RAREFYING OSTEITIS. OSTEOPOROSIS. OSTEO-MALACIA OF THE HORSE. BIG HEAD.

Definition. Distinction from rachitis. Process of rarefaction, cell

proliferation, congestion, solution of earthy salts and fibrous

matrix, osteoclasts, Howship’s lacunæ. Dried bone light, spongy,

friable, though enlarged in repaired cases, dense, heavy. Face

lesions. Dyspnœa. Dropping teeth. Causes: microbian hypothesis,

disturbance of bone nutrition, faulty food, lack of bone salts, cellar

stables, floor on ground, malaria, cold, damp soils, city life, early

life, breed, asses and mules, breeding. Nature. Symptoms: illness,

inappetence, lifelessness, early fatigue and perspiration, stiffness,

lameness, distortions, stumbling, knuckling, arthritis, tender puffed

joints, thickened softened bones, facial swellings, narrowing of

intermaxillary space, chisel teeth, difficult mastication, shedding

teeth, emaciation, marasmus. Phosphates in urine when disease is

active. Relation to exostosis. Prevention and treatment. Hygienic,

move from cellar stable, or ground floor, secure air space under

floor, ventilation, warmth, sunshine, grain feeding, pasture, change

food, rest, salicylates, salicin, salol, phenacetin, blisters,

phosphates, bone dust, phosphorus, bitters, iron, barium chloride.

_Definition._ A form of osteo-malacia occurring in the mature as well as

in the growing horse, characterized by the absorption of earthy salts

from the walls of the cancelli and Haversian canals with excessive

production of the organic basis and cell elements and enlargement,

softening, lightness and fragility of the bones.

It differs from rachitis essentially in this that while the latter

attacks the young growing bone at the chief seats of growth, under the

periosteum and in the epiphyseal ligament, and therefore especially on

the surface of the true bony tissue, osteoporosis attacks the formed and

often the mature bone in its interior, producing attenuation of the

walls of its vascular canals and cancellar cavities and increase of

their fibro-cellular contents. Both result in enlargement of the bone,

but in rachitis this is determined largely by deposition on the surface

while in osteoporosis it takes place by expansion from within. The

further distinction that rachitis appears enzootically and osteoporosis

sporadically applies only to localities in which the latter is not

common. At different points on Long Island, in New Jersey and on the

rich soils in the Mississippi valley and on the Atlantic and Gulf

coasts, osteoporosis often prevails enzootically and has its

recrudescences like rachitis.

The process of rarefaction and softening may be thus stated. In the

Haversian canals and narrow spaces there is an active proliferation of

cells and increase of vascularity, with a gradual solution and removal,

not only of the earthy salts, but also of the fibrous matrix in the

walls of these spaces. As in the normal changes in bone, the absorption

appears to be effected through the large cells or osteoclasts grouped

around the blood vessels. In the osseous tissue, which abuts on the

vascular tissue, are to be found excavations, simple or irregular,

(Howship’s lacunæ), containing granular cells and the larger

osteoclasts. In a similar manner bone is softened and absorbed in

connection with tubercle, or the pressure of tumors, aneurisms,

actinomycosis. In case of recovery, repair takes place by the

disposition of new bone, so that the enlarged and rarefied bone may in

the end become harder than before. This applies especially to the

cancellated bone. On the articular ends of the affected bones, the

granulation tissue makes its way into and through the cartilage of

incrustation with resulting active disease of the joint.

The condition of the bone is well illustrated in the dried or macerated

specimen. Taken from a bad case in the active stage of the disease, it

crumbles under pressure and weighs as light as a sponge, whilst from an

advanced or recovered case, it is hard and resistant, and weighs as much

more than the normal bone as it exceeds it in bulk. The morbid

rarefaction usually affects the whole skeleton more or less, yet in

perhaps the majority of cases; the change is greatest in the bones of

the face, and the resulting distortions are usually symmetrical on the

two sides. It may show mainly in the maxilla, which is thickened to

twice or even five times its normal thickness, it may show in rounded,

general swelling of the nasal and superior maxillary bones and those

around the orbit, or it may involve the turbinated bones, the vomer and

even the cartilaginous nasal septum. Loosening and evulsion of the molar

teeth is common and snuffling breathing may occur as in rachitis

affecting the nasal bones of dogs and swine.

