Hyperostosis is a fancy word that means “above normal bone growth”. It’s an unusual condition that only occurs in certain groups of fishes, for reasons that aren’t exactly known. Those who have wondered about those large “knobby” growths on “old man” pink snapper (Chrysophrys auratus), or have cursed those “hard to fillet” king salmon (Polydactylus macrochir) will be familiar with what I am describing. But what is the role of these bony protuberances, and what causes them?
The first point to note is that hyperostosis is relatively rare in the kingdom of fishes. Of the 30,000+ fish species currently swimming in our world’s oceans, lakes and rivers, hyperostosis is known to occur in only around 100 species from 23 (or so) fish families. The relatively narrow range of fish groups affected does not mean that the condition is “new”, however, as hyperostosis has been observed in fossilised fish, and was first described in modern times as far back as 1655.
In Australia, hyperostosis is consistently seen in pink snapper, trevallies, and threadfin salmons, but usually only in larger adult specimens. The location of the bones that are affected and how the bone growths develop appear to be fairly consistent and predictable within a given species. For example, those humps on the head, nose and spine of pink snapper all develop as a result of hyperostosis, as do those lumps on the ribs and spinal bones of king threadfin. What is really interesting though, is the patterns of abnormal bone growth can be very different between different fish species, even when the species themselves are very closely related. Within the permits, for example, hyperostosis tends to occur only in certain cranial bones of one of the Aussie permits (snubnosed dart, Trachinotus blochii), but in contrast the Caribbean permit (T. falcatus) and the second Aussie permit (oyster cracker, T. anak) both exhibit bone enlargement only in the ribs. Why is this so ? Who knows.
For decades scientists have noticed that within each of the susceptible families of fishes, hyperostosis appears to be species-specific. Furthermore, within each species, the condition can be hit and miss, with some individuals displaying hyperostoses, while others may not. The only consistent factor appears to be that in any given affected species, hyperostoses occur more predictably in larger, older fish.
Given this pattern of occurrence, scientific sleuthing has been able to rule out some of the less likely possibilities, putting the most common of the urban myths to rest in the process. The condition occurs in both male and female fish, and is certainly not due to repeated bumping of affected areas during feeding. So its certainly not caused by an “old man” snapper knocking its head on rocks or using its mouth to crack open shellfish. There are several theories as to what causes hyperostosis, including genetic programming, but given the condition occurs mainly in older wild fish, it is difficult to do the required experiments under controlled laboratory conditions in order to definitively prove one thing or another.
I have personally examined quite a few fish (snapper and king threadfin) affected with hyperostosis, and can confirm the opinions of other scientists that the hyperplastic bony tissue growth is not cancerous, nor does it seem to contain any pathogens which might indicate it is caused by a contagious disease-like condition.
Current thinking suggests that because hyperostosis only occurs in certain fish species which display consistent and characteristic patterns of bone overgrowth as fish age, the condition most likely has a genetic basis. Certainly, some subpopulations of Australian snapper are more likely to exhibit hyperostostis than others, which would be consistent with a genetic cause. In humans, hyperostosis can be associated with conditions like diabetes, which requires the affected person to have a genetic disposition for the condition as well as exposure to certain environmental triggers to express the genes. Perhaps the same situation occurs in those species of fish affected by hyperostosis? A genetically encoded hormonal or biochemical anomaly affecting calcium storage or bone remodeling, that may be triggered by certain environmental or nutritional conditions, cannot be ruled out.
Other scientists have pointed out that fish with the most prominent types of hyperostoses tend to be bottom feeders, and that increases in bone mass would be beneficial for these species by providing negative buoyancy, which would assist them during bottom foraging activity. There certainly may be a grain of truth in this theory in the case of the larger threadfin salmon, which are notorious for their hyperostoses, but also have relatively large swim bladders, and hence tend to be “finely tuned” in relation to their buoyancy. Interestingly, both the king threadfin (P. macrochir) found throughout northern Australia, and the world’s largest threadfin, the giant African threadfin (Polydactylus quadrifilis), are known to be quite sensitive to catch and release fishing. Studies have shown a high percentage of larger specimens (which are almost inevitably female fish) lose equilibrium after long fight times and, especially, if they are held out of the water for more than a minute. Given the shallow water (<8 meters) these fish are usually captured from, this temporary “belly up” situation is clearly not a typical barotrauma (pressure damage) situation. In my opinion, it’s more likely due to lactic acidosis causing a small but significant increase in swim bladder volume, when reduced blood pH affects the gas gland via the Bohr and Root effects, as I have previously suggested for swordfish.
Thinking via the lense of natural selection, if threadfin salmon chased any distance by a large predator (e.g. crocs or sharks) tended to go belly up due to lactic acidosis, they would tend to be removed from the gene pool more often than those which have hyperostoses (see the x-ray of a king threadfin captured from Weipa) which might allow them to swim just that bit further before losing equilibrium. In this context, increasing bone density via hyperostoses to nudge buoyancy in favour of the fish during a predator avoidance event would make sense, as it would provide no selective disadvantage, and possibly even an advantage over threadfin without hyperostoses.
But of course, the ecological situation with large threadfin salmon is very different to some of the other hyperostotic species. For example, the oarfish (Regalecus russellii), also exhibits hyperostosis, but these large ribbon-like fish live in the open ocean at depths of 200+ meters without a swim bladder. Clearly their story is very different to that of the threadfin salmon, and in the case of oarfish scientists have suggested that their hyperostoses might be due to repetitive healing of “stress fractures” in the otherwise fragile bones which support their long dorsal swimming fins. By providing a firmer base for the swimming fin, they hypothesised that the hyperostoses in oarfish may provide a slight selective advantage (or at least, no selective disadvantage) by improving fin performance. A similar pathological stress fracture hypothesis was also ventured by scientists working with cleaner wrasse (Labrus bergylta), who suggested the hyperostoses in this species are induced by “chronic mechanical stress”.
So the jury is still out as to why some fish exhibit hyperostosis, while others (including closely related species) do not. Of course, wherever excessive bone growth provides no selective disadvantage, there is no need for these lesions to be caused by any one particular factor. A variety of causes would be just fine, as natural selection facilitates preservation of genes in the gene pool of a given population regardless of whether a selectively neutral characteristic is genetically induced, or not.
This x-ray of a king threadfin salmon shows several spectacular hyperostoses which occur in the usual positions typical of this species. These excessive bone growths may allow the affected threadfin a slightly wider window of exercise to avoid predators before they suffer from buoyancy issues from lactic acid-induced swimbladder hyperinflation. But other fish species with hyperostosis may tolerate this condition for entirely different reasons.
