflammation.⁴ Still, the basic
biomechanical premise remains the same—accelerated damage to cartilage leads
to bone-on-bone contact, pain, stiffness, and dysfunction. On the biochemical
nature of the disease, some data posit that inflammatory cytokines play a role in
altering the balance between cartilage buildup and breakdown,⁵ suggesting that a
systemic understanding of OA is also necessary.
A DV E R T I S E M E N T

The pathogenesis of OA is dependent on the age at presentation. In the under-40

age group, for example, OA is almost always associated with some injury to the
affected joint,² suggesting that in this minority of patients, trauma is a key factor in
disease development. In patients older than 40, the pathogenesis appears not to
rely on trauma, although it may be contributory. The most significant risk factor for
HOA, or for OA of any joint, is age. The incidence of OA is greatly increased
between the ages of 40 and 70, after which it seems to return to under-40 levels.
The significance of the 30-year window of increased OA development is unknown,
but it is useful in making a differential diagnosis. Any patient within the 40- to 70-
year-old range or any patient with a history of joint trauma should be regarded as
at risk.⁶

Although not necessary for the development of HOA, some kind of occupational or
recreational history involving repeated hand motions is often present. This
supposed link to the “wear and tear” hypothesis is simply that increased usage
causes a thinning of the cartilage and when that damaged cartilage cannot be
replaced, OA results. The effect of activity on HOA is dose dependent and shows
differential distributions of joints involved depending on the particular repetitive
task.⁷ Patients with a history of repetitive use damage should receive counseling
on how to best care for their joints, and an immobilizing splint should be
considered.
A DV E R T I S E M E N T

Whereas the connection between OA and obesity seems somewhat common

sense in the context of the hip joint or the knee joint, obesity is also a known risk
factor for the development of HOA,⁸ a finding that supports the systemic,
biochemical nature of the disease. Proposed mechanisms focus on the endocrine
function of adipose tissue possibly increasing the systemic levels of adipokines,
such as leptin, and thereby impacting cartilage throughout the body.⁵ Published
evidence from knee OA suggests that body fat percentage, not increased weight
or body mass index (BMI), is the important feature in this relationship.⁹ Weight loss,
when indicated, may be therapeutic in overweight patients with HOA and perhaps
is preventative in those who have not yet developed the disease.

Female sex is a risk factor that is particularly predictive of OA of the hand.¹⁰

Unfortunately, another major cause of hand pain, rheumatoid arthritis (RA), also
has higher prevalence in women. These two entities can be differentiated by a
combination of age of onset, clinical presentation, joints presenting with pain, and
laboratory testing. Family history is a pertinent risk factor,¹¹ although a specific
genetic component has not been identified (see Table 1).
A DV E R T I S E M E N T

Table2.DiagnosisofHOA

• Presentingsymptomatology

• Jointdistribution

• Assessmentofriskfactors

• Assessmentoftreatmentgoals

•
Physicalexam(bonyenlargment,extra-articular
manifestations)

• HandX-rays

Diagnosis

Diagnosis of HOA requires a multifaceted approach, as there is no single test or

finding that holds adequate sensitivity and specificity to make the diagnosis on its
own (see Table 2). The European League Against Rheumatism (EULAR) published a
set of recommendations for the diagnosis of HOA that were developed using a
combined evidence-based and expert consensus methodology.¹² Prior to the
EULAR task force, the best resource for the diagnostic criteria of HOA was the
American College of Rheumatology (ACR) Criteria for the Classification and
Reporting of Osteoarthritis of the Hand (1990).

The first step in diagnosis is comparing a patient’s complaints with the typical
presenting symptomatology. HOA most often presents as hand pain on usage, with
or without mild morning stiffness, affecting one or more joints of the hand. The
distal interphalangeal joint (DIP) is most often involved, followed in order by the
thumb base and proximal interphalangeal joint (PIP). This distribution of joints
involved can be somewhat helpful in differentiating OA from other hand arthroses
(Figure 1), but the specificity of this diagnostic approach is low.
A DV E R T I S E M E N T

Similarly, the presence of Heberden’s or Bouchard’s nodes may aid in the diagnosis
but are not specific enough to be considered as a sole diagnostic marker. Some
degree of functional impairment is to be expected but may be very similar to
impairment seen in RA. An important subset of HOA is that of erosive OA. Patients
with this condition may present with abrupt onset of marked pain, functional
impairment, inflammatory signs and symptoms, and mildly elevated C-reactive
protein (CRP). In general, these patients have a worse outcome and more rapidly
developing symptoms than those with nonerosive OA.

Radiologic evaluation of HOA includes a posterior-anterior x-ray of both hands.