_Causes._ We are still in the dark as to the essential cause of

rarefaction of bone. There is a growing tendency to suspect a microbian

origin, and many facts are held to point in that direction. It seems to

have been unknown in England in the early part of the 19th century, and

is not noticed by Blaine, Youatt, Percivall nor other of the early

writers. In Varnell’s cases the same man had two farms not far apart and

equal in soil, drainage and stabling, stocked with horses bred from the

same parents with the same kind and amount of feed and work, yet on one

farm six cases of osteoporosis occurred, and on the other not a single

case. McNeil, in charge of street car stables, found the disease

destructively prevalent in the best appointed stables and absent from

others in the worst hygienic condition. In a superior stable with 220

horses he had 47 cases in two years, and in a fine stable with 100

horses he had 26 cases in the same length of time. In the poorer

stables, the horses bred in the same way on all kinds of soils and with

no difference in feeding nor management escaped. It is the common

experience in Europe and America that a farm or district, which has been

previously free from the disease suddenly has an outbreak in enzootic

form, and this will last for a year or two, then remit only to appear

with its old force after an interval of some years. Even during the

active prevalence of the disease on one or on several adjacent farms,

others in the immediate vicinity, and differing in no appreciable way,

geologically, hydrostatically, in buildings, food, water, general

management nor work, completely escape. Berus, Hoskins and other city

veterinarians have noticed, that it was almost the rule, that a fresh

horse put in the stall of one that had suffered from osteoporosis soon

contracted the disease.

W. L. Williams noticed on two different farms in Central Illinois, on

which the disease suddenly appeared, that for years after the

comparative subsidence of the affection there was an unusual prevalence

of spavins, splints, ringbones and other diseases of the bones. Meyer

has noticed that cases sent from Cincinnati into the country, and that

have got well, will succumb to the affection if brought back into the

city stables in which they originally contracted it.

All of this points very strongly to one of two things; either a

pathogenic germ in the system of the affected animal; or the presence of

a pathogenic microbe in the stable, water, or other part of the

environment, the toxic products of which are taken into the animal

system.

But as yet no specific pathogenic microbe has been demonstrated so that

this doctrine must still be held as a mere plausible hypothesis.

Many veterinarians with long experience in such cases absolutely deny

contagion. The hypothetical contagion undoubtedly extends slowly, and

uncertainly from animal to animal, probably, like actinomycosis, taking

place mainly through the soil, or some outside medium, rather than by

direct contact; or a special susceptibility on the part of the

individual animal may be necessary to render it effectual.

_Accessory Causes_ can be spoken of more confidently but even of these

no one, nor small group, can be advanced as essential. The process of

bone nutrition is readily disturbed by a variety of conditions, and such

disturbances may easily become the occasion of weakening the resisting

power and mayhap of admitting the hypothetical microbe to get in its

pathogenic work.

_Faulty food_ has been a favorite explanation. A lack of lime in the

soil and fodder seems, at times, to have had a baneful effect, if only,

in lowering the general tone and impairing the nutrition. Yet we see

osteoporosis on limestone soils (New York, etc.), and in animals

generously fed on grain. The same remarks apply to phosphorus and

phosphates. Their deficiency apparently contributes to the production of

the disease, and yet under other conditions, their abundance is no

barrier to its development. The excess of free phosphorus produces

osteitis and it is held by some that an over-abundance of phosphates

acts in the same way. It has been sought to incriminate a too

nitrogenous diet in some cases, and in others one too rich in fat or

carbohydrates. The many cases in Philadelphia and Pennsylvania were

mostly in animals that had been well fed and were in good condition when

attacked (Marshall).

Special food may be the direct cause, bran diet has been already noted.

