Why haven’t we cured arthritis? - Kaitlyn Sadtler and Heather J. Faust
While regaling you with daring
stories from her youth,
it might be hard to believe your
grandmother used to be a trapeze artist.
However, the bad backs, elbow pain,
and creaky knees so common in older people
is more than just “old age."
In fact, the source of this stiffness
plagues many young people as well.
The culprit is arthritis:
a condition that causes inflammation
and pain in the joints
of over 90 million people
in the U.S. alone.
But are stiff, creaky joints
really inevitable?
What makes arthritis so pervasive,
and why haven’t we found a cure for
this widespread condition?
The first hurdle is that arthritis
is actually a spectrum
of over 100 different arthritic
conditions.
All these conditions share symptoms
of joint pain and inflammation,
but the origin and severity of those
symptoms vary widely.
Even the most common type,
osteoarthritis,
is trickier to prevent than
one might think.
It’s a general misconception that
arthritis is confined to old age.
The origins of osteoarthritis can often
be traced to a patient’s early life,
from any seemingly ordinary joint injury.
Following impact, immune cells rush in
to help clean and repair the damaged site
and begin pumping out enzymes,
including matrix metalloproteinases
and aggrecanases.
These enzymes clear out the damaged
tissue and contribute to inflammation.
But while this rapid swelling helps
protect the joint during recovery,
inadequately healed tissue can cause these
immune cells to overstay their welcome.
The continuing flood of enzymes starts
to degrade the cartilage,
weakening the joint and leading
to arthritis later on.
Not all forms of arthritis can simply
be traced to an old sports injury.
Take rheumatoid arthritis, which
affects 1.3 million U.S. adults.
This condition is actually an
autoimmune disease
in which autoantibodies target
natively produced proteins,
some of which are secreted
by cartilage cells.
We still don’t know what
causes this behavior,
but the result is that the body treats
joint tissue like a foreign invader.
Immune cells infiltrate the joint despite
there being no tissue damage to repair.
This response leads to chronic
inflammation,
which destroys bone and cartilage.
Yet another condition,
spondyloarthritis,
has similarities to both of the
conditions we’ve covered.
Patients experience continuous
inflammation in the joints
and at the sites where ligaments and
tendons attach to bones,
even without any initial injury.
This leads to the flood of enzymes and
degradation seen in osteoarthritis,
but is driven by different inflammatory
proteins called cytokines.
As the enzymes eat away at cartilage,
the body attempts to stabilize smaller
joints by fusing them together.
This process sometimes leads to
outgrowths called bone spurs,
which also cause intense stiffness
and joint pain.
With so many factors causing arthritis,
our current treatments are tailored
to tackle specific symptoms
rather than underlying causes.
These range from promising
MACI techniques,
which harvest cells from small pieces
of cartilage to grow replacement tissue.
To a technique called microfracture,
where surgeons create small
holes in the bone,
allowing bone marrow stem cells to
leak out and form new cartilage.
As a last resort,
people with withered cartilage can
even undergo full joint replacements.
But outside these drastic measures,
the underlying drivers of
autoimmune arthritis
still present a unique
treatment challenge.
Scientists are making progress with
therapies that block TNF-alpha,
one of the primary proteins causing
inflammation in rheumatoid arthritis.
But even this approach only treats the
symptoms of the condition, not the cause.
In the meantime, some of our best defenses
against arthritis are lifestyle choices:
maintaining a healthy weight to
take pressure off joints,
low-impact exercises like yoga or cycling,
and avoiding smoking.
These arthritis-fighting behaviors
can help us lead longer lives
as we continue to research
cures and treatments
for the huge diversity of
arthritic conditions.
