Background and aims: The steatotic liver disease (SLD) nomenclature incorporates both alcohol consumption and metabolic risk factors. Yet, histological differences across the SLD spectrum remain unexplored by novel techniques. We aimed to investigate whether fibrosis distribution, inflammation and cellular composition differed between patients with MASLD, MetALD and ALD when deploying a quantitative histological AI tool. Method: Single-centre study in Odense, Denmark. Patients were biopsied at first visit. All patients had confirmed MASLD, MetALD or ALD based on metabolic dysfunction and self-reported alcohol intake and phosphatidylethanol measurements. Patients were matched for age and fibrosis stage. A clinical pathologist at Odense performed initial assessment. LiverExplore (PathAI, Boston, Research Use Only; not for use in diagnostic procedures) extracted quantitative histology features from digital H&E whole slide images. The AI-based pathology tool quantitatively differentiated cell subtypes, including distribution and density of immune cells, ballooned and steatotic hepatocytes and fibroblasts. Further, LiverExplore identified different fibrosis subtypes and amount per tissue. We compared the density of cell types and fibrosis distributions using Kruskal-Wallis with p-value correction for multiple testing. Results: We included 80 patients: 38 MASLD, 20 MetALD, and 22 ALD. Fibrosis stages were distributed as follows (n): F0/1, F1/18, F2/24, F3/27, and F4/10. Mean age was 59 ± 9 years, 72% male. Patients with ALD had substantially more perisinusoidal fibrosis than MASLD and MetALD patients, across both F0–2 and F3–4. Additionally, patients with ALD showed more overall fibrosis, already from earlier stages (F0–2). However, when comparing the densities of injured or healthy hepatocytes and immune cells we found no statistically significant difference between the SLD subgroups. PCA analysis revealed no stratification by fibrosis or SLD subtyping. However, distinct patient clusters emerged according to ballooning, steatosis and lobular inflammation (scored by pathologists) agnostic to SLD subtyping. Conclusion: Patients with ALD exhibit a greater fibrosis burden than MASLD, particularly within the perisinusoidal compartment, compared across similar fibrosis stages. These architectural differences do not appear to be driven by increased immune cell infiltration or greater hepatocyte injury. PCA analysis suggests distinct histopathological subtypes that are not a function of the driving risk factors of disease.