THERE are plenty of stories relating to how and why large snapper tend to develop massive knobby bumps on their foreheads. Some stories suggest this might be due to “old man” snapper knocking their heads on underwater obstructions or using their heads to crack open shellfish. Other people seem to favour that affected fish have cancer or some other disease. But as is often the case, the truth can be even stranger than fiction.
The enlargement of particular areas of fish bones is known as hyperostosis, a fancy word that simply means “above normal bone growth”. The condition is not new, it has been observed in fossilised fish and was first described in modern times as far back as 1655. Today, hyperostosis occurs in at least 96 species of mainly marine fishes worldwide in 22 families, but for Australian recreational fishos it’s most commonly seen in snapper, trevallies, and threadfin salmons. Some sharks can also develop abnormal skeletal structures equivalent to hyperostosis in bony fish, though of course the swellings are made of cartilage instead of bone.
The location of the bones that are affected and how they grow appear to be fairly consistent and predictable within a species. For example, the humps on the head and spine of adult snapper (Pagrus auratus) develop as a result of hyperostosis, as do the lumps on the ribs and spinal bones of king threadfin (Polydactylus macrochir).
What is really interesting though is the patterns of abnormal bone growth can be very different, even in very closely related species. For example, hyperostosis is well described in several species of permit (Trachinotus spp.). Within the permits, however, certain species, including one of the aussie permits (snubnosed dart, T. blochii) tend to get bone enlargement only in certain cranial bones, while the Caribbean permit (T. falcatus) and the second aussie permit (oyster cracker, T. anak) exhibit bone enlargement only in the ribs.
Bone enlargement “lumps” can be clearly seen on this fish’s ribs here (centre right).
The cause of hyperostosis is unknown, mainly because it occurs mainly in older wild fish and has never been reproduced under controlled laboratory conditions. However, science has been able to rule out some of the 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 injury or repeated bumping of affected areas during feeding. I have examined several affected fish (snapper and king threadfin) 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 hyperosteosis only occurs in certain fish species which display consistent and characteristic patterns of bone overgrowth, the condition probably has a genetic basis. Certainly it has been found that some sub-populations of Australian snapper are more likely to exhibit hyperostostis than others, which would be consistent with a genetic cause. Hyperostosis in humans can be associated with conditions like diabetes, which requires the affected person to have a genetic disposition for the condition as well as be exposed to environmental triggers to express the genes.
Hence, for 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. Alternatively, other scientists favour a purely genetic cause, pointing out that fish with prominent hyperostosis 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.
Regardless of its cause, hyperostosis doesn’t appear to have any effect on the edibility of a fish, except for the fact it can make badly affected fish pretty hard to fillet!