Magnetic resonance imaging (MRI), scintography, and ultrasound have been
evaluated as imaging modalities, but studies have yet to illustrate a true,
reproducible benefit. X-ray indicators of HOA include joint space narrowing,
osteophyte formation, subchondral bone sclerosis, and subchondral cysts. The
correlation between x-ray findings and clinical OA is very weak in the hand, worse
than in the hip or knee. There currently are no recommended interventions for
asymptomatic HOA found incidentally on hand radiography.
A DV E R T I S E M E N T

There is no laboratory test for OA, but there are tests to evaluate alternative
diagnoses. A strongly positive rheumatoid factor, for example, would lead one
away from diagnosing OA. Inflammatory markers are not typically elevated,
although CRP may be slightly above normal in erosive OA, as mentioned above. For
a typical patient presenting with hand pain, the differential diagnoses include HOA,
psoriatic arthritis, RA, and hemochromatosis.

Management of Pain

For the most part, managing HOA means managing the pain and dysfunction
associated with HOA. To date, there is a lack of any drug or intervention that has
been shown to significantly reverse the plethora of typical pathological changes
seen in the course of the disease. Surgical interventions are available as a last-
resort treatment in HOA of the base of the thumb but not at other affected joints of
the hand. That said, because pain and dysfunction are by far the most common
ailments in patients suffering from HOA, treatment of these two facets of the
disease potentially provides vast improvements in patients’ quality of life,
productivity, and satisfaction with medical care.
A DV E R T I S E M E N T

As with all pain management conditions, it is advisable to start with safer

treatments moving on to more powerful options if safe options are ineffective (see
Figure 2).

Non-drug Therapy: The EULAR strongly suggests that treatment of HOA be a

combination of non-drug therapy and drug therapy. Non-drug therapies consist of
patient education on how to avoid over-exerting the joints that are troubling them.
Wrist and thumb braces have shown some effectiveness when combined with
education and are attractive options because of their low risk profile. In one
randomized trial, a full thumb-wrist brace was shown to be significantly more
effective than a half brace.¹³

Acetaminophen: Acetaminophen is considered the first-line drug for OA of all joints

because of its proven effectiveness, impressive safety record, and low cost.
Although it has been used for decades to treat HOA, there are no randomized
controlled trials investigating its effectiveness in this area. Extrapolated results
from OA in other joints suggest that acetaminophen is less effective in decreasing
pain and increasing function than nonsteroidal anti-inflammatory drugs (NSAIDs),
but its safety record and cost are far superior, shifting the risk-reward balance in its
favor. Using acetaminophen minimizes the risk of gastrointestinal (GI) side effects
compared with NSAID use. Evidence strongly suggests that the often quoted
hepatic damage with acetaminophen can be completely avoided simply by staying
under the maximum daily dosage.¹⁴ Reports of renal damage, similarly, are
unsupported by significant evidence.

Topical Treatments: Topical treatments have the advantage of safety. In particular,

topical NSAIDs avoid the GI toxicity associated with oral formulations, and clinical
trial data indicate that their effectiveness is roughly equivalent. Cost can be an
issue with this mode of treatment, as most are still relatively new and are still
unavailable in generic forms. If insurance plans allow them, topical NSAIDs are a
reasonable second step in management if oral acetaminophen proves insufficient.
Topical capsaicin, likewise, lacks systemic side effects and has proven
effectiveness in treating pain. Topical treatment with both capsaicin and NSAIDs
sometimes requires several days or weeks of application before full effectiveness
is achieved.

Oral NSAIDs: Oral NSAIDs should be used as a third-line treatment after failure of
both acetaminophen and topical treatments. Because of high GI toxicity, these
drugs should be used only when absolutely required and for as short a course as
necessary. This toxicity is dose dependent and increases with age, so oral NSAID
therapy should be especially cautioned in elderly patients, and patient education
should stress the importance of using as small a dose as possible. A proton pump
inhibitor (PPI), misoprostol, or an H2 blocker can be added to protect the stomach
lining. A cyclo-oxygenase-2 (COX-2) inhibitor also is an option in patients with GI
risk, as studies have shown it to have gastric safety equivalent to that of NSAID
plus a gastroprotective agent. Importantly, coxibs should be avoided in patients
with significant cardiovascular (CV) risk factors, as they have been shown to
enhance risk for cardiac events.¹⁵ Similarly, recent studies on non-selective NSAIDs
have revealed an increased CV risk.¹⁶ Therefore, even non-selective NSAIDs should
be used with caution in patients with CV risk factors, and the literature on this topic
should be carefully followed for further updates on risk.

SYSADOA: The group of drugs now referred to as symptomatic slow-acting drugs

for osteoarthritis (SYSADOA) includes glucosamine, chondroitin sulfate, avocado
soybean unsaponifiables (ASU), diacerhein, and intra-articular hyaluronan.

