Osteopetrosis is a rare group of sclerosing bone dysplasia characterized by diminished skeletal resorption [1] . It was first described by German radiologist Albert Schonberg in 1904. Its hallmark feature of increase bone density as seen on radiography results from abnormality in osteoclast differentiation or function. It is variably referred to as marble bone disease or Albers-Schonberg disease [2] . Osteopetrosis comprises a clinically and genetically heterogeneous group of conditions. Traditionally, the disorder has been divided into two forms, the benign (adult, autosomal dominant) osteopetrosis variety that has autosomal dominant inheritance and present with relatively mild symptoms, and the malignant precocious (congenital, infantile, autosomal recessive) osteopetrosis that has autosomal recessive inheritance and present with severe early symptoms, those affected rarely survive beyond the first decade [3] .

Typical osteopetrosis has the hallmark feature of increase bone mass with related symptoms and signs as a result of increase bone density. Macrocephaly, altered craniofacial morphology, altered modeling and remodeling system, encroachment of bone on bone marrow space and increase bone surface area that can lead to defect on bone marrow system and nervous systems [2] . Autosomal dominant osteopetrosis, was classified into type I and type II according to radiological appearance of the axial skeleton. Autosomal dominant type I is characterized by sclerosis of the skull mainly on the vault and is associated with calvarial thickening. Spine shows little sclerosis apart from the density of the vertebral arches. Autosomal dominant type II, sclerosis is mainly on the base of the skull, and presents with normal calvaria, thickening of vertebral end plates (sandwich-like or rugger jersey appearance) and presence of subcristal sclerosis of pelvic bone (convex arcs of sclerosis parallel to each iliac crest). Type II has high risk of fracture as compared to type I [3] . The mean number of fracture per patient has been reported as 4.4, predominantly involves the long bone [3] . Symptoms vary from fatal with autosomal recessive osteopetrosis to asymptomatic with autosomal dominant osteopetrosis.

Atypical osteopetrosis has typical features of increase bone sclerosis, and other systems are affected. Atypical symptoms vary in severity according to different mutation mechanism, gene and protein involved. Most Intermediate Recessive Osteopetrosis (IRO), type II carbonic anhydrase deficiency and other varieties are considered as atypical osteopetrosis. Type II carbonic anhydrase deficiency is associated with renal tubular acidosis and other symptoms like mental deficiency, hypotonia, apathy and muscular weakness which can be explained by metabolic acidosis [4] .

Of recent, X-link inheritance pattern and intermediate recessive osteopetrosis has been classified to those affected to the degree between severe autosomal recessive osteopetrosis and mild autosomal dominant osteopetrosis. These patients with intermediate recessive osteopetrosis may present with short stature, anaemia, hepatomegaly and multiple fractures depending on severity of the defect [5] .

Some literature classify as classic osteopetrosis, neuropathic osteopetrosis and autosomal recessive osteopetrosis (ARO) with renal tubular acidosis (RTA) [2] . Classification of the condition has been challenging as one disease has different inheritance pattern, different mutation mechanism, gene and protein involved (Table 1).

Autosomal recessive osteopetrosis has estimated incidence of 1 in 250,000 births and autosomal dominant osteopetrosis has an incidence of 5 in 100,000 births. The overall incident is difficult to estimate as a single disease has many genes and different inheritance pattern [6] . Likewise, the presentation and severity of symptoms vary widely, ranging from neonatal onset with life threatening complication to the asymptomatic and those with typical symptoms and those with atypical symptoms. Current more than 10 genes variant have been identified as the cause of osteopetrosis [4] [6] .

In this study, we present three cases of osteopetrosis. It was considered worth reporting these cases and discussing its clinical presentation, treatment options, outcomes and complications. The aim of describing these cases scenario is to help colleagues faced with similar cases.

Prospective single centered Case series study was conducted at Kilimanjaro Christian Medical Center (KCMC) in the Department of Orthopedics. KCMC is Institution of the Good Samaritan Foundation of Tanzania located in Moshi Municipality, North-eastern Tanzania. The hospital has 650 bed capacity and is the second largest consultant zonal referral hospital in the country serving patients from northern and central regions of Tanzania. It is the teaching hospital for the Kilimanjaro Christian Medical University College, which offers undergraduate and post-graduate training.

Three cases were followed up for more than 5 years. All of them attended as outpatient and admitted several time in the course of their management. All of them had a history of recurrent trivial injury that led to fractures, and all of them were subjected to nonoperative treatment for most of their fractures. Two proximal femur fractures were operated on.