This is a review from the first half of the 20th century about literature related tot he etiology of fibrositis (an old name for back mice).
The author deals with different factors that have been related to fibrositis by several authors.
Related factors: sedimentation rate, focal sepsis, diet and intestinal symptoms, vascular disturbances, pain substances, acid uric, epidemic viruses, panniculitis, nodules, postural stresses, psychological components. (Personal note: he just announces them, in a certain chaotic way. It is true that it is an extensive review which contributes many references from that period, which may be interesting, but it does not facilitate a clear picture about the entity itself).
He just presents a short summary with his own conclusions about factors related to the etiology of fibrositis (after performing the extensive review):
-He recommends the Bath Spa Hospital classification of fibrositis.
-He states that there is NOT any laboratory test value in fibrositis.
-He mentions that “epidemic myalgia” appears to be a separate entity.
-Subcutaneous fibrositis differs from panniculitis.
-He discusses the pathology of fibrositic nodules, especially Copeman’s works (Valentine does not give a clear conclusion).
-He considers the role of the PERIPHERAL VASCULAR SYSTEM to be important.
-He exposes theories about the causation: bacterial toxins, metabolites, postural or occupational stresses and psychological factors.
“HE CONSIDERS FIBROSITIS a TISSUE REACTION of varying pathology and of several CAUSAL factors”.
The author did not publish anything else related to fibrositis.
Etiology of Fibrositis: a Review
By Max Valentine
Published in the Ann Rheum Dis
Free on line article PUBMED LINK
Valentine considered the Bath fibrositis classification to be the most valuable, the National Mineral Water Hospital Bath 1940 classification.
It divided FIBROSITIS as follows:
- intramuscular
- periarticular
- bursal and tenosynovial
- subcutaneous
- perineuritic (brachial, sciatic…)
He mentions other classifications:
- Devonshire Royal Hospital, Buxton, 1940
- Ministry of Health report, 1924
- Herrogate Royal Bath Hospital report, 1940
- Ray, 1934
- Comroe, 1941
- Patterson, 1938
Laboratory test findings in fibrositis
NO BIOCHEMICAL ABNORMALITIES have been demonstrated in fibrositis.
Some authors said that the sedimentation rate may be normal or slightly increased.
Case analysis findings in fibrositis
-Several reports from hospitals found an incidence of fibrositis (from 22 to 52%),
for example, in 1943 an incidence of 31% at a Spa Hospital:
- More common between 40 and 60 years old.
- Among the under forties it was commoner in females.
- There was a familial tendency to “rheumatism” in 23% of cases.
OTHER RELATED AND DISCUSSED findings, factors related to the etiology of fibrositis
1-FOCAL SEPSIS relation. Bacteriological theories controversy
Some authors like Lewellyn and Jones (1915) concluded that there were primary and secondary factors in production of fibrositis. The primary cause being by a BACTERIAL or AUTO-INTOXICATIVE cause. They alleged that most fibrositic subjects suffer from a focal sepsis (mainly septic teeth) and some improve dramatically after this focal sepsis has been eradicated.
Many authors questioned the WIDELY-ACCEPTED relation between dental sepsis and rheumatic disease: Valentine explains that the theory that the majority of fibrositic subjects suffer from FOCAL SEPSIS DID NOT MEET BY THEN GENERAL AGREEMENT. He refers that many authors DID NOT AGREE with the “treatments” that were used based on that theory.
2-INTESTINAL relation. Theories about hypersensitivity to diet or associated intestinal symptoms
Thomson and Gordon (1926) had the theory that strain or chill would be a contributory cause, but a toxin derived from the colon or a focal sepsis was the essential causative agent. They noticed that the fibrositic subjects are particularly liable to gastro-intestinal disorders.
LLewellyn (1927) related one case of LUMBAGO for the hypersensitivity to certain protein food.
3-THYROID relation. Hypothyroidism
In general, there is little evidence of relation, despite some authors related it to hypothyroidism.
4-DRAINAGE relation. Vascular deficiency and metabolites
In early works (1933), Copeman mentioned the poor adaptability of the skin capillaries to changing atmospheric conditions, with secondary accumulation of metabolites and effusion of serum.
Ray (1936) also mentions capillary stasis like Gordon (1936) that expressed inefficient circulation and metabolites tendency to collect in fibrous tissue.
