Joint pain and Tenosynovitis

Overview

Joint pain can have multiple causes, a

reflection of the diverse joint diseases
which arise from inflammation, cartilage
degeneration, crystal deposition, infection,
and trauma. The initial aim of the
evaluation of a patient with joint pain is to
localize the source of the joint symptoms
and to determine the type of
pathophysiologic process responsible for
their presence.
The differential diagnoses of joint pain are
generated in large part from the history
and physical examination. [1] Screening
laboratory test results serve primarily to
confirm clinical impressions and can be
misleading if used indiscriminately.

Pathophysiology
Joint pain may arise from structures within
or adjacent to the joint or may be referred
from more distant sites. Sources of pain
within the joint include the joint capsule,
periosteum, ligaments, subchondral bone,
and synovium, but not the articular
cartilage, which lacks nerve endings.
Determination of the anatomic part
responsible for joint pain is often a difficult
task, but it is critical, in that it guides the
approach to diagnosis and therapy.
Knowledge of the anatomy of complex
joints (eg, the knee, shoulder, and ankle)
aids in this assessment.
The evaluation of joint pain, both in terms
of the history and the physical
examination findings, is best achieved
through an understanding of the basic
pathophysiologic types of joint disease.
These include synovitis, enthesopathy,
crystal deposition, infection, and structural
or mechanical derangements. These
types of joint disease are not mutually
exclusive. Examples of pathologic
processes that commonly coexist include
crystal deposition in osteoarthritis,
synovitis in enthesopathies, and cartilage
destruction in chronic synovitis.

Tenosynovitis is inflammation of a tendon

and its sheath (see the image below).
Most acute cases of flexor tenosynovitis
(FT)—which involves disruption of
normal flexor tendon function in the hand
—result from infection. However, FT also
can develop secondary to acute or chronic
inflammation from a noninfectious cause,
such as diabetes, overuse, or arthritis.

Background
De Quervain's tenosynovitis (or de
Quervain tenosynovitis) is caused by
stenosing tenosynovitis of the first dorsal
compartment of the wrist. The first dorsal
compartment at the wrist includes the
tendons of the abductor pollicis longus
(APL) and the extensor pollicis brevis
(EPB). Patients with this condition usually
report pain at the dorsolateral aspect of
the wrist, with referral of pain toward the
thumb and/or the lateral forearm. This
condition responds well to nonsurgical
treatment

Pathophysiology
In the first dorsal compartment of the
wrist, a tendon sheath encloses the
abductor pollicis longus and the extensor
pollicis brevis tendons at the lateral border
of the anatomical snuffbox. Inflammation
at this site commonly is seen in patients
who use their hands and thumbs in a
repetitive fashion. Thus, de Quervain
tenosynovitis can result from cumulative
(repetitive) microtrauma. Inflammation
also may occur after an isolated episode
of acute trauma to the site. [6]
The first dorsal compartment of the wrist
often contains a septum, which can
complicate treatment by making target
structures more difficult to inject. Up to
50% of patients may have first dorsal
compartments with septa. These septa
have an average length of 5 mm. [7]

Epidemiology
Frequency
United States
De Quervain tenosynovitis is relatively
prevalent, especially among individuals
who perform repetitive activities using
their hands (eg, certain assembly line
workers, secretaries). [8]
A randomized study of 300 undergraduate
students showed that those who texted
more mobile phone messages per day
were more likely to have a positive
Finkelstein test (indicative de Quervain
tenosynovitis). The investigators
concluded that students who use their
mobile phones to send more than 50 texts
per day have a higher probability of
developing de Quervain tenosynovitis