All findings in fatteners with impaired moving activity in this farm led to the assumption, that M. hyosynoviae as an infectious factor was involved in disease pathogenesis in combination with osteochondropathy. Since degenerative joint diseases, such as OC, are important predisposing factors in M. hyosynoviae disease [20], other aetiological cartilage pre-damages might also contribute to the adhesion of M. hyosynoviae. In puppies the negative impact of an undersupply with P onto the musculoskeletal system has been described. Affected puppies showed a loss of muscle strength, deviation of the limb axis and hyperflexion of joints, indicating the demand of P also for the connective tissue [21]. Several studies have shown that P-reduced feeding can cause degenerative but also other pathological skeleton alterations. It is known, that embedding of bone mineral elements in later life in mammals depends on the supply in the early stages of growth and bone development [19]. During skeletal development growth cartilage in the plate of the physis is responsible for longitudinal growth, while the articular–epiphyseal cartilage is shaping the long bone ends. Within a sequential progress including matrix mineralization enchondral ossification is achieved by parallel continuous production of cartilage and its replacement by bone [22]. The rate and direction of growth is assumed to be affected also by nutritional and metabolic factors [22].
In this case the result of bone marker determination hinted at a potential insufficient mineral supply. Serum osteocalcine has been found to be a more accurate indicator of bone mineralization in pigs than alkaline phosphatase in serum [23]. Disadvantages are that osteocalcine is relatively unstable and serum samples should therefore be processed and frozen within one hour after collection. Suppressive effects might occur, when the animal is pretreated with corticosteroids [24]. Results from the one pooled sample analysed in this study might suggest, that bone formation with respect to accretion of minerals is reduced. Since diagnostic imaging or invasive procedures such as a bone biopsy are still difficult to perform in swine, diagnostic methods easy to implement and providing meaningful results are of high practical impact. While it is usually not feasible to perform radiography in several pigs of a herd, taking several blood samples and pooling them for bone marker analysis is much more practical.
Nevertheless, the hypothesis of an additional nutritional impact on disease development could not be supported by bone composition and blood parameters in this case. Bone ashing in pigs is a further diagnostic approach to verify the suspicion of impaired mineralization of bone. Standardization of the method has been improved in the recent years, so that preliminary reference values could be elaborated for the femur [25]. Of high importance is the removal of adjacent tissue from the bone before starting the diagnostic procedure. Ca and P contents in dry matter of bone ash were within the reference ranges [25]. Bone ash diagnostic is of value for diagnostic of long-lasting marginal supply with minerals, which was not the case in this study. In growth periods with insufficient Ca and P supply, at first bone mass in total will be reduced, while bone formation and composition itself will be preserved, resulting in a lower ratio of the diameter of the long bones to body mass [25]. This might finally result in higher pressure forces (N/cm2) onto the articular cartilage especially in pigs with high growth rates.
Blood parameters shown in Table 5 vary within the reference range. A hypothesised low dietary P intake would be reflected by low P concentrations in blood as shown in Table 6 with data recorded in a feeding experiment [25]. A comparison of P concentrations in blood of case animals (Table 5) with these experimental data revealed, that P concentrations in blood can be assessed as high. Blood concentrations reflect only the current P supply and are of diagnostic value for acute P deficiency.
For this reason, analysis of diet composition and feeding anamnesis are fundamental in the diagnostic procedure. The authors assume, that a marginal mineral supply during a specific iuvenile phase of life with high growth rates might predispose for disease development in later life. In individuals with high growth rates (900–1000 g average daily weight gain) the uptake of digestible P might have been insufficient at the end of nursery/beginning of fattening, also with a high P digestibility of 60% as shown in Table 2. These pigs would be undersupplied with only 4.6 g P/kg in the respective diets (Table 1), especially in the case that feed processing as pelletizing or granulating had reduced phytase activity. To diagnose a marginal mineral supply in critical growth phases, the demand of the pigs with respect to feed intake and growth rate must be calculated. Different batches of compound feed vary in P and Ca concentrations, which can lead to deficiencies especially if original concentrations are low. Labelled diet compositions are only based onto an analysis in the first charge. In general, digestibility of dietary P is markedly improved by a fermentation of the liquid diet (for about 24 h) prior to its offer and by adding phytase to the compound feed [26–28]. Both strategies were realised in the study farm.
The primary hypothesis was, that the development of the disease was a multifactorial process starting with an impaired bone mineralization. Mineral deficiency osteopathy, caused by inadequate P or insufficient P availability in the diet, might trigger development of osteochondropathy of the joints [29]. But there were also studies which could not indicate hypophosphatemia as an etiological factor in the development of OC [30]. Next to hereditary factors rapid growth with early excess weight is a major risk for dyschondroplasia in physeal and epiphyseal locations [31, 32], which is accompanied by a premature regression of blood supply. Microscopic focal lesions or necrotic chondrocytes below the interface of articular or within the epiphyseal growth cartilage, which were replaced by fibrous connective tissue, can undergo calcification. Lesion development can already start in the age of 4 weeks of life with a widening of growth plate parts. Resulting deformation of the bones with incongruity in cartilage surfaces can result in osteoarthritis. The progress might be triggered by moving pigs from a relatively soft plastic floor in the nursery to a hard concrete floor in fattening. Especially heavyweight pigs might suffer from the sudden change in flooring, to which neither claw horn nor joints have been adapted to. The claw lesions found in lame pigs (Fig. 3) support the impact of flooring in this case.
Although the authors suggest, that a trias of three factors as marginal dietary P supply, degenerative joint alterations and joint infection might be responsible for the spectrum of symptoms, so far no connection between the development of OC and an undersupply of calcium or P has been proven [2]. Whether cartilage alterations as shown in these pigs predispose for colonization and infection with M. hyosynoviae is also still hypothetical. Other authors have also considered that OC could predispose joints to infection with M. hyosynoviae [33]. However, these assumptions were also refuted by authors who did not find M. hyosynoviae more frequently in individuals at the slaughterhouse with OC than in individuals without OC [8]. The infection of the joints with M. hyosynoviae can be asymptomatic, but the joints can also be filled macroscopically with a yellow/brownish viscous fluid, which often has an enlarged volume, whereby in chronic cases the joint capsule can be extended [1]. In the present study a mild to moderate lymphoplasma-histiocytic inflammation as well as one fibrino-suppurative synovialitis were detected by histology. A slight increase in synovia volume was found in two of the pigs. While no periarticular edema was present, in one pig surrounding joint tissue was thickened. Infectious arthritis caused by M. hyosynoviae often results in decreased profitability due to higher medication costs and time-consuming measures to be taken, as e.g. separation of diseased pigs in recovery pens. This infectious agent is in addition further impairing skeletal health in fatteners, which is an important welfare issue [2]. Due to the differing outcome of infection the identification of other trigger factors in affected farms is of high importance.