One would be mistaken by thinking the name of a condition determines whether the biology has been fully established or not. For instance, Guillain–Barré syndrome, is still known as this, even though the biology is well known.
Fibromyalgia is a clearly recognised clinical syndrome for which the pathophysiology is gradually unravelling. Patients start out with normal pain perception, and move to a state of hightened pain perception along with a host of other changes. This may or may not respond to the usual treatment of aerobic exercise and cognitive based therapies, with so far, little good evidence for response to pharmacological agents ( though Naltrexone looks promising ).
Although the pathogenesis of fibromyalgia is not completely
understood, research shows biochemical, metabolic, and
immunoregulatory abnormalities. These substantiate the proposal that
fibromyalgia can no longer be considered a subjective pain condition. 
There are a number of biological changes that can be detected:
The important biologic elements here include proinflammatory
cytokines, the HPA axis, other neuroendocrine axes, and the autonomic
nervous system. Growth hormone abnormalities are also thought to
contribute to symptoms in fibromyalgia. 
There appears to be a genetic basis for fibromyalgia:
High-throughput genotyping is rapidly identifying a series of
single-nucleotide polymorphism (SNP) haplotypes that influence
neurotransmitter levels and receptor levels in the brain and thus
contribute to the various abnormalities in pain processing. Such
SNP haplotypes constitute vulnerability elements in the development of
fibromyalgia and other central sensitivity syndromes. 
A recent study using Resting-state functional-connectivity MRI is also interesting showing network disruption in CNS processing 
The study included 18 patients with fibromyalgia and 18 healthy
individuals matched for age. They evaluated resting (intrinsic)
connectivity in 3 brain networks: (1) the default mode network (DMN),
which is most active at rest and is deactivated during performance of
externally focused tasks; (2) the executive attention network (EAN),
involved with cognitive processing of memory and attention; and (3)
the medial visual network, which served as a control and is involved
in processing visual information.
Fibromyalgia patients had greater connectivity within the DMN and
right EAN and greater connectivity between the DMN and the insular
cortex, a region of the brain that processes evoked pain. In addition,
they found a direct link to ratings of self-reported spontaneous pain
at the time of the scan and the extent of both right EAN and DMN
connectivity to the insula.
According to the researchers, the findings "strongly implicate the
insular cortex as being a key node in the elevated intrinsic
connectivity in patients with fibromyalgia."
"The results of this study provide direct evidence of disrupted
intrinsic connectivity within multiple brain networks in patients with
fibromyalgia," Dr. Napadow and colleagues conclude. Their approach
"represents a novel step forward in finding the neural correlates of
spontaneous clinical pain," they add.
I think the difference between a disease and syndrome is often semantic, and doesn't contribute to management or understanding.