Hinebauch found an acute osteitis with bone softening and arthritis in

horses fed on millet, green, partially matured and ripe. Horses

elsewhere have fed on millet, without such results, but not perhaps, in

the same environment, nor in presence of the hypothetical microbe.

Millet is not the sole nor common cause of osteoporosis, but there is

reason to suspect that it is at times an important accessory cause.

Of all prejudicial conditions none is to be so dreaded as _unwholesome

stables_. Of 200 cases reported by Berus, in Brooklyn, almost all were

in cellar stables or those with floors laid on the soil. Meyer finds

that “most all cases can be traced to an unwholesome atmosphere, or

gases arising from vaults, sewers, cellars, filthy streams, or from a

hollow space under the floor.” Harbaugh says every case was stabled in

damp, ill-drained, unventilated and badly lighted buildings. The worst

outbreak was in a basement with a damp wall, on one side, and none

suffered except those that stood next to this wall. The horses standing

on the opposite side, which was on a level with the ground outside,

escaped. Removal from a cellar stable to the floor above, put a sudden

stop to the appearance of new cases. James, of St. Louis, found 20

successive cases in a stable on a dirt floor, and Jasme, of Charlestown,

finds nearly all his many cases on earth floors in malarial regions.

_Malaria_ has been blamed, especially by southern observers, accustomed

to see the disease on the warm alluvial seaboard and river bottoms. That

this environment predisposes to the disease, by undermining the health,

is doubtless the case, but in spite of occasional remissions in the

symptoms, malarial germs cannot be set down as the constant cause. One

of the worst cases I ever saw, with every bone in the body soft, spongy

and light, developed at Inglis Green laundry, Edinburgh, where malaria

is absolutely unknown, but where the brook received large quantities of

chlorine.

_Cold_ is an undoubted factor, though the disease is most prevalent in

our warm southern states. Many veterinarians have noticed its

coincidence with rheumatism, in which cold is so often the dominating

accessory cause. Some have even suspected that it is only a modified

type of the rheumatic condition. Hinebauch found his cases of _millet

disease_ in cold basement barns, or with leaking roofs, so that the

floor and bedding were constantly wet. He found that cold always

aggravated the disease, and bad air even more so, while salicylates

seemed to have a marked curative influence.

_Damp soils_ should be named in this connection. These not only chill

the air by evaporation, and condense the cold dews at night,

contributing to produce the extremes of hot noon day and cold night

temperature, with corresponding disturbances of the bodily health, but

they favor the preservation of the infinitesimal forms of life

(bacteria, protozoa) and therefore of the hypothetical microbe of the

disease.

_City life_ is a most potent cause. Berus tells us that hundreds of

horses die yearly in Brooklyn of osteoporosis, and that if sent early to

the country a large proportion recover. The same is true of New York

City and Philadelphia. Of Cincinnati, Meyer says that he has failed to

find a case more than five miles outside the city limits, and that cases

sent to the country make a partial or complete recovery. If returned to

their former city stables, nearly all contract the disease anew within a

year.

Many cases, however, are found in the country and often within a

circumscribed area. These indicate, as in the city cases, a localized

cause, bacteridian or otherwise.

_Early life_ predisposes, the majority of cases taking place before the

sixth or seventh year, yet the disease occurs at all ages up to twenty

years and over.

_Breed_ does not seem to make a material difference, and though Shetland

ponies have acquired a bad reputation, their propensity to become fat

and soft, their too often idle, pampered life, and the confined quarters

in which they are frequently kept, account for much of the mortality.

_Asses and mules_ habitually escape, even in the South, where the latter

animal is so numerous and often so poorly kept. In Hinbauch’s millet

disease, the mules suffered more than the horses.

_Breeding horses_, male and female, have often acute attacks and die

early. The drain on the system and confinement seem to act injuriously.