A large meta-analysis of glucosamine, chondroitin, and their combination recently

showed no impact on pain or structural OA in the hip and knee.¹⁷ Although this
study did not investigate the effectiveness of these drugs in HOA, extrapolating
the data is not encouraging. None of the other drugs in the SYSADOA category has
been studied as rigorously as glucosamine and chondroitin. A systemic review on
the effects of ASU on knee and hip OA suggest decreased pain and improved
function in the treatment group compared with placebo.¹⁸ Diacerhein has been
shown to have a small effect on decreasing pain and slowing progression in OA of
the hip but also has been shown to be the only SYSADOA with significant side
effects, as it causes diarrhea. There is inadequate evidence to suggest a large
enough benefit to warrant the toleration of this side effect based on the evidence
available today.

Intra-articular hyaluronan has been evaluated in the trapeziometacarpal joint in a

study that found that 5 weekly injections decreased pain by 46% at 5 months post-
treatment.¹⁹ Furthermore, a second trial indicates that hyaluronan injection may be
more effective and longer lived than corticosteroid injection for this joint.²⁰

SYSADOA is a class of drugs with intriguing potential, as they have shown some
very modest ability to modify the structural dysfunction in OA, but the evidence for
their effectiveness in pain management is lacking, and their mechanism of action is
not completely understood. The safety profile and modest findings suggest that
the oral treatments in this group be left to patient discretion, as no side effects
have been noted. Research on utility of hyaluronan injections should be followed,
as its potential for replacing steroid injections is enticing. Finally, diacherin should
not be recommended because of its lack of strong evidence and clear GI side
effects.

Steroids: Expert consensus opinion suggests that intra-articular injection with

long-acting corticosteroids (such as triamcinolone) is effective for flare-ups of
HOA, especially in the trapeziometacarpal joint. No adequately powered
randomized controlled trials have been published to support or refute the validity
of this recommendation. Possible side effects from the injection of corticosteroids
include localized depigmentation and weakening of the ligaments in the area, as
well as known systemic side effects that go along with steroids.

Surgery: Although surgery remains a mainstay treatment for end-stage OA of the

hip and knee, it is uncommonly used in HOA, and evidence for its effectiveness is
lacking. However, for HOA at the base of the thumb, evidence does support
effectiveness of surgical therapy when conventional therapies have failed. These
surgical interventions include trapeziectomy, arthrodesis, osteotomy, ligament
reconstruction, and joint replacement. Surgery for areas other than the thumb base
is not yet widely available as a treatment option.

New treatments: This section very briefly reviews some possible new
pharmacologic approaches to the management of OA yet to gain Food and Drug
Administration approval.

Nerve growth factor (NGF) is a neurotrophin that has been identified as a major
signaling molecule in the sensitization of nociceptors. Tanezumab, a monoclonal
antibody against NGF, is currently under investigation in Phase III clinical trials and
has been shown to significantly decrease OA pain when administered as an IV
infusion every 8 weeks.²¹ Tanezumab also is under review for its effects on low
back pain, pelvic pain, and neuropathic pain.

COX-inhibiting nitric oxide donors (CINODs) represent a potential solution to the GI

and CV toxicity inherent in traditional NSAIDs. The structure of CINODs is that of an
NSAID with a nitric oxide (NO) group covalently bound to it. The NO group is
cleaved when the drugs enter the gut, thereby releasing the free NSAID to act as
anti-inflammatory and analgesic, and the free NO moiety to counter the dangerous
side effects of NSAIDS. In Phase III clinical trials, naproxcinod (the naproxen version
of a CINOD) has shown non-inferiority to naproxen alone in treating knee OA, and
early endoscopy studies show less GI damage.²¹ Furthermore, early data on
CINODs demonstrate a decrease in blood pressure that may ameliorate the
potential cardiovascular side effects inherent in COX inhibition.

Calcitonin is a hormone that participates in calcium and phosphorus metabolism.

When given in pharmacologic doses, salmon calcitonin has been shown to affect
osteoclasts, increase bone formation, inhibit cartilage-degrading
metaloproteinases, and promote cartilage growth. An ongoing Phase III,
randomized, placebo-controlled trial is investigating the effectiveness of salmon
calcitonin in reversing some radiographic, structural changes in OA of the knee.²¹

Conclusion

Osteoarthritis in the hand is an incredibly common disorder in the elderly that can
present in many different ways. Pain management in this setting should be
individualized for specific patients based on the severity of symptoms, their
desired functionality, and their individual risk factors. Treatment goals should be
discussed and agreed on with the patient, as should steps for assessment of
treatment effectiveness.
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This article was originally published August 31, 2011 and most recently updated October 21, 2015.
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