5-PAIN SUBSTANCES relation. Physiological reports
Lewis (1932) related the pain with what he called the P-factor. The P-factor seems to depend on the state of the local circulation, if the ischemic muscles are exercised, pain is produced. The pain remains constant if the exercise is stopped, but pain disappears rapidly when circulation is restored.
Kellgren (1939) reported that the pain depends on the DEPTH at which the tissue is stimulated rather than on the nature of the tissue.
In general, there are no evidences with alteration with lactic acid.
6-URIC ACID relation. Gouty alterations.
Like Buckley (1940), some authors related fibrositis to increased blood uric acid.
7-VIRUS INFECTION relation. Myalgia and epidemic myalgia.
Some authors related the fibrositic pain after exposure to certain viral infections, even sometimes it presented in an epidemic way.
8-PANNICULITIS relation. Subcutaneous fibrositis.
Some authors relate certain subcutaneous superficial tenderness with the panniculitis like Dercum’s disease.
9-NODULES relation. The fibrositic nodule
“The fibrositic nodule is by no means universally recognized to EXIST” Valentine
-Stockman (1920) described it as: an inflammatory hyperplasia of connective tissue in patches, containing numerous fibroblasts and SERO-FIBRINOUS EXUDATE, it is swollen, painful and tender, tends to contract and can be massaged away.
-Gordon (1940) said: “the nodule is the hallmark of the fibrositic subject but the tombstone of the fibrositic attack”.
-Copeman (1943) said that: chill, trauma and focal sepsis may reactivate nodules that have lain dormant since their inception during previous acute infections.
-Collins (1940) described: fatty nodules that many considered “typical fibrositic nodules” and that have been proved to be FATTY MASSES (similar to the ones of panniculitis by Stockman).
-Copeman and Ackerman (1944) describe: edematous fatty lobules whose removal resulted in the cure of painful low back pain.
–Copeman and Pugh (1945) demonstrated: NODULAR FATTY LOBULES enclosed within fibrous walls in the subcutaneous tissues, which constituted trigger points for fibrositic pain. These “fat-herniae” structures are liable to present “non-inflammatory edema with the production of pain and tenderness (that’s why they test the dehydration therapy)
Llewellyn and Jones (1915) described certain areas of muscular spasm: commonly trapezius, latissimus dorsi, and sacroespinalis. Copeman and Pugh related this to the irritation process localized outside the muscle.
10-POSITION AND OCCUPATION relation. Postural and occupational stresses
-Seze (1939) considered that the sciatic pain is mainly caused by discogenetic disease of the space between the fourth and the fifth lumbar vertebrae, brought about by deficient musculature of the abdominal wall consequent upon man’s assumption of the erect posture.
-Weil (1939) thought that continued strain, indicated by the word “microtraumatism”, is the main cause of fibrositis. He postulates individual predisposition of endocrine or sympathetico-vascular type, accompanied by abnormalities in the blood chemistry.
-Many authors relate local fibrositis with the occupation activities, by causing postures favoring fibrositis.
11-Psychological factors relation
–Gordon 1940 distinguished 3 varieties of psychological components related to fibrositis.
-Lindstedt (1938) stated that there was a depressive and psychoneurotic disposition in most cases of sciatica. He also considered that the Lasegue’s sign was the result of stretching the tender muscles and not from the neuritis.
12-VESSELS relation. The peripheral vascular system
Pemberton and Pierce (1935) found dysfunction of the smaller vessels of the skin in arthritis. They also point out vascular abnormalities in muscular rheumatism.
Valentine (1943, referring to his own thesis) himself says that the vessels show to be narrow, spastic and closed all together. He also noticed a phenomenon of RED FLARE similar to one that is produced by histamine after pressuring over the tender areas, the phenomenon is not to the same extent over the unaffected areas. Some authors also studied this relation with histamine.
They also relate fibrositis with low blood pressure.
They also hypothesize that the same vessel affection that occurs in the fibrous tissue could also occur across the bone tissue and could cause osteophytes.
Published in October 2018 By Marta Cañis Parera 
Reference of the article
1947 M. Valentine. Aetiology of Fibrositis: A review. Ann Rheum Dis. 1947; 6 (4): 241-250.