_Nature._ Until we know the essential cause or causes of osteoporosis,

we must be in doubt as to its pathology. We are even debarred from

pronouncing authoritatively upon the essential identity or difference of

the various forms of softening, or rarefaction of bone. In obedience to

the clinical manifestations and structural changes, rachitis, fragilitas

ossium and osteoporosis have been separately described, but we cannot

positively say that they are not all due to one essential cause,

manifesting itself differently according to the activity of trophic

processes in the bones of the victim. In the growing foal the active

developmental processes in the epiphyseal ligament and periosteum may

determine that the symptoms shall be pre-eminently those of rickets, yet

we often see these complicated by the facial and other lesions of

osteoporosis. Both may be the result of one etiological factor, or there

may be a complex disease resulting from the presence of two. Again in

the pregnant cow in which the relaxation of the ischio-pubic symphysis

and pelvic ligaments means a profound change in the bone nutrition at

this point, the presence of the hypothetic microbe, or other essential

factor, may determine a decalcifying and fragility of the pelvic bones

generally. Again in the mature male and non-breeding female, in the

absence of the disturbing conditions of nutrition just named, the

vascular elements in the Haversian canals and cancelli may determine the

simple rarefaction and expansion of the bone which characterizes

osteoporosis. When present in the bone in any of these conditions, acids

doubtless fulfill an important rôle in the decalcifying and softening

process, but behind these it may be surmised that there is an unknown

cause or causes, which it is for the bacteriologist, chemist or botanist

to discover.

_Symptoms._ These are largely the same as in brain disease. There may be

first a period of illness, with poor appetite, lack of spirit and

energy, early perspiration and fatigue, or if at large, leaving the

herd, soon followed by some stiffness of gait and lameness, which may be

intermittent, disappearing under exertion, or shifting from one joint or

limb to another after the manner of rheumatism. Sometimes it shows in

stiffness of the neck, so that the patient finds difficulty in lowering

the head to graze; in others the back and loins are stiff and arched so

that the animal has difficulty in rising and turns slowly and painfully;

in still other cases the dorsal and lumbar vertebræ are depressed so

that the back is hollow. Even before the manifestation of lameness, the

affected limb may stand forward at the fetlock or knee, the gait is

clumsy and awkward, and the patient may suddenly stumble and fall,

showing little or no power of prompt recovery of balance. A horse, and

especially a young horse, with this habit of stumbling is always to be

suspected. The long bones of the limbs tend to enlarge or thicken, and

this is likely to be more uniform than in rachitis, and not to be

confined so much to the epiphysis. The implication of the stifle, hock

or other joint, with marked synovial distention, and mobility or

dislocation of the patella, is common and may be the earliest

manifestation of illness. The bones of the face usually show early

changes. The superior maxillary and nasal bones, beneath the zygomatic

spine and infra-orbital foramen and along the line of the molar alveoli

become especially bulging and rounded, the other facial and cranial

bones suffering to a lesser degree. In the lower jaw, also, the disease

predominates along the region of the molar alveoli, and the loosening of

the molars permits them to deviate inward so that the grinding surfaces

come perceptibly nearer to the median line, and the outer half of the

tooth is rapidly worn while the inner edge projects as a sharp cutting

ridge (chisel teeth).

For the same reason, the softening branches of the lower jaw deviate

inward, tending to still further destroy the due approximation of the

upper with the lower molars, and to diminish the breadth of the

intermaxillary space. The great thickening of the rami of the maxilla

tends still further to reduce the intermaxillary furrow.

Fractures and detachment of tendons and ligaments are common results of

the rarefaction, a portion of the bone often remaining adherent to the

tendon.

Cary gives the following statistics of fifteen cases: lame in the fore

limbs 11 (mostly shoulder), in hind limbs 11 (mostly hip and stifle),

stiff in loins 8, unable to rise without aid 3, had indented ribs 4, had

shifting lameness 8, had chronic indigestion 6; mares 5; geldings 8;

mules 2; ages were—_one_ 3 years, _five_ 6 years, _three_ 7 years, _one_

8 years, _two_ 9 years and _three_ 10 years.

When the bones are enlarged their softness and friability may be shown

by pricking with a needle, which will often freely penetrate the

rarefied bony tissue. It should be first rendered antiseptic by dipping

in strong carbolic acid.

From the first the general health fails, there is difficulty in

mastication, digestion is more or less impaired, nutrition is imperfect

and muscular flabbiness, weakness and wasting advance more or less

rapidly. In advanced cases emaciation is often a marked feature.

Examination of the urine gives valuable indications, though the results

obtained have been supposed to be contradictory. While rarefaction of

the bone is advancing rapidly the urine is charged with an excess of

phosphates in ratio with the activity of the morbid process. When on the

other hand the disease has come to a standstill and the process of

repair in the rarefied bones has begun, the absence of phosphates is no

less characteristic. A patient therefore may show greatly enlarged and

softened bones with persistent lameness, and yet the urine may show

little or no phosphate. The phosphaturia may, therefore, be made the

basis of a reasonable prognosis. Excess of phosphates indicates an

active pathological process, with an uncertain outcome, while the

absence of phosphates indicates an arrest of rarefaction and holds out

good hope of recovery.

I have long observed the same in cases of obstinate and intractable

spavins, splints, ringbones and other bone diseases. Phosphaturia

bespeaks a faulty nutrition of the bone and explains the failure of

remedial measures, while lack of phosphates in the urine, or a reduction

to the normal amount is likely to become a guarantee of improvement

under local treatment. The treatment however, must be first

constitutional to correct the condition of malnutrition and then local

to correct the osteitis.

_Prevention and treatment._ As in rachitis hygienic measures give the

most uniformly good results. The change of stable is especially demanded

from a cellar or basement stable, one with joists laid on the ground or

one with an earth floor saturated with urinary and feculent products. In

different cases an enzootic has been arrested, coincidently with the

removal of the stock to the floor above, and in others with the removal

of the filth saturated earth beneath a ground floor, and the laying of a

new floor with ample space beneath for the free circulation of air. In

the same line would be thorough drainage of the site and to carry off

liquid manure to a well ventilated receptacle. Exposure to cold and wet

is to be sedulously avoided as greatly favoring the onset of the

disease, and hurrying the milder cases into a fatal activity. Free air

and sunshine are all important and it is the universal experience that

city cases taken early and sent to dry, sunny pastures, mostly recover,

or at least undergo marked amelioration. The fact that certain cases

originate during an open air life does not invalidate this position but

merely shows that other pathogenic conditions may be too potent to be

overcome by this hygienic one.

A liberal allowance of sound grain is essential to success, even in the

case of patients sent to pasture. Those that have recovered or improved

at pasture, should be retained in the country and on no account returned

to the same city stables in which they contracted the disease. Even in

the country a different stable should be secured if possible.

Any food that has manifestly contributed to the disease, should be

withheld (bran, millet, musty or fermented food or that drawn from

particular fields).

Overwork must be forbidden, and indeed any work at all during the active

stage of the disease. The victim should also be withdrawn from breeding,

at least until it has fully recovered the normal consistency of its

bone.

In cases aggravated by cold or wet, or which show the rheumatic

propensity to shift from place to place, sodium salicylate in ounce

doses several times a day may appear to benefit, and as a germicide this

may be tried on all cases. Salicin, salol, or phenacetin may be used as

substitutes. Where the disease has been largely localized, blisters have

appeared to be beneficial.

Phosphates and phosphorus have been lauded by German veterinarians, but

in other hands, and when the morbid process was active they have proved

useless, or even hurtful. Bone dust or phosphate of lime or soda may be

freely used at any time and appears to act as a general tonic, beside

supplying lime and phosphoric acid which may possibly be availed of for

bone nutrition. Phosphorus and phosphorated oil in excess always softens

the bone and much more so when this process is already excessive. In

small doses (gr. ⅙ to ½) and after the process of rarefaction has

ceased, it is valuable in hastening bone consolidation and fitting the

patient to return to work.

Bitters, iron and other tonics are valuable in improving the general

tone and indirectly the bone nutrition.

Cary had prompt improvement in connection with intravenous injection of

barium chloride once a week for four weeks, and ½ oz. doses of sodium

salicylate thrice a day. It remains to be seen whether or not this is

generally applicable.

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